Fact

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.
Fact About Baldness That You Must Know!

Fact About Baldness That You Must Know!

Covid-19, Fact·

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!