What is Rheumatoid Arthritis ? Find it Out Here!

What is Rheumatoid Arthritis ? Find it Out Here!

What is Rheumatoid Arthritis ? When we are talking about autoimmune disease it is not about one kind of disease. There are many different types of autoimmune disease or even a hundred. When the body senses danger from a virus infection, the immune system kicks into gear and attacks it. This is called an immune response. In our normal conditions, an immune response cannot be triggered against the cells of one’s own body. Sometimes, healthy cells and tissues are caught up in this response, resulting in autoimmune disease.1 

Autoimmune diseases affect approximately 8% of the population, 78% of whom are women. The reasons for the high prevalence in women are unknown, but circumstantial evidence links autoimmune diseases with preceding infections.4 Autoimmune diseases are the third most common category of disease in the United States after cancer and heart disease; they affect approximately 5%-8% of the population or 14-22 million persons.2  Autoimmune diseases can affect virtually every site in the body, including the endocrine system, connective tissue, gastrointestinal tract, heart, skin, and kidneys. At least 15 diseases are known to be the direct result of an autoimmune response, while circumstantial evidence implicates >80 conditions with autoimmunity.3

Now, we want to discuss one of these autoimmune diseases called Rheumatoid Arthritis(RA). The global prevalence of  RA between 1980 and 2019 was 460 per 100.000 population, with variations due to geographical location and study methodology.5

Also Read What is Sudden Death? is it Necessary to Watch Out?

Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a disease of unknown origin, which is characterized by inflammatory(redness, swelling, pain, tenderness, heat, and disturbed function of an area of the body, especially as a reaction of tissue injury)  changes of the synovial tissue of joints, of cartilage and bone and, less frequently, of extra-articular(means outside of or other than a joint)sites. Somehow people can’t make the difference between arthritis and rheumatoid arthritis. Whenever there’s joint pain, there must be rheumatoid arthritis, is a big NO. 

The fact is not every arthritis was an autoimmune disease. For example: Rheumatoid arthritis and osteoarthritis  both cause joint pain, stiffness and limited range of motion, but the two diseases are distinct in their root cause and treatment. RA is a complex disease that affects approximately 0,5% of the adult population worldwide, and occurs in 20-50 cases per 100.000 annually, mainly in women after their 40s.5

Sign & Symptoms

RA commonly involves multiple joints of both hands with morning stiffness that may last for several hours. It has symptom duration of fewer than six months is defined as early, and when the symptoms have been present for more than months, it is defined as established.6,7,8

There are times when symptoms get worse, known as flares, and times when symptoms get better, known as remission. Sign and symptoms of RA include:9

  • Pain or aching in more than one joint
  • Stiffness in more than one joint
  • Tenderness and swelling in more than one joint
  • The same symptoms on both sides of the body (such as in both hands or both knees)
  • Weight loss
  • Fever 
  • Fatigue or tiredness
  • Weakness

Risk Factor

An autoimmune disease like rheumatoid arthritis, something goes awry. Instead of protecting the body from infection or disease as it normally does the immune system attacks and destroys the body’s healthy tissue. When the disease affects many organs, as in lupus, it’s called a systemic autoimmune disease.  

Researchers had found many mechanisms that cause the risk of RA. And here some characteristics that increase risk of having RA :9

  • Age: RA can happen at any stage of your life, but likelihood increases with age. The onset of RA is highest among adults in their sixties.
  • Sex: New cases of RA are typically two-to-three times higher in women than men.
  • Genetics/inherited traits: there are specific genes that more likely this person will develop RA. These genes, called HLA /Human Leukocyte Antigen class II genotypes, can also make your arthritis worse. This risk of RA may be highest when people with these genes are exposed to environmental factors like smoking or when a person is obese. 
  • Smoking: multiple studies show that cigarette smoking increases a person’s risk of developing RA and can make the disease worse.
  • History of live births: women who have never given birth may be at greater risk of developing RA.
  • Early life exposures: some early life exposures may increase risk of developing RA in adulthood.10 For example: one study found that children whose mothers smoked had double the risk of developing RA as adults. 
  • Obesity: Being obese can increase the risk of developing RA. 

If there are some characteristics that can cause people to develop RA. Is there any characteristic that could be decreasing the risk???


Breastfeeding women: In a new study of over 7,000 older Chinese women published online today in the journal Rheumatology, breastfeeding especially for a longer duration is shown to be associated with a lower risk of rheumatoid arthritis (RA). Specifically, it showed that women who had breastfed their children were around half as likely to have RA, compared to women who had never breastfed.11

Figure 1. Bone joint differentiation of normal and Rheumatoid arthritis the pathophysiological mechanism of rheumatoid arthritis and the immune response involves a sequence of events. (Source: Pradeepkiran, Jangampalli Adi. Insight of rheumatoid arthritis risk factors and associations. Elsevier: Journal of Translational Autoimmunity. August 2019.)

Diagnostic & Treatment

There is no specific test for diagnosis of RA. In 2010, the American College of Rheumatology and European League Against Rheumatism collaborated to create new classification criteria for RA. The 2010 new criteria rates on a scale from 0-10 points were assigned in four separate domains of signs and symptoms namely:1) joint involvement 2) serology 3) duration of symptoms 4) acute phase reactants. Patients are definitely diagnosed with RA if they score 6 or more points according to the following criteria. This criteria can be applied to any patient with and there is no explanation for synovitis which can not be attributed to other entities and there is no explanation for synovitis.13 

Many rheumatic conditions can be diagnosed or suspected based on taking history and physical examination. Sometimes, diagnosis of RA maybe possible based on clinical grounds alone, nevertheless there are no disease-specific clinical features or laboratory tests to be diagnostic for RA.14 Early symptoms of RA may appear as vague pain with gradual appearance without classic symptoms of joint swelling or tenderness. Prolong duration of morning stiffness with arthralgia , or arthritis in a limited number of joints may be a clue for considering RA diagnosis.15 

The therapy is complex and includes different classes of drugs with different routes of application but also non drugs interventions. The most important are patient education followed by exercise and physical and occupational therapy. Patient and the medical staff must go together to get the goal of the treatment. Because of an increased risk of coronary atherosclerosis, efforts should be made to reduce risk factors such as smoking, hyperlipidemia , hypertension, and obesity. To relieve pain and swelling fast and to gain control of the inflammation, glucocorticoids  are used widely in acute disease flares either orally or as joint injections .16 Oral glucocorticoid is for short-term use (up to 3-4 month) only should be tapered to prevent side effects as soon as possible.17 To control inflammation in the long run, Disease Modifying Anti-Rheumatic Drugs (DMARD) to spare glucocorticoid are needed. 


  1. https://www.hopkinsmedicine.org/health/wellness-and-prevention/autoimmune-disease-why-is-my-immune-system-attacking-itself.  Access: 24 June 2021
  2. National Institutes of Health Autoimmune Disease Coordinating Committee Report 2002. Bethesda (MD): The Institutes; 2002.
  3. Rose NR An immunology primer. In: Morton CC, Fagan T, editors. Proceedings from Sex Differences in Immunology and Autoimmunity, Society for Women’s Health Research, Boston, MA, 8 Nov 2001. Washington: Society for Women’s Health Research; 2002. p. 7–9.
  4. Women and Autoimmune Diseases. DeLisa Fairweather, Noel R. Rose. Emerg Infect Dis. 2004 Nov; 10(11): 2005–2011. doi: 10.3201/eid1011.040367. PMCID: PMC3328995
  5. Almutairi K, Nossent J, Preen D, Keen H, Inderjeeth C. The global prevalence of rheumatoid arthritis: a meta-analysis based on a systematic review. Rheumatol Int. 2021 May;41(5):863-877. doi: 10.1007/s00296-020-04731-0. Epub 2020 Nov 11. PMID: 33175207.
  6. Carbone F, Bonaventura A, Liberale L, Paolino S, Torre F, Dallegri F, Montecucco F, Cutolo M. Atherosclerosis in Rheumatoid Arthritis: Promoters and Opponents. Clin Rev Allergy Immunol. 2020 Feb;58(1):1-14.
  7. Cai Q, Xin Z, Zuo L, Li F, Liu B. Alzheimer’s Disease and Rheumatoid Arthritis: A Mendelian Randomization Study. Front Neurosci. 2018;12:627.
  8. Voigt A, Seipelt E, Bastian H, Juche A, Krause A. [Improved early diagnostics of rheumatic diseases : Monocentric experiences with an open rheumatological specialist consultation]. Z Rheumatol. 2018 Nov;77(9):844-849
  9. Rheumatoid Arthritis. Access: https://www.cdc.gov/arthritis/basics/rheumatoid-arthritis.html
  10. Colebatch AN, Edwards CJ. The influence of early life factors on the risk of developing rheumatoid arthritis. Clin Exp Immunol. 2011;163(1):11-16. doi:10.1111/j.1365-2249.2010.04263.x
  11. Oxford University Press (OUP). “Breastfeeding is associated with a lower risk of rheumatoid arthritis, according to a new study.” ScienceDaily. ScienceDaily, 7 January 2014. <www.sciencedaily.com/releases/2014/01/140107093037.htm>.
  12. Pradeepkiran, Jangampalli Adi. Insight of rheumatoid arthritis risk factors and associations. Elsevier: Journal of Translational Autoimmunity. https://doi.org/10.1016/j.jtauto.2019.100012. August 2019.
  13. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative.Aletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd, Birnbaum NS, Burmester GR, Bykerk VP, Cohen MD, Combe B, Costenbader KH, Dougados M, Emery P, Ferraccioli G, Hazes JM, Hobbs K, Huizinga TW, Kavanaugh A, Kay J, Kvien TK, Laing T, Mease P, Ménard HA, Moreland LW, Naden RL, Pincus T, Smolen JS, Stanislawska-Biernat E, Symmons D, Tak PP, Upchurch KS, Vencovský J, Wolfe F, Hawker G. Arthritis Rheum. 2010 Sep; 62(9):2569-81.
  14. Heidari, Behzad. “Rheumatoid Arthritis: Early diagnosis and treatment outcomes.” Caspian journal of internal medicine vol. 2,1 (2011): 161-70.
  15. Emerging trends in diagnosis and treatment of rheumatoid arthritis.. Birch JT Jr, Bhattacharya S. Prim Care. 2010 Dec; 37(4):779-92, vii.
  16. Kohler M.Birgit, Gunther Janine, Kaudewitz Dorothee, Martin Lorenz-Hanns. Current Therapeutic Options in the Treatment of Rheumatoid Arthritis. J. Clin. Med. 20198(7), 938; https://doi.org/10.3390/jcm8070938
  17. Hoes, J.N.; Jacobs, J.W.G.; Boers, M.; Boumpas, D.; Buttgereit, F.; Caeyers, N.; Choy, E.H.; Cutolo, M.; Silva, J.A.P.D.; Esselens, G.; et al. EULAR evidence-based recommendations on the management of systemic glucocorticoid therapy in rheumatic diseases. Ann. Rheum. Dis. 200766, 1560–1567.
Becker’s Nevus Syndrome, What kind of Syndrome is This?

Becker’s Nevus Syndrome, What kind of Syndrome is This?

Becker’s Nevus Syndrome – A simple nevus but many distributed to our body may not be so disturbing. But, how could it be? If those nevus appeared only on one side of your body following hypertrichosis?

