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Dermatology 2002;205(4):374-7
Hair pain (trichodynia): frequency and relationship to hair loss and patient gender.
Background: Patients complaining of hair loss frequently claim that their hair has become painful. Objective and Methods: The aim of the study was to evaluate the frequency of this phenomenon and its relationship to hair loss. Patients seeking advice for hair loss either spontaneously reported or were questioned about painful sensations of the scalp. Hair loss activity was quantified by a hair pull, daily count and wash test. Telogen percentage was obtained by a hair pluck. The scalp surface was examined by dermatoscopy. Results: Of 403 examined patients, 20% of women and 9% of men reported hair pain, irrespective of the cause and activity of hair loss. A minority presented scalp telangiectasia. This strongly correlated with hair pain. Conclusions: Hair pain (trichodynia) affects a significant proportion of patients complaining of hair loss and may increase the anxiety. The symptom neither allows discrimination of the cause nor correlates with the activity of hair loss. A higher prevalence of female patients might be connected to gender-related differences in pain perception in relation to anxiety. The role of vasoactive neuropeptides in the interaction between the central nervous system and skin reactivity is discussed. In the absence of any correlation with quantitative parameters of hair loss or specific morphologic changes of the scalp, management remains empiric and tailored to the individual.
Ann Dermatol Venereol 2002 May;129(5 Pt 2):831-6
Alopecia areata: update on therapy
The management of patients with alopecia areata is obviously not restricted to the prescription of a treatment inducing hair growth. It requires thorough exploration (history of hair loss, treatments and concomitant pathologies), detailed clinical examination of the integument and palpation of the thyroid. The patient must, systematically, be given a simple explanation of his/her pathology, thus avoiding any feelings of mystery, hopelessness and guilt and hence paradoxically turning alopecia into "just another disease", even if flares are unpredictable and cannot always be treated. Innovations over the past few years have not met dermatologist's expectations: in particular immunosuppressors administered locally have not shown efficacy in human, as opposed to animal models of alopecia areata. Moreover, we must remain critical and rigorous with regard to "false" innovations: several recent publications are, methodologically, open to criticism. Older products provide clear descriptions of their indications and use, and relatively standardize the therapeutic approach to alopecia. Some of them lead to hair growth on the treated area: localized immuno-therapy that in certain cases induces hair growth where other treatments have failed. PUVA-therapy, however, because of frequent relapses on withdrawal and the characteristic recurrence of alopecia, rapidly leads to the use of high cumulative doses; balneo-PUVA therapy is effective with lower doses (PUVA-turban). Recently, UVB TL01 has shown efficacy in anecdotal studies. Local corticosteroids; notably injectable and anthralin, an old treatment which remains a useful therapeutic approach in alopecia areata plaques and in the ophiasic forms in children and adults. Finally, among the available treatment arms, systemic corticosteroids still have a place in recent extended forms: although still under experimentation, the bolus appears efficient during the primary episodes of alopecia areata, when administered within the first three months
Ther Umsch 2002 May;59(5):217-22
Diffuse hair loss in women
The complaint "Doctor, I am losing my hair" represents a particular challenge to the physician, and involves making a specific diagnosis, selecting an appropriate therapy, and expressing empathy for the patient's anxiety. Diffuse hair loss in women was formerly classified as an entity of its own. Since the identification of female pattern hair loss, most cases have been recognized to be due to androgenetic alopecia, often during phases of life characterized by fluctuations of sexual hormone levels or in connection with intake or cessation of hormonal therapy. The most difficult differential diagnosis includes androgenetic alopecia, chronic telogen effluvium, and psychogenic pseudo efflvuium. Androgenetic alopecia is due to androgen-induced, non-synchronized, progressive shortening of the hair growth cycle and gradually leads to thinning of the central scalp area. Idiopathic chronic telogen effluvium typically occurs in women, starting abruptly without a recognizable initiating factor, and involves the entire scalp area with increased shedding of telogen hair. It is believed to be due to synchronization phenomena of the cyclic hair growth. Psychogenic pseudo effluvium affects fashion-oriented, self-conscious women suffering of a discrepancy between the actual state of their hair and idealized expectations. Later the problem of age-related hair thinning oft becomes a surrogate for the more generalized problem of senescence. Rational therapy of androgenetic alopecia aims at blocking the androgen effect on hair follicles with estrogens and antiandrogens or at pharmacologically reversing vellus hair transformation with topical minoxidil. In contrast, women with idiopathic chronic telogen effluvium should be reassured that their problem is rather a state of exaggerated "hair shedding" than of actual "hair loss".
Br J Dermatol. 2003 Mar;148(3):553-7.
Compound heterozygosity for mutations in the hairless gene causes atrichia with papular lesions.
BACKGROUND: Congenital atrichias represent a complex and heterogeneous group of genodermatoses, which have been shown in several consanguineous families to result from homozygous mutations in the hairless gene (HR). OBJECTIVES: To identify the molecular basis of congenital atrichia in a non-consanguineous family. METHODS: Genetic analysis was carried out in a two-generation family with two children with congenital atrichia and one healthy child. RESULTS: We established a diagnosis of atrichia with papular lesions based on clinical and histopathological data. We identified a heterozygous 11-bp deletion (189-199del) in the two affected children and their mother. In addition, the two affected children and their father were shown to carry a non sense mutation (Q478X), which has previously been described in a Pakistani family. Haplotype analysis revealed that mutation Q478X occurred independently in the two families. CONCLUSIONS: We have identified the first case of compound heterozygosity for mutations in HR as well as the first instance of a recurrent mutation in this gene. These data further expand our understanding of the molecular pathomechanisms underlying congenital atrichias.
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