There is no clear association between low serum ferritin and chronic diffuse telogen hair loss.

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Br J Dermatol 2002 Nov;147(5):982-4

There is no clear association between low serum ferritin and chronic diffuse telogen hair loss.

BACKGROUND: Low iron stores are considered a possible cause of chronic diffuse telogen hair loss in women. Estimation of serum ferritin is recommended as part of the initial assessment when women present with chronic diffuse telogen hair loss, and iron supplementation therapy is commonly recommended for those found to have low iron stores. OBJECTIVES: To evaluate the relationship between low serum ferritin ( 20 micro g L-1. Cessation or reversal of hair loss was not seen in any of these women. CONCLUSIONS: No direct relationship between low serum ferritin and hair loss can be established. The usefulness of serum ferritin in the routine investigation of women with chronic diffuse telogen hair loss is unclear, as is the role of iron supplementation therapy in the management of hair loss.

Clin Exp Dermatol 2002 Jul;27(5):389-5

Telogen effluvium.

The term telogen effluvium, first coined by Kligman in 1961, refers to the loss of club (telogen) hair in disease states of the follicle. Kligman's hypothesis was that whatever the cause of hair loss, the follicle tends to behave in a similar way, namely the premature termination of anagen. "The follicle is precipitated into catagen and transforms into a resting stage that mimics telogen." Ipso facto the observation of telogen hair loss does not infer a cause. To establish the cause of the hair loss, one requires a history to identify known triggers, biochemical investigations to exclude endocrine, nutritional or autoimmune aetiologies and in many cases histology to identify the earliest stages of androgenetic alopecia. The duration of the hair loss at presentation helps predict those patients in whom further investigation will have the greatest yield. "It is unfortunate that baldness has been approached with an eye toward "regrowing" or "restoring hair", and thus with a tendency toward commercialism. Locked within the metamorphosing hair follicles in the balding scalp are all the secrets of growth and differentation. Searching for these secrets should transcend the eagerness to "regrow" hair on a bald scalp, an achievement which is of no great consequence. When we know these answers, we shall have the key, not to hair growth alone, but to all growth, which is, after all, the basis of all biological phenomena." William Montagna, 1959.

J Theor Biol 2002 Feb 7;214(3):469-79

The follicular automaton model: effect of stochasticity and of synchronization of hair cycles.

Human scalp hair consists of a set of about 10(5)follicles which progress independently through developmental cycles. Each hair follicle successively goes through the anagen (A), catagen (C), telogen (T) and latency (L) phases that correspond, respectively, to growth, arrest and hair shedding before a new anagen phase is initiated. Long-term experimental observations in a group of ten male, alopecic and non-alopecic volunteers allowed determination of the characteristics of hair follicle cycles. On the basis of these observations, we previously proposed a follicular automaton model to simulate the dynamics of human hair cycles and the development of different patterns of alopecia [Halloy et al. (2000) Proc. Natl Acad. Sci. U.S.A.97, 8328-8333]. The automaton model is defined by a set of rules that govern the stochastic transitions of each follicle between the successive states A, T, L and the subsequent return to A. These transitions occur independently for each follicle, after time intervals given stochastically by a distribution characterized by a mean and a standard deviation. The follicular automaton model was shown to account both for the dynamical transitions observed in a single follicle, and for the behaviour of an ensemble of independently cycling follicles. Here, we extend these results and investigate additional properties of the model. We present a deterministic version of the follicular automaton. We show that numerical simulations of the stochastic version of the automaton yield steady-state level of follicles in the different phases which approach the levels predicted by the deterministic equations as the number of follicles progressively increases. Only the stochastic version can successfully reproduce the fluctuations of the fractions of follicles in each of the three phases, observed in small follicle populations. When the standard deviation is reduced or when the follicles become otherwise synchronized, e.g. by a periodic external signal inducing the transition of anagen follicles into telogen phase, large-amplitude oscillations occur in the fractions of follicles in the three phases. These oscillations are not observed in humans but are reminiscent of the phenomenon of moulting observed in a number of mammalian species.

Hum Genet. 2003 Apr;112(4):400-3. Epub 2003 Feb 14.

Notch4, a non-HLA gene in the MHC is strongly associated with the most severe form of alopecia areata.

Alopecia areata (AA) is a disorder primarily affecting the hair and nails in which associated autoimmune or atopic disease is common. Genetically, it is a complex trait with evidence of a role for genes of the major histocompatibility complex (MHC), the interleukin-1 cluster and chromosome 21 in the pathogenesis. The strongest association is with HLA class II alleles, although whether this indicates a direct contribution to the pathogenesis or results merely from linkage disequilibrium with nearby disease genes is unknown. Notch4 is a recently defined gene in the HLA class III region. Notch signalling is a direct determinant of keratinocyte growth arrest and entry into differentiation. A possible role for Notch in hair growth has been indicated by transgenic mouse findings that activation of the Notch pathway in the hair cortex leads to aberrant differentiation of adjacent hair-shaft layers. Notch4 is therefore a plausible candidate gene for AA. We have examined two polymorphisms in the coding sequence of the Notch4 gene at positions +1297 and +3063 in a case-control study of 116 AA patients and 142 ethnically matched, healthy control subjects. The initial analysis showed a significant association of AA in the overall data set with the Notch4(T+1297C) polymorphism (P<0.001) but not with Notch4(A+3063G). To confirm this association, we genotyped an additional 62 patients and found that the risk for disease was higher in Notch4(+1297C) homozygotes [odds ratio (OR) 3.43 (1.63, 7.19)] than in heterozygotes [OR 2.58 (1.57, 4.24)]. On classifying the patients by severity of disease, the association appeared to be confined to the severest form (alopecia universalis) [OR 4.02 (1.64, 9.88), P=0.0014]. These results support previous findings showing that different HLA susceptibility alleles are associated with mild and severe AA.

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