Becker’s nevus syndrome (BNS) is characterized by the simultaneous occurrence of a circumscribed patch of light or dark brown hyperpigmentation with a sharply outlined but irregular border (resolving into small spots reminiscent of an archipelago) and hypertrichosis (the so-called Becker’s nevus).1,2 

Becker’s nevus was first described  by Becker in 1949. Happle in 1997, described Becker’s nevus syndrome or hairy epidermal nevus syndrome, where BNS was associated with multiple skin and musculoskeletal(is made up of bones, muscles, joints, tendons and ligaments which all work together to provide the body)  abnormalities, mostly on the same side. Becker nevus usually presents as numerous macules, especially located unilaterally(only on one side) on the trunk and shoulders. It mostly appears in the adolescent period, being five times more frequent in men than in women.3

Also Read What is Sudden Death? is it Necessary to Watch Out?


1. Skin Manifestation

The nevus is characterized by the presence of light or dark brown macule with a sharply outlined but irregular and bizarre borders that resolve into small spots reminiscent of an archipelago.4 Becker’s Nevus mainly appears in the first and second decades of life, sometimes after sun exposure, and it is rarely described at birth. 

Most lesions are one side of the body area, localized to the upper quadrant of the chest and shoulder, but they can be found on any area of the body including the forehead, face, neck, lower, trunk, extremities, and buttocks.5,6,7   After its appearance, Becker’s Nevus may grow for a year or two but then remains fixed in size. In the course of time, pigmentation can fade however.6

2. Breast Manifestation

Another Becker’s nevus manifestation has reported in some cases unilateral hypoplasia(incomplete development/underdevelopment of an organ or tissue) of the breast. Both men and women are equal in prevalence, but this manifestation is more seen in women. 

A case report: A 24-year old woman was presented with a brown discoloration which initially appeared as a little spot on her left breast 11 years ago and then expanded with time. IN addition, the underlying left breast tissue had not grown during the peripubertal period(the 40-60 days period before first ovulation when a majority of these dynamic changes occur is referred to as the peripubertal period). From USG and MRI of the left breast showed hypoplasia.8 

3. Maxillofacial  Abnormalities

A case of 14-year-old boy with Becker’s nevus presented with abnormal symptoms including an asymmetric face, hemi maxillary enlargement, and abnormal teeth, all constituents of HATS syndrome.9 HATS or hemi maxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings is a rare developmental disorder involving the first and second branchial arches.

4. Maxillofacial  Abnormalities

Bone and muscle anomalies are frequently observed. They can include scoliosis(is a medical condition in which a person’s spine has a sideways curve. The curve is usually “S”- or “C”-shaped over three dimensions.). Vertebral defects (including hemivertebrate  and spina bifida occulta, fused or accessory cervical ribs(A cervical rib is an extra rib that forms above the first rib, growing from the base of the neck just above the collarbone), pectus excavatum (is a condition in which a person’s breastbone is sunken into his or her chest)  or carinatum (or pigeon chest is when part of your child’s breastbone is pressed outwards or raised up), asymmetry of scapulae(also known as the shoulder blade), short limb or other forms of limbs asymmetry, bilateral tibial torsion(is the twisting of a child’s shinbone, also known as the tibia and caused a toddler’s legs and feet to turn inward, giving them a pigeon-toed appearance), ipsilateral hypoplasia of the shoulder girdle (including absence of the pectoralis major muscle/large muscle in the upper chest, fanning across the chest from the shoulder to the breastbone), hypoplasia of the sternocleidomastoid muscle, and umbilical hernia.10, 11, 12, 13

5. Other Anomalies

A 15- year old female patient presented with a large dark-colored patch over genitals, upper and inner aspects of both the thighs, and in front of the neck.

The lesions started at the age of 5 years. The lesions were smaller in size initially and they gradually increased. The patients started walking and speaking at the age of 5 years. She was a dwarf, deaf, and had not attained her menarche.14

What caused Becker’s Nevus Syndrome ?

The exact cause of Becker’s Nevus remains unclear. There are 2 main hypotheses concerning this disorder. First, genetics. Genetic associates the syndrome with the occurrence of a postzygotic autosomal fatal mutation(is a change in an organism’s genome  that is acquired during its lifespan, instead of being inherited from its parents through fusion of two haploid gametes  that can “survive” only in a mosaic pattern: it is corroborated by the fact that the majority of cases are sporadic and familial grouping is very rare, similar to what happens in other neurocutaneous phenotypes.

The second hypothesis states that BNS is a hormone-dependent disorder; this theory is based on the increased number of androgen receptors  in the affected areas: for this reason, the appearance of lesions is more frequent in puberty, and alteration such as hypertrichosis and acneiform eruptions are restricted to the regions.15, 16, 17, 18 


There is no special treatment for treating BNS. Therefore, patients should be recommended to come to regular clinical follow up to examine whether any associated abnormalities are developed in time. Although patients may feel significantly disturbed because of the conspicuousness of BNS, therapeutic modalities are limited. The treatment is essentially cosmetic. Potential therapeutic options include electrolysis , waxing, makeup, or laser treatment.19

There is also medication that is used for treating hormonal problems such as Spironolactone . Spironolactone is an antiandrogen used in other dermatological diseases due to the hormonal action. In relation to breast hypoplasia, its action is not fully understood but has been proposed to respond to negative feedback of androgen receptors. In a dosage of 50 mg/day, improvement of breast hypoplasia has been described.20

In some cases, breast hypoplasia and bone abnormalities, such as scoliosis, were corrected surgically.21


  1. Tymen R, Forestier JF, Boutet B, Colomb D. Late Becker’s nevus. One hundred cases [article in French]. Ann Dermatol Venereol 1981;108(01):41–46
  2. Danarti R, König A, Salhi A, Bittar M, Happle R. Becker’s nevus syndrome revisited. J Am Acad Dermatol 2004;51(06):965–969)
  3. Cosendey FE, Martinez NS, Bernhard GA, Dias MF, Azulay DR. Case Report Becker nevus syndrome. An Bras Dermatol. 2010;85:3.
  4. Cucuzza et al. Becker’s Nevus Syndrome. Journal of Pediatric Neurology. 2018. DOI https://doi.org/ 10.1055/s-0038-1667168. ISSN 1304-2580.)
  5. Van Gerwen HJ, Koopman RJ, Steijlen PM, Happle R. Becker’s nevus with localized lipoatrophy and ipsilateral breast hypoplasia. Br J Dermatol 1993;129(02):213)
  6. Rasi A, Berenji AH, Tabaie SM. Hypertrichosis is not so prevalent in Becker’s nevus: nevus: analysis of 47 cases. IRSN Dermatol 2014;201:953747. doi: 10.1155/2014/953747)
  7. Fegeler F, Schreiner H. Familiäres Vorkommen von systematisierten Pigmentnaevi mit circumscripter Sklerodermie im gleichen Hautsegment. Hautarzt 1954;5(06):253–255)
  8. Suzan Demir Pektas, Gulsen Akoglu, Ahmet Metin, Nuran Sungu Adiyaman, Mustafa Erol Demirseren. Indian J Dermatol. 2014 Nov-Dec; 59(6): 634. doi: 10.4103/0019-5154.143587. PMCID: PMC4248539)
  9. HATS syndrome: hemi maxillary enlargement, asymmetry of the face, tooth abnormalities, and skin findings.Al Shaiji JM, Handler MZ, Huo R, Freedman A, Schachner LA. Cutis. 2014 Oct; 94(4):E18-21.)
  10. Happle R, Koopman RJ. Becker nevus syndrome. Am J Med Genet 1997;68(03):357–361)
  11. Sugarman JL. Epidermal nevus syndromes. Semin Cutan Med Surg 2004;23(02):145–157)
  12. Ruggieri M, Pavone V, Polizzi A, et al. Tuberculosis of the ankle in childhood: clinical, roentgenographic and computed tomography findings. Clin Pediatr (Phila) 1997;36(09):529–534)  
  13. Sorge G, Ruggieri M, Polizzi A, Scuderi A, Di Pietro M. SHORT syndrome: a new case with probable autosomal dominant inheritance. Am J Med Genet 1996;61(02):178–181)
  14. (Becker’s Nevus Syndrome. Sathyanarayana B Dasegowda, GB Basavaraj, KC Nischal, MR Swaroop, NP Umashankar, Suchetha S Swamy. Indian J Dermatol. 2014 Jul-Aug; 59(4): 421. doi: 10.4103/0019-5154.135530PMCID: PMC4103296)
  15. Ruggieri M, Praticò AD. Mosaic neurocutaneous disorders and their causes. Semin Pediatr Neurol 2015;22(04): 207–233)
  16. Ruggieri M, Iannetti P, Pavone L. Delineation of a newly recognized neurocutaneous malformation syndrome with “cutis tricolor”. Am J Med Genet A 2003;120A(01):110–116)
  17. Lionetti E, Pavone P, Kennerknecht I, et al. Neurological manifestations in individuals with pure cutaneous or syndromic (Ruggieri-Happle syndrome) phenotypes with “cutis tricolor”: a study of 14 cases. Neuropediatrics 2010;41(02):60–65
  18. 4 Wagner RF Jr, Grande DJ, Bhawan J, Hellerstein MK, Longcope C. Unilateral dermatomal superficial telangiectasia overlapping Becker’s melanosis. Int J Dermatol 1989;28(09):595–596) 
  19. Metelitsa A, Rohrer T, Arndt KA. Laser and light therapy for cutaneous hyperpigmentation. UpToDate. 2017. Available at: https://www.uptodate.com/contents/laser-and-light-therapyfor-cutaneous-hyperpigmentation. Accessed December 18, 2017
  20. Taheri A, Mansoori P, Sandoval LF, Feldman SR. Treatment of Becker nevus with topical flutamide. J Am Acad Dermatol 2013; 69(03):e147–e148
  21. 5 Ruggieri M, Praticò AD, Evans DGE. Diagnosis, management and new therapeutic options in childhood neurofibromatosis type 2 and related disorders. Semin Pediatr Neurol 2015;22(04):240–258
What is Sudden Death? is it Necessary to Watch Out?

What is Sudden Death? is it Necessary to Watch Out?

What is Sudden Death? People nowadays are more critical yet still not knowing much about medical or medical term in the medics problem. The term that I want to bring up right now is about sudden death. People said the sudden death was someone who experienced an unexplained condition before death, or death while they’re sleeping. 

From American Heart Association journal, sudden death has come into the focus of the discussion on ischemic heart disease (IHD). At the present time, the meaning of the attribute “sudden” in this context is subject to considerable variation, ranging from death occurring within a few minutes to death within 24 hours2 of the onset of acute symptoms.   

In adults, the most common cause of sudden death is coronary heart disease or defects in the cardiac conduction system3 however there are some cause of sudden death is not from cardiac problems.

Data from Open Heart Journal in North Carolina(U.S) by following adjudication, 190 sudden unexpected deaths including 122 men and 68 women were identified. Estimated incidence was 32,1 per 100.000 person/years overall: 42,7 among men and 22,4 among women. The majority of victims were white, unmarried men over age 55 years, with unwitnessed deaths at home. Women who were under age 55 years with coronary disease accounted for over half of female participants with coronary artery disease. Hypertension and dyslipidemia were common in men and women.4

Also Read What Is Irritable Bowel Syndrome? What is The Cause?


Sudden death is a sudden, natural and unexpected death: in witnessed cases as an acute change in cardiovascular status with time to death being <1 hour and in un-witnessed cases as a person last seen alive and functioning normally <24 hours before being found dead. 


