Tag: medical in sanur

What is Rheumatoid Arthritis ? Find it Out Here!

What is Rheumatoid Arthritis ? Find it Out Here!

Autoimmune, Covid-19·

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???

YES, THERE IS IT. 

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. 

References

  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. 2019, 8(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. 2007, 66, 1560–1567.
Becker’s Nevus Syndrome, What kind of Syndrome is This?

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

Covid-19, Fact·

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?

Manifestations

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 

Treatment

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

References

  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?

Covid-19, Fact·

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?

Definition

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. 

Causes

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. 

References

  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.