Hair Loss

Common Nonscarring Alopecia(Hairloss)

1) Androgenic alopecia(Pattern hair loss).
2) Telogen effluvium -(Non pattern hair loss-Generalised).
3) Alopecia areata –usually patchy.
4) Hyper & Hypothyroidism
5) Hypoparathyroidism :Calcium levels
6) Hypopituitarism
7) Diabetes mellitus
8) Decreased Serum Ferritin levels : Anemia
9) Low Serum Protein : Aminoacids
10) Deficiency of Vitamin. A, C, E, Zinc, Selenium, Copper, etc.
11) Dieting, Stress, Anxiety, Lack of Sleep
12) Additional cause:
1) Drugs
2) Weight loss
3) Acute blood loss
4) General anesthesia-
5) Reversible (but may be become chronic)
6) Post-partum
Hair Abuse: Heat drying
Hair Abuse: Straightening
Hair Abuse: Perming
Hair Abuse: Dyes
Common Scarring alopecia
Discoid lupus erythematosus
Lichen planopolaris
Sever fungal,viral,bactarial infection
Trauma or Burns

Common Nonscarring Alopecia(Hairloss)

Androgenic alopecia or Pattern hair loss

An androgenic alopecia is by far the most common form of alopecia in men and women. The development and occurrence of AGA depends on genetic predisposition and an interaction of endocrine factors How does pattern hair loss occurs( Pathogenesis) AGA involves both genetic and hormonal factors. Different gene loci have been linked to the development of AGA After puberty, androgen triggers a series of events within theses genetically programmed hair follicles, predominately in fronto- parietal scalp area that transform terminal to miniaturized follicles. In AGA, hair cycle dynamic change. The time between shedding of hair and anagen regrowth become longer, leading to reduction of present hair on the scalp. GENETICS The development of AGA shows a strong genetic involvement. The risk of AGA increases significantly with positive family history. Inheritance is POLYGENIC (Kuester & Happel,1984) The Expression of Insulin like growth factor(IGF)-1, in dermal papilla may play important role in development of pattern baldness. Gene locus on chromosome 12(12q22-q23) may responsible for male pattern baldness. More recent study shows that 17q21.31 may be locus for early onset AGA. CYP17 gene on chromosome 10q24.3 was held responsible for female pattern baldness. Ellis shows there is no role of 5µ-reductase isoenzymes in causation of male pattern baldness. In balding scalp ,higher expression of the androgen receptor gene was found which is located at band q12 in the X chromosome. The involvement of the X chromosome in development of AGA stresses the importance of the maternal line in inheritance.

Hormonal Factors

5µ-reductase plays the key role in AGA.Two 5µ-reductase isoenzymes are found in dermal papilla cells of beard and scalp follicles. In the balding scalp a predominance of 5µ-reductase isotype 1 can be found. All enzymes can be located in the sebaceous gland and different parts of the hair follicle of the scalp skin. Therefore pilosebaceous unit has the potential to mediate androgetic action without relying on elevated systemic levels or production of testosterone or DTH Increased level of AROMATASE(Detoxifying by removal of excess androgens) in female explain the difference in male and female patterns of balding and sparing of the frontal hair line.

Role of Androgen in Female Pattern Baldness

Increases level of 5µ-androstane-3µ,17b-diolglucuronide and 5µ-reductase hyperactivity was found. Testosterone level is normal. Male Pattern Baldness More than 90% of hair loss problem in men are AGA. Out of 10 males 6 are suffering from MPB. AGA usually start at an early age and progress slowly. Thinning of hair can occur as early as the age of 12 or any time later in life. Most cases start between the age of 15 and 25. The clinical course is gradual. Many men reach their maximum pattern by their forties. Usually there is strong family history but in about 12% cases family history is negative.