In one retrospective study assessed the underlying causes of sudden unexpected death in 162 subjects (aged 9 to 39 years) over 10-years period (1976 to 1985). In this study they divided into 3groups there are Cardiac, Non-cardiac causes and Unidentifiable causes in subjects aged <20 years the major underlying causes were Myocarditis , hypertrophic cardiomyopathy  and conduction system abnormalities . In subject aged ≥30 years the most frequent cause is coronary artery disease  followed by myocarditis. In the 20-29 year old age group, coronary artery disease and myocarditis were the most frequent causes, followed by hyperthrophic cardiomyopathy. The noncardiac cause happened to 8 subjects with Intracranial hemorrhage  as the most common cause. The hemorrhage(bleeding) was intra cerebral(brain) in 4 subjects, subarachnoid  in 3 and combined in 1. Circle of Willis  aneurysm (is weakening and bulging of an artery wall) was identified only in 1 of 8 subjects. Glioblastoma multiform  accounted for intracranial bleeding  in 1 younger subject.5In 6 subjects, infectious disease, mostly respiratory tract infection. Cardiac causes of sudden death were more frequent in men (105 of 134 [78%]) than in women (13 of 28 [46%]; p <O.Ol). Non-cardiac causes were more often encountered in women (11 of 28 [39%]) than in men (14 of 134 [IO%]; p <O.Ol).5

Coronary artery disease is the most common cause of sudden cardiac death, accounting for up to 80% of all cases. The most common causes of non-ischemic sudden cardiac death are cardiomyopathy  related to obesity, alcoholism, and fibrosis .6 Another resource that I found, there are 6 case reports have been published linking recent use of cannabis with sudden death.7,8 

Can Sudden Death be Prevented ?

Since this can occur people even seem to be in good health, so prevention is too difficult. However, as explained above, the most frequent cause is heart problems so everyone must know how to live a healthy life. 

Here’s what you should know: if there is a person in your family history who died with heart problems before, or having hypertension (high blood pressure), cholesterol problem or diabetes (high blood glucose level) or even obesity, you should care more about your future. Unexplained death wasn’t completely unknown, if there is a risk factor that can be the trigger. If you are the one who has those risk factors, you should have a routine medical check-up, control your diet, and keep a good and healthy lifestyle. 


  1. Working Group on Ischaemic Heart Disease Register, Report (Part I). Copenhagen, World Health Organization, Regional Office for Europe, 1969
  2. Sudden Unexpected Death. Suggestion for Classification Adopted by the International Society of Cardiology, Geneva, 1969
  3. Aquilla, Isabella PhD,MD; Boca,Silvia MD; Caputo, Fiorella MD; Sacco, Matteo A. MD; Gratteri, Santo PhD, MD; Fineschi, Vittorio PhD, MD; Ricci, Pietrantonio PhD, MD. An Unusual Case of Sudden Deathh Is There a Relationship Between Thyroid Disorders and Fatal Pulmonary Thromboembolism? A Case Report and Review of Literature. The American Journal of Forensic Medicine and Pathology. September 2017. Vol 38, Issue 3. P 229-232. DOI: 10.1097/PAF0000000000000317
  4. Lewis ME, Lin F-C, Nanavati P, et al. Estimated incidence and risk factors or sudden unexpected death. Open Heart 2016; 3:e000321.doi:10.1136/openhrt-2015-000321
  5. Drory Y, Turetz Y, Hiss Y, Lev B, Fisman EZ, Pines A, Kramer MR. Sudden unexpected death in persons less than 40 years of age. Am J Cardiol. 1991 Nov 15;68(13):1388-92. doi: 10.1016/0002-9149(91)90251-f. PMID: 1951130.
  6. Yow AG, Rajasurya V, Sharma S. Sudden Cardiac Death. [Updated 2020 Aug 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507854/ 
  7. A.M. Dines, D.M. Wood, M. Galicia, C.M. Yates, F. Heyerdahl, K.E. Hovda, I. Giraudon, R. Sedefov, D.E.N.R.G. Euro, P.I. Dargan, Presentations to the emergency department following cannabis use—a multi-centre case series from ten European countries, J. Med. Toxicol. 11 (4) (2015) 415–421.
  8. J. Orsini, C. Blaak, S. Rajayer, V. Gurung, E. Tam, J. Morante, B. Shamian, R. Malik, Prolonged cardiac arrest complicating a massive ST-segment elevation myocardial infarction associated with marijuana consumption, J. Community Hosp. Intern. Med. Perspect. 6 (4) (2016) 31695.
World Blood Cancer Day – Leukaemia

World Blood Cancer Day – Leukaemia

Cancer was the scariest diagnosis that people can hear. May 28 became the world blood cancer day, which is a global day of awareness dedicated to the fight against blood cancer. 

The World Health Organization in 2019 estimated that cancer is the first or second leading cause of death before the age of 70 years in 112 of 183 countries and ranks third of fourth in further 23 countries.1,2 Between 30 and 50%of cancers can currently be prevented by avoiding risk factors and implementing existing evidence-based prevention strategies. Many cancers have a high chance of cure if diagnosed early and treated appropriately. Many of the known risk factors for cancer can be prevented. Tobacco use, infectious agents, unhealthy diet, excess body weight, physical inactivity, and alcohol consumption account for the majority of cancer deaths caused by known factors.3 

According to the Global Cancer Observatory in 2018, World Health Organization reports deaths in Indonesia caused by Leukemia was 11.314 people.

Also Read Fact About Baldness That You Must Know!


Figure 1: National ranking of Cancer as a Cause of Death at Ages <70 Years in 2019. The numbers of countries represented in each ranking group are included in the legend. Source: World Health Organization.4

Blood Cyclopedia

Blood is a body fluid in humans that delivers necessary substances such as nutrients and oxygen to the cells and transports metabolic waste products away from those same cells. Blood performs many important functions within the body, including:5  

  • Supply of oxygen to tissues (bound to hemoglobin , which is carried in red cells)
  • Supply of nutrients such as glucose, amino acids , and fatty acids 
  • removal of waste such as carbon dioxide, urea , and lactic acid 
  • immunological functions, including circulation of white blood cells , and detection of foreign material by antibodies 
  • Coagulation , the response to a broken blood vessel, the conversion of blood from a liquid to a semisolid get to stop bleeding
  • Messenger functions, including the transport of hormones  and the signaling of tissue damage
  • Regulation of core body temperature

Blood also has 4 main parts:7 

  1. Blood Plasma: is yellowish liquid component of blood that holds the blood cells, proteins and other constituents of whole blood in suspension.6 Plasma function is to transports nutrients, waste products, and proteins, and other molecules responsible for affecting the function of various parts of the body, including regulating body temperature and fluid balance.
  2. Red Blood Cells: the cells responsible for transporting oxygen to lungs and tissue.
  3. White Blood cells: The cells responsible for protecting against infections.
  4. Platelets: The cells that form blood clots and prevent blood loss. 

Blood Cancer Definition

Blood cancer is a complex group of disease linked by their origins in the bone marrow , where blood is produced. Blood cancer arises from abnormalities in the blood cells affect normal blood cell production and function. 

Then, why is there blood cancer ?

It is important to know that every second of every day a person’s body is replenishing its cells, including its blood cells, by making and destroying old ones. A person’s body can make the right number of each type of cell to keep the person healthy. To make blood cells, stem cells(basic material cell) in the bone marrow mature and develop into one of four types(blood plasma, red blood cells, white blood cells, and platelets) of blood cells. 

If the DNA in the stem cells that tells the body how to make blood cells changes (mutates), these blood cells might start to develop abnormality, or fail to die when they should. These are the “cancerous” cells that cause blood cancer. These abnormal blood cells prevent the blood from performing many of its usual functions, like fighting off infections, bringing oxygen to other tissues or helping to repair the body. 

Blood cancer is a complex group of disease linked by their origins in the bone marrow , where blood is produced. Blood cancer arises from abnormalities in the blood cells affect normal blood cell production and function. 


Leukaemia are a group of hematologic disorders characterized by the dysfunction proliferation and development of leukocytes . They classified as acute or chronic, according to the degree of cell differentiation and as myelocytic  or lymphocytic  according to the predominant type of cell involved. Symptoms are nonspecific and can include fever, fatigue, weight loss, bone pain, bruising, or bleeding. Definitive diagnoses often require bone marrow biopsy , the result of which inform interprofessional treatment ranging from chemotherapy  to stem cell transplantation. 

Leukaemia has 2 major classification and 4 major subtypes.

  • Acute vs Chronic : acute leukemias are characterized by abnormal cells that are less mature, develop quickly, and leave the bone marrow as dysfunctional cells called “blasts (immature cells)”. These blasts crowd out healthy cells in the bone marrow , causing the rapid onset of symptoms. Blasts normally make up 1%$ top 5% of marrow cells, and having more than 20% blasts in the bone marrow is required for a diagnosis of acute leukemia. In contrast, chronic leukemias develop slowly and may take years to develop symptoms. They are composed primarily of more mature and functional cells and there are generally not elevated numbers of blasts.
  • Myeloid vs. Lymphoid : Hematopoietic stem cells  give rise to two types of blood cells: myeloid and lymphoid . Myeloid cells  include monocytes , macrophages , neutrophils , basophils , eosinophils , erythrocytes/red blood cells, and megakaryocytes .   
  • Acute lymphoblastic leukemia (ALL): ALL occurs when primitive white blood cells of lymphoid origin reproduce without developing into normal B and T cells. It is the most common leukemia in pediatrics, accounting for up to 80% of cases in this group vs. 20% of cases in adults.
  • Acute myelogenous leukemia (AML): AML is also characterized by the hyperplasia  of blasts, but in this case, of myeloid origin. It accounts for half of the leukemia cases diagnosed in teenagers and people in their 20s. It is the most common acute leukemia in adults.
  • Chronic lymphocytic leukemia (CLL): CLL occurs when mature but abnormal white blood cells of lymphoid origin undergo hyperplasia, leading to a monoclonal population  of dysfunctional lymphocytes. Most cases occur in people between ages 60 and 70.
  • Chronic myelogenous leukemia (CML): A monoclonal population of self-renewing, dysfunctional myeloid cells (e.g., neutrophils, basophils, eosinophils, macrophages) characterizes CML. Most cases occur in people between ages 25 and 60.

Several Risk Factors are associated with a higher risk of developing leukemia: Exposure to ionizing radiation is associated with an increased risk of multiple subtypes of leukemia; Exposure to benzene is a risk factor for leukemia in adults, particularly AML12; Previous exposure to chemotherapy, especially alkylating agents  and topoisomerase inhibitors , increase the risk for acute leukemia later in life10,11 ; A history of any hematologic malignancy is a risk factor for subsequently developing another subtype of leukimia13; Viral Infections (e.g., human T-cell leukemia virus, Epstein Barr virus) are linked with subtypes of ALL13;Several genetic syndromes (e.g., Down syndrome, Fanconi anemia() , Bloom syndrome , Li-Fraumeni syndrome ) are associated with an increased risk of AML and ALL14.


Leukaemia and other blood cancers are usually not easily caught. The symptoms of it are not special so we also consider other differential diagnoses. One must rule out infection, drug effects, vitamin/micronutrient deficiencies, and other myelodysplastic disorders that can cause abnormalities in blood cell lines. These some of condition that you must be considered due to abnormalities on your blood count: B12 and folate deficiencies, Copper deficiencies, Viral infections (e.g., HIV, Cytomegalovirus, Epstein Barr virus), Drugs (chemotherapeutic agents, valproic acid, ganciclovir , myocophenolate mofetil ), Autoimmun  conditions (e.g., systemic lupus erythematosus


We must understand that cancer is not one disease, but many, influenced by genetic mutations that affect both disease development and treatment options. For blood cancer, there are 2 main model therapies. 1called Curative therapy and the other one called Palliative therapy. 

Chemotherapy and radiotherapy was included in curative and palliative treatment to cure blood cancer. Curative therapies aim to cure the disease. These treatments eliminate the blood cancer cells, whereas palliative treatments ease the pain caused due to symptoms, but not actually remove the cancer.  

Now, the advance technology, science, and medication has been approved to help the treatments for blood cancer such as CAR-T , CRISPR technologies , PARP inhibitors . We also hope that every kid and adult who has this kind of disease can be manageable and we can also reduce the recurrence.


  1. World Health Organization (WHO). Global Health Estimates 2020: Deaths by Cause, Age, Sex, by Country and by Region, 2000-2019. WHO; 2020. Accessed December 11, 2020. who.int/data/gho/data/themes/mortality-and-global-health-estimates/ghe-leading-causes-of-death
  2. Bray F, Laversanne M, Weiderpass E, Soerjomataram I. The ever-increasing importance of cancer as a leading cause of premature death worldwide. Cancer. In press.
  3. Jemal,Ahmedin. Torre,Lindsey. Soerjomataram, Isabelle. Bray, Freddie. The Cancer Atlas. American Cancer Society. 2019. P 18
  4. Sung, H, Ferlay, J, Siegel, RL, Laversanne, M, Soerjomataram, I, Jemal, A, Bray, F. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2021: 71: 209- 249. https://doi.org/10.3322/caac.21660
  5. https://en.wikipedia.org/wiki/Blood Access: 26 May 2021
  6. https://en.wikipedia.org/wiki/Blood_plasma Access: 26 May 2021
  7. https://www.yalemedicine.org/conditions/blood-cancers#:~:text=Leukemia%3A%20Your%20doctor%20will%20obtain,be%20examined%20under%20a%20microscope. Access: 26 May 2021
  8. State of the Nation: Blood Cancer in Australia. Final Report to the Leukaemia Foundation. February 2019. Page 1-2
  9. Lyengar V, Shimanovsky A. Leukemia. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560490/
  10. Bispo JAB, Pinheiro PS, Kobetz EK. Epidemiology and Etiology of Leukemia and Lymphoma. Cold Spring Harb Perspect Med. 2020 Jun 01;10(6)
  11. Miranda-Filho A, Piñeros M, Ferlay J, Soerjomataram I, Monnereau A, Bray F. Epidemiological patterns of leukaemia in 184 countries: a population-based study. Lancet Haematol. 2018 Jan;5(1):e14-e24.)
  12. Snyder R. Leukemia and benzene. Int J Environ Res Public Health. 2012 Aug;9(8):2875-93.
  13. Davis AS, Viera AJ, Mead MD. Leukemia: an overview for primary care. Am Fam Physician. 2014 May 01;89(9):731-8.
  14. Stieglitz E, Loh ML. Genetic predispositions to childhood leukemia. Ther Adv Hematol. 2013 Aug;4(4):270-90.)

Covid-19 Variants in Indonesia and How is it?

Covid-19 Variants in Indonesia and How is it?

The latest headline news in Indonesia recently was that the Ministry of Health stated that they found new Covid-19 variants in Indonesia, mutated strains of the coronavirus that cause COVID-19. The variation of new COVID-19 strains are widely happening around the world. 

The Indonesia Ministry of Health has announced on May 4th that new corona virus variants have already entered Indonesia, such as B.1.1.7 ; B.; and B. Press secretary of Indonesian Ministry of Health said  3 types of variants classified with Variant of Concern (VoC) that are aware of these types and this variant B.1.1.7 is known to have a higher transmission rate approximately 36 to 75 percentage compared to other strains of virus previously.1 The distribution of new Covid-19 variants in Indonesia includes 1 case variant type B.1617 found in Riau Island, and 1 case in DKI Jakarta. 2 cases variant B.117 found in North Sumatera, 1 case from South Sumatera, 1 case from Banten, 5 cases from West Java, 1 case from East Java, 1 case from Bali and 1 case from East Kalimantan. Meanwhile, variant B 1351 was found 1 case in Bali.1 


I. What’s the meaning of Virus Mutation ?

Viruses are simple entities, lacking an energy-generating system and having very limited biosynthetic capabilities. Viruses are subject to mutations, the genomes of different viruses can recombine to form novel progeny, the expression of the viral genome can be regulated, and viral gene products can interact.2

Viruses are continuously changing as a result of genetic selection. They undergo subtle genetic changes through mutation and major genetic changes through recombination. Mutation occurs when an error is incorporated in the viral genome. Recombination  (produced by the combining of genetic material from more than one origin) occurs when co-infecting(living with two or more viruses at the same time) viruses exchange genetic information, creating a novel virus.2 

All viruses, including SARS-CoV-2, evolve over time. When a virus replicates or makes copies of itself, it sometimes changes a little bit, which is normal for a virus. These changes are called mutations and one or more new mutations is referred to as a variant of the original virus.3

II. What is the difference between new Covid-19 variants in Indonesia ?

  • B.1.1.7 : This variant was first discovered in the South East of England (known as B.1.1.7 or VUI 202012/01) are more likely to have a cough, sore throat, fatigue, or myalgia than those infected with other variants, the Office for National Statistic has reported.4 The B.1.1.7 variant is thought to be much more infectious and possibly more deadly, although this is still being investigated.6 The report, which covered cases in England from 15 November 2020 to 16 January 2021, said, “Loss of taste and loss of smell were significantly less common in new variant compatible positives than triple positives, whereas other symptoms were more common in new variant compatible positives, with the largest differences for cough, sore throat, fatigue, myalgia, and fever. There is no evidence of difference in gastrointestinal symptoms, shortness of breath, or headaches.
  • B. : this variant first detected in South Africa in October 2020 also known as 501Y.V2. This variant is linked to higher viral load and increased transmission (approx. about 50% increased transmission)7 But, there is still no evidence that B. is associated with increased severity of disease.8  
  • B. : This variant was first detected in India in October 2020. The B. variant carries two mutations including the L452R and E484Q which have been seen separately before in other variants but never together in one variant. The L425R mutation which has been spotted in fat-spreading variants in California can reportedly increase the binding power of the virus’s spike protein with human cells, making it more transmissible and can also potentially increase viral replication. The E484Q is reportedly similar to the E484K mutation found in the UK and South African variants of the coronavirus which have shown to lower the effectiveness of antibodies generated by vaccine or a previous infection of COVID-19. Researchers are still trying to find the answer about this double mutation. Is it more deadlier than other variants and do existing vaccines work against it? It’s still in search.9 

III. The Impact of Vaccine to the New Variants of COVID-19

WHO said that the COVID-19 vaccines that are currently in development or have been approved are expected to provide at least some protection against new virus variants because these vaccines elicit a broad immune response involving a range of antibodies and cells. Therefore, mutations in the virus should not make vaccines completely ineffective. In the event that any of these vaccines prove to be less effective against one or more variants, it will be possible to change the composition of the vaccines to protect against these variants. And WHO and all researcher still in searching and learn more about that.10

IV. What Should We Do ?

Some variants and also Covid-19 variants in Indonesia appear to spread more easily between people and also may spread more easily. But we know we can all still having part to control the spread of COVID-19 and its new variants by keeping the health protocols (included: Washing our hands, Wearing a mask, Staying at least 1 m apart, and limiting time in or avoiding enclosed/crowded spaces)3and get the vaccine!


  1. https://www.kemkes.go.id/article/view/21050500003/virus-corona-varian-baru-b-117-b-1351-b-1617-sudah-ada-di-indonesia.html. Visited: May 13,2021
  2. Fleischmann WR Jr. Viral Genetics. In: Baron S, editor. Medical Microbiology. 4th edition. Galveston (TX): University of Texas Medical Branch at Galveston; 1996. Chapter 43. Available from: https://www.ncbi.nlm.nih.gov/books/NBK8439/
  3. WHO.COVID-19 new variants. https://www.who.int/news-room/feature-stories/detail/the-effects-of-virus-variants-on-covid-19-vaccines?gclid=CjwKCAjw-e2EBhAhEiwAJI5jg6LtkOylLSj2pwQ9is0C79Rft0WuJiY-Da3fRZGVz8w-ondGiJdaMBoC75wQAvD_BwE. Visited: May 13, 2021
  4. Office for National Statistics. (Covid-19) infection survey: characteristics of people testing positive for covid-19 in England. 27 Jan 2021. https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/articles/coronaviruscovid19infectionsinthecommunityinengland/characteristicsofpeopletestingpositiveforcovid19inengland27january2021 
  5. Mahase E. Covid-19: What have we learnt about the new variant in the UK?BMJ 2020;371:m4944. https://www.bmj.com/content/371/bmj.m4944 . doi: 10.1136/bmj.m4944 pmid: 33361120
  6. Iacobucci G. Covid-19: New UK variant may be linked to increased death rate, early data indicate. BMJ 2021;372:n230. https://www.bmj.com/content/372/bmj.n230 . doi: 10.1136/bmj.n230 pmid: 33500262 
  7. Pearson CAB, Russell TW, Davies NG, et al. Estimates of severity and transmissibility of Novel South Africa SARS-CoV-2 variant 501Y.V2. visited:May 13 2021
  8. WHO. SARS-CoV-2 Variants. https://www.who.int/csr/don/31-december-2020-sars-cov2-variants/en/. Visited: May 13 2021
  9. Ray, Siladitya. “Double Mutant” Covid Variant: Here’s What We Know as Israel Reports Vaccine Efficacy Against Variant First Detected in India.  Forbes. Apr;l 20, 2021. https://www.forbes.com/sites/siladityaray/2021/04/20/double-mutant-covid-variant-heres-what-we-know-as-israel-reports-vaccine-efficacy-against-variant-first-detected-in-india/?sh=4b82b7052fb3
  10. WHO. The effects of virus variants on COVID-19 vaccines. https://www.who.int/news-room/feature-stories/detail/the-effects-of-virus-variants-on-covid-19-vaccines. Visited: May 13 2021
What Is Irritable Bowel Syndrome? What is The Cause?

What Is Irritable Bowel Syndrome? What is The Cause?

What is Irritable Bowel Syndrome? Is this just simple constipation? But I got this for such a long time. As you can say, I’m living with this gut. Alright, you might not really worry about your constipation, because you are living with this condition in a long term period 6-7 years.

But do you know that constipation might be linked to one of the symptoms of Irritable Bowel Syndrome (IBS)? Yes, it’s linked. For mine, I am also a post IBS’s patient, and not knowing this diagnosis for about almost 7 years. So, In this month this IBS awareness month, so I loved to share this information for all of you so you can be more aware and go get your medical check up if you possibly get the symptoms of IBS.

Also Read Fact About Baldness That You Must Know!

What is Irritable Bowel Syndrome (IBS) ?

Irritable bowel syndrome is a common medical condition characterized by chronic, recurrent, abdominal pain and discomfort, and altered bowel habits that occur in the absence of other organic gastrointestinal (GI) disease.1 IBS is the most common reason to visit a gastroenterologist and the second most common reason, after common flu, to be absent from work.1 Usually, women are more commonly affected than men, in ratio of 2:1, and the peak of the disease often starts in early adulthood.2 In general, patients are evenly distributed among 3 subtypes diarrhea-predominant [IBS-D], constipation-predominant [IBS-C], or mixed [IBS-M]. 

The underlying cause is still being defined but is thought to be multifactorial.1

Signs and Symptoms 

Common sign and symptoms of IBS are abdominal pain, bloating, straining during defecation, sensation of incomplete evacuation3, mucus with stools, urgency, postprandial symptoms, depression, and anxiety.5

Things Cause IBS

  1. Food Intolerance

One of the most common factors causing symptoms in IBS patients is food intolerance.6 They believed that specific types of food trigger their symptoms. Foods that contain fermentable oligosaccharides, disaccharides, monosaccharides and polyols  (FODMAP) are known triggers that worsen IBS symptoms because of their osmotic and fermentation effects.7 

Table 1. High FODMAP Foods

2. Enteric Infection

Enteric infection known as post-infectious IBS6 and usually occurs after an acute bacterial, viral or protozoal gastroenteritis, when around 20% of patients will develop symptoms of IBS.9 The groups of pathogens that lead to IBS symptoms are still unknown, but colonic spirochetosis  was linked previously with colonic eosinophilia , lymphoid follicles, and IBS-D(IBS Diarrhea).10,11 

3. Stress-depression

Up to 75% of patients with IBS symptoms usually have coexisting or depression.10 One study that compared anxiety and depression levels in IBS patients and healthy individuals found that the activity of the dorsolateral prefrontal cortex  in IBS patients was dysregulated in behavioral selection duties.12 Norepinephrine  production by stressful stimuli appears to enhance the growth of many intestinal pathogens, including Campylobacter jejuni13, Escherichia coli (E.coli) and E. Coli 0157:H7, with activation of the HPA axis.14 It appears that this stress stimulation also affects the non-pathogenic bacteria, such as Lactobacilli and Bifidobacteria, promoting even more invasion from other potential pathogens.15

4. Microbiota

IBS patient assumed have altered microbiota in their intestines.16 Observation from a study in 110 IBS patients show that patients with IBS have different intestinal microbiota.17 

Lactobacillus and Bacteroides species, known beneficial bacteria, are also depleted, while the number of pathogenic bacteria, such as Streptococcus spp., are increased.18 In a study of IBS patients with abdominal pain, the investigators observed that patients with pain had 5 times smaller amounts of Bifidobacteria in their intestines.19 


Inflammatory Bowel Syndrome is a disease that is manageable. The cause IBS is multifactorial and not completely elucidated. The initiation of treatment of IBS starts with identifying the severity and predominant symptoms of the disorder. If symptoms do not significantly affect quality of life, management with lifestyle modification and education is a reasonable choice. Treatment is based on a trial of lifestyle changes and symptom management. The low FODMAP diet and exercise should be recommended for lifestyle changes. Pain and bowel cramping can be treated with antispasmodics  and peppermint oil, tricyclic antidepressants , counseling, probiotics, or a trial of rifaximin.1

This month awareness of IBS just wants people to be more concerned about their gut changes activity. If you find something uncomfortable, painful, or even bloody stool please be more concerned and go to see your doctor!

Stay safe and Healthy!


  1. Defrees DN, Bailey J. Irritable bowel syndrome: epidemiology, pathophysiology, diagnosis, and treatment. Prim Care 2017;44:655-671.
  2. Mayer EA. Clinical practice. Irritable bowel syndrome. N Engl J Med 2008;358:1692-1699.
  3. Enck P, Aziz Q, Barbara G, et al. Irritable bowel syndrome. Nat Rev Dis Primers 2016;2:16014.
  4. Böhn L, Störsrud S, Törnblom H, Bengtsson U, Simrén M. Selfreported food-related gastrointestinal symptoms in IBS are common and associated with more severe symptoms and reduced quality of life. Am J Gastroenterol 2013;108:634-641.
  5. Jerndal P, Ringström G, Agerforz P, et al. Gastrointestinal-specific anxiety: an important factor for severity of GI symptoms and quality of life in IBS. Neurogastroenterol Motil 2010;22:646-e179.
  6. Chey WD, Kurlander J, Eswaran S. Irritable bowel syndrome: a clinical review. JAMA 2015;313:949-958.
  7. Shepherd SJ, Parker FC, Muir JG, Gibson PR. Dietary triggers of abdominal symptoms in patients with irritable bowel syndrome: randomized placebo-controlled evidence. Clin Gastroenterol Hepatol 2008;6:765-771.
  8. Vakil, Namish. Dietary Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols (FODMAPs) and Gastrointestinal Disease. Nutrition in Clinical Practice. Vol 00 Number 0. 2018;1-8. American Society for Parenteral and Enteral Nutrition. DOI: 10.1002/ncp.10108
  9. Keely S, Walker MM, Marks E, Talley NJ. Immune dysregulation in the functional gastrointestinal disorders. Eur J Clin Invest 2015;45:1350-1359.
  10. Holtmann GJ, Ford AC, Talley NJ. Pathophysiology of irritable bowel syndrome. Lancet Gastroenterol Hepatol 2016;1:133-146.
  11. Walker MM, Talley NJ, Inganäs L, et al. Colonic spirochetosis is associated with colonic eosinophilia and irritable bowel syndrome in a general population in Sweden. Hum Pathol 2015;46:277-283.
  12. Aizawa E, Sato Y, Kochiyama T, et al. Altered cognitive function of prefrontal cortex during error feedback in patients with irritable bowel syndrome, based on FMRI and dynamic causal modeling. Gastroenterology 2012;143:1188-1198
  13. Xu F, Wu C, Guo F, et al. Transcriptomic analysis of Campylobacter jejuni NCTC 11168 in response to epinephrine and norepinephrine. Front Microbiol 2015;6:452.
  14. Raskov H, Burcharth J, Pommergaard HC, Rosenberg J. Irritable bowel syndrome, the microbiota and the gut-brain axis. Gut Microbes 2016;7:365-383 
  15. Pigrau M, Rodiño-Janeiro BK, Casado-Bedmar M, et al. The joint power of sex and stress to modulate brain-gut-microbiota axis and intestinal barrier homeostasis: implications for irritable bowel syndrome. Neurogastroenterol Motil 2016;28:463-486.
  16. Bhattarai Y, Muniz P DA, Kashyap PC. Irritable bowel syndrome: a gut microbiota-related disorder? Am J Physiol Gastrointest Liver Physiol 2017;312:G52-G62
  17. Tap J, Derrien M, Törnblom H, et al. Identification of an intestinal microbiota signature associated with severity of irritable bowel syndrome. Gastroenterology 2017;152:111-123.
  18. Parkes GC, Rayment NB, Hudspith BN, et al. Distinct microbial populations exist in the mucosa-associated microbiota of subgroups of irritable bowel syndrome. Neurogastroenterol Motil 2012;24:31-39.
  19. Jalanka-Tuovinen J, Salonen A, Nikkilä J, et al. Intestinal microbiota in healthy adults: temporal analysis reveals individual and common core and relation to intestinal symptoms. PLoS One 2011;6:e23035.

Fact About Baldness That You Must Know!

Fact About Baldness That You Must Know!

Fact About Baldness – Baldness in a medical term named alopecia. Androgenic alopecia is a common form of hair loss in both men and women. This baldness condition in men also known as male-pattern baldness, and in women named female pattern hair loss (FPHL). Androgenic alopecia (AGA) is considered to be the most common type of baldness characterized by progressive hair loss. It is estimated that prevalence rates in Caucasian populations is around 30% for men in their 30s, 40% for men in their 40s and 50% for men in their 50s.1

In the Indian context, a population based study of 1005 subjects showed a 58% prevalence of AGA in males aged 30-50 years. In oriental races, a lower prevalence has been shown.2 In a Chinese study by Wang et al.,1 the overall prevalence was 21.3%, while in a Korean study, the overall prevalence was 14.1%.3 All studies demonstrate a gradual increase in incidence with age.4

In women androgenic alopecia, a study by Norwood,4showed a total prevalence of around 19% in a population of 1006 Caucasian patients. In a Chinese population study, the prevalence was only 6.0% and a Korean study had a relatively similar lower prevalence of 5.6%, suggesting that like in men, the prevalence is considered to be lower in oriental races compared to Caucasians.1,3 The incidence of AGA in women also tends to increase with age.4,5

Also Read Save Your Scrotum! I mean, Save Your Balls!

Do you know if our hair has a cycle of life?

Fact about Baldness – A normal hair cycle has 3 stages: Active growth phase or Anagen, Regression phase or Catagen, Resting phase or Telogen.

Anagen is the active growth phase of hair follicles during which the root of the hair is dividing rapidly, adding to the hair shaft. During this phase the hair grows about 1cm every 28 days. Scalp hair stays in this active phase of growth for 2-7 years. At the end of the anagen phase an unknown signal causes the follicle to go into the catagen phase.6 

Catagen is a short transition stage that occurs at the end of the anagen phase. It signals the end of the active growth of a hair. This phase lasts for about 2-3 weeks while the hair converts to a club hair. A club hair is formed during the catagen phase when the part of the hair follicle in contact with the lower portion of the hair becomes attached to the hair shaft. This process cuts the hair off from its blood supply and from the cells that produce new hair. When a club hair is completely formed, about a 2-week process, the hair follicle enters the telogen phase.6 

Telogen is the resting phase of the hair follicle. When the body is subjected to extreme stress, as much as 70% of hair can prematurely enter the telogen phase and begin to fall, causing a noticeable loss of hair. This condition is called telogen effluvium. The club hair is the final product of a hair follicle in the telogen stage, and is a dead, fully keratinized hair. 50 to 100 club hairs are shed daily from a normal scalp.7

Does the baldness in all populations are the SAME? 

Fact about Baldness – Baldness or in medical terms named alopecia, has many types due to the etiology that caused baldness. Alopecia divided into 2 main groups, Non cicatricial alopecia and cicatricial alopecia(Scarring hair loss, also known as cicatricial alopecia, is the loss of hair which is accompanied with scarring. It can be caused by a diverse group of rare disorders that destroy the hair follicle, replace it with scar tissue, and cause permanent hair loss). The  non cicatricial alopecia type: Androgenic Alopecia, Alopecia areata, Telogen Effluvium. Anagen Effluvium, Loose Anagen Syndrome, Trichotillomania, and Traction Alopecia. Cicatricial Alopecias type : Chronic Cutaneous Lupus Erythematosus, Lichen Planopilaris, Central Centrifugal Cicatricial Alopecia.9

I. Non Cicatricial Alopecias

  • Androgenetic Alopecia(AGA)9

Androgenetic alopecia (AGA) is a multifactorial disorder caused by interactions between several genes and environmental factors.4 Also known as patterned hair loss, is the most common type of alopecia in both men and women. Although AGA is a physiological condition, the psychological impact of hair loss can be profound. Half of men are affected by age 50, whereas 40% of women are affected by age 70 (Norwood 1975, 2001).

Male pattern: Thinning of the frontal hairline, bitemporal recession, hair loss at the crown, Female pattern: Hair loss at the crown with preservation of the frontal hairline. Caused by the effect of dihydrotestosterone  on hair follicles leading to miniaturization.9 The duration of anagen phase in AGA gradually decreases and that of telogen phase increases. As the duration of anagen phase determines the hair length, the maximum length of the new anagen hair becomes shorter than that of its predecessor, leading to miniaturization and eventually a bald appearance.7,9

  • Alopecia Areata9

Equally affects both sexes, with usual onset before age 30. Most common areas of hair loss are scalp and beard regions. Caused by autoimmune destruction of hair follicles involving cell-based and humoral immunity.

  • Telogen Effluvium9

Acute telogen effluvium is characterized by diffuse scalp hair loss lasting < 6months, whereas the duration is >6month for chronic telogen effluvium. Women between ages 30 to 60 are most commonly affected. A stressor event may or may not be present, usually occurring 2–4 months before onset of hair shedding 20%–50% of scalp hairs transition prematurely to telogen phase and are shed with normal hair shafts.

  • Anagen Effluvium9

Diffuse hair loss characterized by hair breakage during anagen phase. Classic causative agents are radiation therapy and cancer chemotherapy. Affects 80%–90% of scalp hairs with onset within 1–4 week of exposure. Narrowing, fractured hair shafts constitute a characteristic sign.

  • Loose Anagen Syndrome9

Typical patient is a blond female aged 2–5 who presents with diffuse hair loss and short, dull hair 6:1. Female to male ratio among the patient population, which includes adults and dark-haired individuals as well Greater susceptibility to hair breakage caused by premature keratinization  of the inner root sheath, causing impaired adhesion with the hair shaft cuticle. Shorter anagen phase leads to reduced hair length.

  • Trichotillomania9

Patients experience an irresistible urge to pull out their own hair despite negative impacts to their occupational and social function. Childhood trichotillomania affects more boys than girls and resolves spontaneously. Adult trichotillomania affects women much more frequently than men. Often comorbid with mood or anxiety disorders. Short, fractured hairs distributed sparsely and irregularly in affected areas.

  • Traction Alopecia9

Results from tension applied to hair for a prolonged period of time, from hairstyles such as tight ponytails and braids, as well as hair-styling devices. Areas under greatest pressure are most affected, usually scalp margins. Especially common among African-American females because of their association with certain hairstyles. Typically hair loss is transient; scarring or inflammation may be observed. 

II. Cicatricial Alopecias9

  • Chronic Cutaneous Lupus Erythematosus 

Scaly, erythematous plaques(a big patch redness in the scalp) with well-demarcated borders that eventually atrophy(decrease in size of a body part, cell, organ, or other tissue), found on sun-exposed areas including scalp. Most common form is discoid lupus erythematosus, accounting for 50%–85% of all cases. Affects more women than men, usually between ages 20–45 Associated with carpet tack sign, describing follicular spikes on the undersurface. Cases among African-Americans are often more severe.

  • Lichen Planopilaris9

Considered to be a variant form of lichen planus . Classic lesions are smooth white areas with absent follicle ostia and central scarring; edges are characterized by erythema and scaling around hair follicles. Mostly affects adult women at the crown and parietal areas of the scalp. Due to autoimmune attack on hair follicles mediated by T lymphocytes.

  • Central Centrifugal Cicatrical Alopecia

Scarring hair loss that usually begins at the crown and expands outward to affect the entire scalp. Middle-aged African-American females are most commonly affected; individuals of other races rarely present with this condition. May be associated with chemicals and pressure applied to hair Lymphocyte-rich infiltrates observed at edges of balding lesions with signs of inflammation.

Treatment You Need

There are many types of alopecia. Each of it has different etiology and different kind of treatment. From topical medication, oral medication, mesotherapy, microneedling treatment, light treatments, hair transplant, and also cognitive behavioral therapy/CBT  (for Trichotillomania).

  1. Minoxidil

This is a piperidino pyrimidine derivative and potent vasodilator that is effective orally for severe hypertension. Minoxidil was first approved in 1979 by the FDA for the treatment of hypertension. It’s 2% and 5% were approved for the treatment of male AGA in 1988 and 1991, respectively. In Female Pattern Hair Loss, 2% minoxidil was approved by the FDA in 1991 and a 5% minoxidil foam with once daily application was approved in 2014.10

2. Hair Supplement (Viviscal)

A double-blind, placebo-controlled study evaluating the efficacy of oral hair supplement in women showed women aged 21 to 75 years of age who were in generally good health, but complained of self-perceived thinning hair. Subjects were randomized in double-blind fashion to receive hair oral supplement (Viviscal Maximum Strength) or placebo. Viviscal contains AminoMar C marine complex, a proprietary blend of shark and mollusk powder, an organic form of silica derived from Equisetum sp. (horsetail), vitamin C derived from Malpighia emarginata (acerola cherry), microcrystalline cellulose (E460), natural orange flavor, magnesium stearate, hypromellose, and glycerol. Subjects were instructed to take one tablet of their assigned treatment each morning and one tablet each evening with water following a meal.11 

When women with thinning hair were treated with the study medication, the mean number of terminal hairs in the target scalp area increased from 271.0 at baseline to 571 after three months of treatment and increased further to 609.6 after six months. Both were significantly greater than the mean number of terminal hairs among placebo-treated subjects at baseline (256.0), which remained unchanged throughout the study. These results support the hypothesis that Viviscal increases hair growth in women with thinning hair.11

3. Mesotherapy

Mesotherapy or intradermal therapy(injected into the scalp) is a technique defined as multiple intradermal injections or pharmaceutically active substances in low dose, at numerous points, near/over the affected sites, at longer time intervals than conventional routes. Once the drug is administered, it achieves a longer lasting effect and a great local bioavailability . The injectable blend for mesotherapy may contain several drugs. In one case report a 47-year old healthy male with a complaint of hair loss and the patient had diffuse thinning on his scalp hair and recession of the frontal and temporal hairline(Hamilton-Norwood Scale IV) without evidence of inflammation or scarring. He also had a positive family history of hair loss.

The patient received 10 sessions of sterile injectable blend containing 1ml minoxidil 0,5%, 1ml finasteride 0,05%, 2ml biotin 5mg/ml, and 2ml D-panthenol 50mg/ml, with total volume of injection is 6ml per session. At the 10th session, we noted a significant improvement in hair density, less hair fall, and an increase in hair thickness. We decided to maintain the injections for more than 10 sessions due to a good clinical response. The patient reported remarkable hair regrowth, and the photographic assessment showed excellent improvement after the 20th session (Figure 1). The treatment was well‐tolerated, with no evidence of adverse events.12

4. Platelet Rich Plasma (PRP)

Platelet-rich plasma (PRP) is an autologous source of growth factors derived from platelet sequestration and concentration via gradient density centrifugation. And its gained popularity in the treatment of androgenic alopecia.13

5. Microneedling

Microneedling is a minimally invasive dermatologic procedure in which fine needles are rolled over the skin to puncture the stratum corneum. Through the physical trauma from needle penetration, microneedling induces a wound healing cascade with minimal damage to the epidermis that induces collagen formation, neovascularization, and growth factor production of the treated areas. Microneedling has shown promising results as an adjuvant therapy for enhanced drug delivery in the treatment of atrophic scars , AGA, alopecia areata, and pigmentation disorders such as melasma. 14

That’s all article fact about baldness that we can share to you. Wish that discussion will help you to know fact about baldness well. See you on the next articles!

Save Your Scrotum! I mean, Save Your Balls!

Save Your Scrotum! I mean, Save Your Balls!

Save Your Scrotum – You might have seen a dozen Hollywood box office movie which give you an extra scene when they have fought the gangster they will always show you the kick right into the balls. And it seems really painful (just looking at the picture above). For a man, its really painful when they get trauma there (in the testicles area). Some of you might think that the stunt men or the actor just made it so the scene will looks funny, but its actually really painful. Am I right sir ?

So actually the pain from your testicles not always comes from a trauma or accident (sports accident, fight,etc) but it can also causes by several factors including infection. You might be not really care with your balls before you understand it that your balls having a major roles for your fertility! So from now you must take care and save your scrotum! I mean, save your balls!

Also Read Vaginal Discharge Is it SEXUAL TRANSMITTED INFECTION ?


Originally men has two balls and it located under the Mr.Banana. those two balls are protected by a skin layers in the external area that we usually called scrotum. The scrotum is a male reproductive structure located under the penis. This sac divided into two compartments by the scrotal septum. Each sac included external spermatic fascia, testes (your balls), epididymis, and spermatic cord. The average wall thickness of the scrotum is about 8 mm and it has two layers. First, the parietal layer has the function of covering the inner aspect of the scrotal wall and the second was the visceral layer which coats the testis and epididymis. The scrotum responsible for protecting the testes. It helps with the thermoregulation of the testicles. It keeps the temperature of the testis several degrees below the average body temperature, which is an essential factor for sperm production.

Figure 1. The Male Genital Organs, The scrotum. On the left side the cavity of the tunica vaginalis has been opened; on the right side only the layers superficial to the Cremaster have been removed. Contributed by Gray’s Anatomy Plates (Source: Anatomy, Abdomen and Pelvis, Scrotum. NCBI Bookshelf. 2021

The balls or testes are male reproductive gland that is responsible for producing sperm and making androgens.They are oval shaped reproductive structures that are bean-shaped and measures 3cm by 5cm in length and 2cm to 3cm in width.2 The double-layered tunica vaginalis envelop the testes except at the posterior and superior borders where the epididymis and spermatic cord are attached. The visceral or inner layer of the tunica vaginalis is close to the epididymis, testes and vas deferens. On the posterior lateral surface of the testes, there is a small space between the testes and body of the epididymis which is known as the sinus of the epididymis. Deep to the tunica vaginalis is located the tunica albuginea, which is a durable fibrous covering of the testes.

The epididymis is a small curved shaped elongated structure which is highly convoluted and tightly compressed. When open in a straight line, it is estimated that its length is about 20 feet. The epididymis is found on the posterior border of the testis and consists of three parts which include the head (caput), body (corpora), and tail (Cauda). The head of the epididymis lies at the upper pole of the testes and receive seminal fluid from the ducts of the testis. It then permits passage of sperm into the distal portion of the epididymis. Because of its length, the epididymal ducts have ample space for storage and maturation of sperm.2

Figure 2. Testicle, Vas (Ductus) Deferens, Head of Epididymis (shown lifted from testis), Body of Epididymis, Tail of Epididymis, Testicular Artery, Pampiniform Plexus, Efferent Ductules, Septa, Lobules, Tunica Albuginea. Contributed Illustration by Beckie Palmer. (source: Anatomy, Abdomen and Pelvis, Testicles. NCBI Bookshelf.

Vascularization of the testis has two main roles: transport and mobilizations of endocrine factors and metabolites, as well as regulation of testicular temperature. In men, testicular temperature is about 3°-4°C below core body temperature and about 1,5°-2,5° C above the temperature of scrotal skin.3

Story behind Testicular Pain

When your balls get kicked, you might get experiencing painful sensation not only in your balls area. You will experience pain in your tummy, your back, your thigh also you may experience vomit and headache! This kind of pain called referred pain. You must save your scrotum, i mean your balls okay ?

Sensory innervation of the testis and epididymis is conducted by autonomic(The part of the nervous system that controls muscles of internal organs (such as the heart, blood vessels, lungs, stomach, and intestines) and glands (such as salivary glands and sweat glands))4 and sensory (sensory nerve, also called an afferent nerve, is a nerve that carries sensory information toward the central nervous system (CNS) and all those nerves which can sense or recognize the stimuli (Internal or External) are known as sensory nerves. Fibers that travel through the spermatic cord. The somatic fibers of the cremaster muscle and the parietal and visceral layers of the pouch that surrounds testicles travel via the genital branches of the genitofemoral nerve (originating in L1-L2) and ilioinguinal nerve, arising from the first lumbar spinal nerve (L1). Testicular nociceptive fibers travel via the sympathetic plexus (T10 to T12), whereas the deferential and epididymal nociceptive fibers travel via the pelvic plexus (T10 to L1) throughout the vas deferens.5

Causes of testicular pain are various, such as trauma, testicular torsion, post-vasectomy pain, epididymitis, varicocele and chronic orchialgia.

  • Trauma

Trauma must be considered in all ages as the cause of acute pain. Severity varies from simple organ contusions to testicular rupture (a force of 50kg is required to tear or break the tunica albuginea)4The uncommon, but more severe dislocation of the testis is a result of trauma and produces damage or avulsion(an injury in which a body structure is torn off by either trauma or surgery) of the fascia  surrounding the testis and/or of the scrotal ligament

  • Testicular torsion

Testicular torsion is a medical emergency, requiring prompt treatment or risking the loss of the testicles. The incidence is 1 in 4.000 males under the age of 25 years. The classical presentation of testicular torsion is acute onset, intense, unilateral scrotal pain also may complain of nausea and vomiting. Testicular torsion requires immediate surgical intervention with scrotal exploration, detorsion and orchidopexy .6

  • Epididymitis

Epididymitis  is another common cause of acute scrotal pain that must be differentiated from the more severe testicular torsion.5 Sexually active men younger than 35 years are usually infected with Chlamydia trachomatis and Neisseria gonorrhea, whereas older patients, patients who have undergone recent genitourinary surgery, and patients with anatomical abnormalities often have infection with urinary tract infections. Fungal agents such as Candida species, very rarely, can also cause epididymitis.

  • Post-vasectomy pain

Vasectomy is a surgical procedure for male sterilization or permanent contraception. During the procedure, the male fibromuscular tube that has function to excretory sperm are cut and tied or sealed so as to prevent sperm from entering into the urethra and thereby prevent fertilization of a female through sexual intercourse.Most common adverse event affecting the patient’s quality of life after a vasectomy is pain. The presenting symptoms included testicular pain (9cases), pain during intercourse (8cases), pain with ejaculation (4cases) and epididymal pain (2cases).6

  • Varicocele

A varicocele is an abnormal dilation of the spermatic veins commonly due to an anatomical abnormality with an incidence of 10% to 20% in the general male population and 2% to 15% in adolescent males6 and more common in younger ages 15-25.7 Varicocele pain typically presents as a dull, aching, and throbbing sensation in the scrotum without sharp radiating components.6

  • Chronic Orchialgia

Orchialgia or testicular pain. It is defined as intermittent or constant testicular pain for a period of 3 or more months that interferes with daily activities.8 The etiology of chronic orchialgia remains largely unknown with up to 50% of patients presenting with an unknown cause, but has been found to be associated with nerve damage to the spermatic cord after vasectomy, trauma, inguinal herniorrhaphy () , and epididymitis.6


Males has always to more concern about their testicles, because taking good care and save your scrotum or balls will save your future! The testicles pain etiology so many, but there are hundred cases that shows the cause of testicles pain are from trauma. Each treatment depends on the variation degree of the damage cell in your testicles, it could be only pain killer drugs, scrotal support, cold compress and the last thing is surgery.

Some tips here for you who loves sport (especially male in age of school and university) please try to wear athletic cup or jockstrap . While sports-related genital injuries are not very common, they still can give you testicular pain, but if you are not well treated it can become significant injuries.9

A Geisinger study showed that 18 percent of athletes experienced a testicular injury, and 36.4% observed injuries in team members, yet only 12.9% of athletes reported wearing athletic cups.
“A hard hit to the groin can cause severe pain and even nausea or vomiting for boys and men,” said Joel Sumfest, M.D., a Geisinger urologist who co-authored the study.

“And if the hit is hard enough, it can also lead to testicular fracture or testicular rupture.”10


  1. Rosa A.Garcia, Hussain Sajjad. Anatomy, Abdomen and Pelvis, Scrotum. 2021. StatPearls Publishing LLC. Bookshelf ID: NBK549893PMID: 31751083. Access: https://www.ncbi.nlm.nih.gov/books/NBK549893/ March 20 2021)
  2. Manpreet S. Tiwana, Stephen W. Leslie. Anatomy, Abdomen and Pelvis, Testicles. 2020. StatPearls Publishing. Bookshelf ID: NBK470201PMID: 29261881. Access: https://www.ncbi.nlm.nih.gov/books/NBK470201/ March 20 2021
  3. G.F. Weinbauer. E. Nieschlag et al. (eds.), Andrology, DOI: 10.1007/978-3-540-78355-8_2. Springer-Verlag Berlin Heidelberg. 2010. Page 37
  4. Autonomic nervous system. National cancer institute. Access: https://www.cancer.gov/publications/dictionaries/cancer-terms/def/autonomic-nervous-system#:~:text=(AW%2Dtoh%2DNAH%2D,salivary%20glands%20and%20sweat%20glands).  March 20 21021
  5. Juan Fernando Uribe-Arcila, Andres Delgado-Montoya, Federico Gaviria-Gil. Etiology of testicular pain 2019: Classification into ten logical subgroups. Revista Mexicana de URología ISSN: 2007-4085, Vol. 80, núm. 4, julio-agosto 2020:pp. 1-19. Access: https://revistamexicanadeurologia.org.mx/index.php/rmu/article/download/498/922/ March 20 2021
  6. Chirag G Gordhan, Hossein Sedeghi-Nejad. Scrotal pain: Evaluation and management. The Korean Urological Association. 2015. Korean J Urol 2015;56:3-11. http://dx.doi.org/10.4111/kju.2015.56.1.3 pISSN 2005-6737  •  eISSN 2005-6745)
  7. Condition Treated. What is a Varicocele. UCLA Health. Access: https://www.uclahealth.org/urology/body.cfm?id=478&action=detail&ref=19 March 23 2021
  8. Davis BE, Noble MJ, Weigel JW, Foret JD, Mebust WK. Analysis and management of chronic testicular pain. J Urol 1990;143:936-9.
  9. Urology Associates. Protect Your Male Athletes from Genital Injuries&Testicular Pain. 2018. Access: https://denverurology.com/urology-blog/genital-injuries-testicular-pain/, March 23 2021
  10. Why your athletic son needs to wear a cup. Geisinger. 2016. Access: https://www.geisinger.org/health-and-wellness/wellness-articles/2017/02/21/19/38/why-your-athletic-son-needs-to-wear-a-cup, March 23 2021

Save Your Scrotum

Save Your Scrotum!

Save Your Scrotum!

Antibiotics From Hero To Zero?

Antibiotics From Hero To Zero?

Improper Use Of Antibiotics Can Cause Double Trouble

Antibiotics From Hero to Zero – Since everyone knows about the efficacy of antibiotics to treat such an illness, everyone without any hesitation will easily to buy all kind of antibiotics without any prescription. Consumption of antibiotics for treating illness, infection or etc are not always right to do. Basically, antibiotics is made for treated infection caused by bacteria. But we have to know that bacteria which cause problem to our illness are not always the same bacteria. For example: you can not treat skin infection with antibiotics for lung infection, yea maybe it will help but we need more specific antibiotics and the right choice of antibiotics will clearly heal the infection.

Everyone knows antibiotics. Not only they who lives in a city, but also everyone in rural place, village they all knows that antibiotics sometimes become their “life saver” when it faces with infection. Nevertheless, society are not well known how to properly using antibiotics. When you feel sick and miserable, and you really wanted to get better faster, you’ll probably thinking antibiotics is the answer. You can’t take antibiotics for all kind of cough, flu or else before the diagnosis and proper diagnostic examination has been done to you by medical doctor. When antibiotics are not needed for your symptoms, actually it will not help you either! Unfortunately antibiotics will cause harm your body.


The History of Antibiotics

The term antibiotics also known as antibacterial, which is a type of antimicrobial substance active against bacteria. It is the most important type of antibacterial agent for fighting bacterial infections, and antibiotic medications are widely used in the treatment and prevention of such infections. Sometimes, the term antibiotic literally “opposing life”, from the Greek roots ἀντι anti, “against” and βίος bios, “life”—is broadly used to refer to any substance used against microbes, but in the usual medical usage, antibiotics (such as penicillin) are those produced naturally (by one microorganism fighting another), whereas nonantibiotic antibacterials (such as sulfonamides and antiseptics) are fully synthetic.1

Antibiotics have been used since ancient times. Many civilizations used topical application of moudly bread, with many references to its beneficial effects arising from ancient Egypt, Nubia, Serbia, Greece, and Rome. The first person to directly document the use of molds to treat infections was John Parkinson.1 In the 1920s, British scientist Alexander Fleming  was working in his laboratory at St. Mary’s Hospital in London when almost by accident, he discovered a naturally growing substance that could attack certain bacteria. In one of his experiments in 1928, Fleming observed colonies of the common Staphylococcus aureus bacteria that had been worn down or killed by mold growing on the same plate or petri dish. He determined that the mold made a substance that could dissolve the bacteria. He called this substance penicillin, named after the Penicillium mold that made it. Fleming and others conducted a series of experiments over the next 2 decades using penicillin removed from mold cultures that showed its ability to destroy infectious bacteria.2

Before long, other researchers in Europe and the United States started recreating Fleming’s experiments. They were able to make enough penicillin to begin testing it in animals and then humans. Starting in 1941, they found that even low levels of penicillin cured very serious infections and saved many lives. For his discoveries, Alexander Fleming won the Nobel Prize in Physiology and Medicine. It was used widely for treating soldiers during World War II, curing battlefield wound infections and pneumonia. By the mid- to late 1940s, it became widely accessible for the general public. Newspaper headlines hailed it as a miracle drug (even though no medicine has ever really fit that description).2

Antibiotics From HERO to ZERO

Antibacterials are specifically designed to treat bacterial infections. When it used in proper right time, they can cure many infections or even life threatening illness. This recent worldwide concern is antibiotic resistance. Can you imagine if we are get infected by bacteria but in the end we cannot survive without being noticed we couldn’t get help because the bacteria had already resistance for some of antibiotics that usually we used.

Do you know what is Resistance of Antimicrobial mean?

Antibiotic resistance occurs when bacteria change in response to the use of these medicines.

Bacteria, not humans or animals, become antibiotic-resistant. These bacteria may infect humans and animals, and the infections they cause are harder to treat than those caused by non-resistant bacteria. Antibiotic resistance leads to higher medical costs, prolonged hospital stays, and increased mortality.3

Can you imagine how many infectious diseases in this world? And by the time, we cannot put our hope in antibiotic anymore because of this. WHO said Antibiotic resistance is rising to dangerously high levels in all parts of the world. New resistance mechanism are emerging and spreading globally, threatening our ability to treat common infectious disease. A growing list infections such as pneumonia, tuberculosis, blood poisoning, gonorrhea, and foodborne disease are becoming harder, and sometimes impossible, to treat as antibiotics become less effective.3

Data from CDC about Antibiotic Resistance threats in the US 2019 reported more than 2.8 million antibiotic-resistance infections occur in the US each year and more than 35.000 people die as a result. In addition, 223.900 cases of Clostridioides difficile(a bacteria which transfer into human gut and passed in the faces and spread to food, surfaces and objects when people who are infected don’t wash their hands thoroughly. If you touch a surface contaminated with C.defficile sproes, you may then unknowingly swallow the bacteria) occurred in 2017 and at least 12.800 people died.5Drug-resistant infections are already estimated to kill at least 700.000 people a year, and could kill 10 million people a year by 2050 if left unchecked.4 WHO reported the rate of resistance to ciprofloxacin, an antimicrobial frequently used to treat urinary tract infections, varied from 8,4% to 92,9% in 33 reporting countries.6

WHO is concerned that the trend will further be fueled by the inappropriate use of antibiotics during the COVID-19 pandemic. Evidence shows that only small proportion of COVID-19 patients need antibiotics to treat subsequent bacterial infections and the Organization has issued guidance not to provide antibiotic therapy or prophylaxis to patients with mild COVID-19 or to patients with suspected or confirmed moderate COVID-19 illness unless there is a clinical indication to do so.6

WHO Recommendation to Prevention and Control Antibiotic Resistance


To prevent and control the spread of antibiotic resistance, individuals can:

  • Only use antibiotics when prescribed by a certified health professional.
  • Never demand antibiotics if your health worker says you don’t need them.
  • Always follow your health worker’s advice when using antibiotics.
  • Never share or use leftover antibiotics.
  • Prevent infections by regularly washing hands, preparing food hygienically, avoiding close contact with sick people, practising safer sex, and keeping vaccinations up to date.
  • Prepare food hygienically, following the WHO Five Keys to Safer Food (keep clean, separate raw and cooked, cook thoroughly, keep food at safe temperatures, use safe water and raw materials) and choose foods that have been produced without the use of antibiotics for growth promotion or disease prevention in healthy animals.

Health professionals

To prevent and control the spread of antibiotic resistance, health professionals can:

  • Prevent infections by ensuring your hands, instruments, and environment are clean.
  • Only prescribe and dispense antibiotics when they are needed, according to current guidelines.
  • Report antibiotic-resistant infections to surveillance teams.
  • Talk to your patients about how to take antibiotics correctly, antibiotic resistance and the dangers of misuse.
  • Talk to your patients about preventing infections (for example, vaccination, hand washing, safer sex, and covering nose and mouth when sneezing).


  1. Wikipedia. Access 13 Maret 2021 https://en.wikipedia.org/wiki/Antibiotic
  2. The History of Antibiotics. Access 13 Maret 2021https://www.healthychildren.org/English/health-issues/conditions/treatments/Pages/The-History-of-Antibiotics.aspx
  3. WHO. Antibiotic Resistance. Access 13 Maret 2021. https://www.who.int/news-room/fact-sheets/detail/antibiotic-resistance
  4. Prof. David Heymann, Emma Ross. Preserve the Effectiveness of Antibiotics with a Global Treaty. https://www.chathamhouse.org/2019/06/preserve-effectiveness-antibiotics-global-treaty?gclid=Cj0KCQiAv6yCBhCLARIsABqJTjY5nugDmzgzNRT2s3TcWcsewA_srRO0NleXC8D0sfJrtVG4yHd6TdsaAuKmEALw_wcB
  5. Biggest Threats and Data. Access: 13 Maret 2021. https://www.cdc.gov/drugresistance/biggest-threats.html#:~:text=2019%20AR%20Threats%20Report,-CDC’s%20Antibiotic%20Resistance&text=According%20to%20the%20report%2C%20more,at%20least%2012%2C800%20people%20died. )
  6. WHO. Record number of countries contribute data revealing disturbing rates of antimicrobial resistance. Access: 13 Maret 2021. https://www.who.int/news/item/01-06-2020-record-number-of-countries-contribute-data-revealing-disturbing-rates-of-antimicrobial-resistance

Antibiotics From Hero to Zero

Antibiotics From Hero to Zero

Antibiotics From Hero to Zero



Are you in the term of sexuality active age? A women or a girl either active or not in sexual activity may concern about the physical findings in their miss V area. Something coming up in your pants, and it doesn’t look nice. You may worry more about that discharge, but you have to know what the things really is in your pants. Sometimes you have to worry about vaginal discharge, but beforehand you must try to figure it out which vaginal discharge you have. Is it the normal vaginal discharge or is it abnormal?

Vaginal discharge is caused by non-sexually and sexually transmitted infections. If you still don’t know about the difference between normal and abnormal miss V discharge, here I wanted to share with you all. The term vaginal discharge is often used by patients to refer to any genital discomfort.1

Basic Things to Know

Normal genital secretions are a mixture of transudate (is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system)2 through mucous membranes, secretions from gland cells, and desquamated(commonly called skin peeling, is the shedding of the outermost membrane or layer of a tissue)vaginal epithelial cells. Both the amount and consistency of cervical secretions and the desquamation of epithelial cells are hormone dependent and may increase during ovulation(when a mature egg is released from the ovary), premenstrually, with pregnancy, or with the use of oral contraceptives. Normal discharge is asymptomatic except for occasional complaints of excessive secretions.1 A physiologic discharge is usually clear to white, nonadherent to the vaginal wall, and pooled in the posterior fornix (The posterior fornix is the larger recess, behind the cervix. It is close to the recto-uterine pouch.)3. It can appear nonhomogenous with clumps of desquamated epithelial cells. It has a pH of less than 4.5, no offensive odor, and an abundance of epithelial cells on saline microscopy. (Women with copious amounts of desquamated cells who are otherwise asymptomatic are often those who present frequently with “recurrent vaginal discharge.”)1

We conclude that normal physiological vaginal discharge is a white or clear, non-offensive discharge that can vary over time. It is thick and sticky for most of the menstrual cycle but becomes clearer, watery, and stretchy for a short period around the time of ovulation. It is heavier and more noticeable during pregnancy, with contraceptive use and with sexual stimulation. It decreases in volume at menopause due to fall in estrogen levels.4

Figure 1. Sagittal section of the lower part of a female trunk, right segment ( wikipedia )

Causes of Vaginal Discharge

– Physiological
– Cervical Ectopy (also known cervical erosion, is a common condition caused when cells from inside the cervical canal, known as glandular cells, are present on the outside surface of the cervix. is not harmful condition)
– Foreign bodies, such as retained tampon
– Vulvar Dermatitis (it happens when the soft folds of skin around the opening of the vagina become red, painful, and itchy. Dermatitis can be caused by heat or wetness or can be a reaction to scented soaps, powder, creams, toilet paper, or clothing)
Non-sexually transmitted infection
– Bacterial Vaginosis
– Candida Infections
Sexually transmitted infection
– Chlamydia trachomatis
– Neisseria gonorrhoeae
– Trichomonas vaginalis

The abnormal vaginal discharge is characterized by change in color, consistency, volume, and/or odor and may be associated with symptoms such as itching, soreness, dysuria(painful or difficult urination), pelvic pain, or intermenstrual or postcoital bleeding.

The major causes of abnormal vaginal discharge are either vaginal or cervical infections. Causes of vaginal infections are Gardnerella vaginalis, Trichomonas vaginalis, and Candida albicans. Primary cervical infections causing vaginal discharge are Neisseria gonorrhoeae , Chlamydia trachomatis , and Herpes simplex. In the prepubertal girl, N. gonorrhoeae causes a vaginal rather than cervical infection.

Noninfectious causes of vaginal discharge include atrophic vaginitis, foreign body, malignancy, contact dermatitis, or other mechanical or chemical irritation. An intrauterine contraceptive device can sometimes cause vaginal discharge related to chronic irritant cervicitis(an inflammation of the cervix, the lower, narrow end of the uterus that opens into the vagina) or endometritis(is a condition where tissues similar to the lining of the womb starts to grow in other places, such as the ovaries and fallopian tubes).

Bacterial vaginosis will be the diagnosis in 40 to 50% of women presenting to office practices with vaginitis. Most recently it has been called Gardnerella, after its associated organism.

Gardnerella is a short, gram-negative to variable bacillus that may be a colonizer in the vagina. It is controversial whether Gardnerella itself produces the signs and symptoms of the disease or whether its symbiotic relationship with vaginal anaerobes is necessary to produce the characteristic gray, homogeneous, malodorous discharge. The disease is limited to sexually active women, but clear evidence for sexual transmission is lacking, and the need for treatment of partners is unclear. Diagnosis is made by laboratory methods.

Candida vaginitis, or “yeast,” occurs less frequently than patients or physicians believe. In one group of self-referred women who offered to be part of a study on chronic recurrent yeast infections, only 50% were found to have Candida vaginitis. When it occurs, the offending pathogen is usually Candida albicans. Again, it is controversial whether this is a normal colonizer of the vagina. Its pathogenicity is not related to its concentration in the vagina; small amounts can cause excruciating symptoms. Normal bacterial colonization has been thought to be important in the defense against Candida infection; for example, some lactobacilli inhibit the growth of Candida. However, women with Candida still have predominant lactobacilli on gram stain of vaginal fluid. This belief in the efficacy of lactobacilli has led to the home remedy of yogurt containing lactobacillus, used intravaginally with an applicator or as a douche, for treatment of vaginitis. Sexual transmission has not been proven to be important in most cases, although treating male partners may help in recalcitrant cases. Host factors (e.g., recent antibiotic treatment, pregnancy, oral contraceptives) all predispose to yeast infection. It is not known why pregnancy and use of oral contraceptive pills predispose to yeast infection. Diabetes mellitus out of control facilitates yeast growth in the vagina, but most women with recurrent yeast do not have diabetes. Women with diabetes are at risk for all forms of sexually transmitted diseases and must be examined and treated appropriately.

Candida vaginitis has the most characteristic with pruritus being the most prominent symptom, often with sparse or no discharge. The discharge, when present, may resemble cottage cheese. Erythema and swelling of the vulva and vaginal walls are marked. Diagnosis is suggested by history and confirmed by physical examination and laboratory lab test for vaginal specimen culture. Trichomonas vaginalis is a protozoan that grows well at a pH of 6 and has role in sexually transmitted disease.  However, it is a common organism often found asymptomatically in sexually inactive postmenopausal women. It can be associated with other sexually transmitted diseases, especially gonorrhea. The ectocervix may be involved, with punctate hemorrhages producing the typical strawberry cervix, but this is seen only 2 to 5% of the time. Discharge may be gray or greenish yellow and is not usually frothy, but is usually excessive. Occasionally wet-mount examination of vaginal discharge yields only white blood cells with no evidence of trichomonas or of mucous from the cervix. These women are usually at low risk for sexually transmitted diseases. Cervical ectopy with inflammation, rather than infection, may be the cause. Over-the-counter douches, scented toilet paper, and contraceptive products are some of the more common etiologies for local irritation and contact dermatitis. Forgotten diaphragms and tampons must be looked for with malodorous discharges. Postmenopausal women with atrophic vaginal mucosa may develop a watery, irritating, sometimes malodorous discharge secondary to local irritation, especially from intercourse. This may be mixed with blood, and can be mistaken for postmenopausal bleeding. Cervicitis has been a poorly defined term used to refer to a variety of conditions including a pathologic diagnosis, cervical ectopy, and true cervical infection. It is to be hoped that the expanded interest in sexually transmitted diseases will lead to more precise criteria for its use. At present, the most important infectious cervical pathogens that can produce vaginal discharge include N. gonorrhoeae, C. trachomatis, and herpes simplex.


Vaginal discharge serves an important housekeeping function in the female reproductive system. Fluid made by glands inside the vagina and cervix carries away dead cells and bacteria. This keeps the vagina clean and helps prevent infection. Most of the time, vaginal discharge is perfectly normal.6

If you find out something unusual with those discharge especially with changing in color, consistency, volume, and/or odor and may be associated with symptoms please do check up to your doctor.


  1. Gene B. Bishop. Clinical Methods: The History, Physical, and laboratory Examinations. 3rd Edition. Vaginal Discharge. Chapter 172. 1990. Access: https://www.ncbi.nlm.nih.gov/books/NBK281/#:~:text=A%20physiologic%20discharge%20is%20usually,epithelial%20cells%20on%20saline%20microscopy. March 15 2021
  2. John P. Cunha. DO, FACOEP. Transudate vs. Exudate: What’s the Difference?https://www.emedicinehealth.com/transudate_vs_exudate_whats_the_difference/article_em.htm Access 15 March 2021
  3. Wikipedia. Vaginal Fornix. https://en.wikipedia.org/wiki/Vaginal_fornix#:~:text=The%20posterior%20fornix%20is%20the,to%20the%20vesico%2Duterine%20pouch. Access : Maret 15 2021
  4. Vanishree L Rao, Tahor Mahmood. Vaginal Discharge. Elsevier. 2019. Obstetrics, Gynaecology and Reproductive Medicine. 30:1.
  5. Des Spence, Catriona Melville. Vaginal Discharge. BMJ. 2007 Dec 1; 335(7630): 1147–1151. PMCID: PMC2099568. doi: 10.1136/bmj.39378.633287.80 )
  6. Traci C. Johnson, MD. Vaginal Diascharge: What’s Abnormal?. https://www.webmd.com/women/guide/vaginal-discharge-whats-abnormal#:~:text=Vaginal%20discharge%20serves%20an%20important,vaginal%20discharge%20is%20perfectly%20normal. Access: March 15 2021