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PubMed1991

Alopecia in systemic lupus erythematosus. Relation to disease manifestations.

Alopecia was observed in 40/74 (54%) patients with systemic lupus erythematosus (SLE). Patients with alopecia had a significantly higher rating for cutaneous manifestations, Raynaud's phenomenon and muscle tenderness, and most of these signs correlated with the magnitude of alopecia. There was no difference between patients with or without alopecia for arthritis, nephritis or central nervous system manifestations. Alopecia correlated with disease activity index but did not correlate with various specific measurements of disease exacerbation.

Adult↗

PubMed1990

Trial of intralesional interferon alfa in the treatment of alopecia areata.

Eleven patients with alopecia areata, ranging from patchy disease to alopecia universalis, were treated with intralesional interferon alfa-2 on a selected area of alopecia. Follow-up at 3 months revealed local terminal hair growth in one patient. At 12 months, variable disease activity was seen. Regional lymphadenopathy, a new finding with interferon, was seen in four patients during the treatment. Immunohistochemical studies showed some changes in the inflammatory infiltrates and in HLA-DR expression that may be related to the interferon or to the dynamics of the inflammatory infiltrate in alopecia areata. Interferon, at the dosage and treatment schedule used in our trial, had no significant effect on alopecia areata.

Adult↗

PubMed1985

Increase of mast cells in the alopecia lesion of mice.

A histological investigation was made of the quantitative behavior of mast cells in bald areas on mice and in human alopecia areata. C57BL,W/Wv and +/+ mice with alopecia lesions were examined. In C57BL mice and +/+ mice, the number of dermal mast cells (per square mm) in the bald areas was greater than that in controls. The mean number of mast cells was slightly higher in human alopecia areata than in the controls. Since W/Wv mice lacking mast cells developed alopecia lesions, it seems that mast cells are not necessary for the onset of alopecia areata but could play some part in regrowth.

Alopecia Areata↗

PubMed1989

[Planning of a local flap of expanded scalp for repair of alopecia cicatrisata].

Tissue expansion of scalp opens a new way for the treatment of alopecia cicatrisata. From May 1986 to April 1988, 56 cases of alopecia cicatrisata and skull outcrop had been repaired by Chinese tissue expander in our department. All cases got good results. Of them, the area of alopecia was over 120 cm2 and the greatest one (320 cm2) consisting of two third of the total scalp in 21 cases. There were 49 cases repaired by one expansion and other 7 cases followed by a secondary expansion. The characteristics of the expanded scalp and the common types of local flap design had been discussed. It was applicable for all kinds of alopecia cicatrisata and both for children (over 3 yrs) and adults. The results of scalp expansion in children revealed superior than that in adults. We considered that the repairing of alopecia cicatrisata by scalp expansion had more advantages than other methods.

Adolescent↗

PubMed1987

[Endocrine constellation in androgenetic alopecia in the female].

The mechanisms which induce androgenetic alopecia in females are only poorly understood at the molecular biological level. In predisposed, mainly centroparietal areas, androgenic stimulation of genetically predisposed hair follicles is considered to cause transformation from terminal to vellus hair follicles. However, reports on serum androgen levels in androgenetic alopecia in the female show broad variations. In the present study serum androgens, gonadotropins, oestradiol and sex hormone binding globulin were determined in the luteal phase of the menstrual cycle in 25 patients with female pattern androgenetic alopecia by radioimmunosorbent assay. In 16 of these patients skin slices from the alopecic areas were punch biopsied under local anaesthesia for determination of cytosol- and nuclear androgen receptor (AR). Mean values of all serum hormone levels were within the normal range. Cytoplasmatic AR was positive in 75% of cases, with a mean level of 22 fmol/mg protein. In 50% of cases nuclear AR was demonstrated, with a mean level of 119 fmol/mg DNA. No correlation was found between serum androgen levels and AR. Highly positive AR levels indicate a high androgen stimulability in female androgenetic alopecia. These findings support the concept of AR as regulators of genetically determined hair follicles in androgenetic alopecia.

17-alpha-Hydroxyprogesterone↗

PubMed1987

Treatment of alopecia areata with squaric acid dibutylester.

Fourteen of 18 patients with extensive alopecia areata completed a course of weekly treatments with the topical allergen squaric acid dibutylester in acetone. The concentration of squaric acid was varied as needed to maintain a moderate dermatitis. Only one area of alopecia was treated in each patient until marked hair growth occurred. The remainder of the scalp was then treated. Four patients (28.5%) had complete regrowth of hair during treatment; one of these patients had recurrent alopecia after stopping treatment. Ten patients (71.4%) were treatment failures. Of these ten failures, seven developed a moderate dermatitis and hair regrowth but experienced recurrent alopecia with continued treatment. One patient failed to maintain an adequate persistent dermatitis, and two failed to grow any hair despite the presence of dermatitis. Successful results in these patients correlated with (1) a duration of alopecia of less than two years, (2) the development of a moderate dermatitis within three weeks of starting treatment, (3) persistent hair growth within two months of developing dermatitis, and (4) an age of 16 years or older.

Allergens↗

PubMed1983

[Genetic control of alopecia in sheep].

A hypothesis is suggested which turns down the opinion that alopecia or pathological wool shedding in sheep is due to some pathological processes or disease. We suppose that this trait is controlled by a gene of natural wool shedding inherited from sheep far ancestors, and we propose to designate the recessive alopecia gene as Alp3 and its dominant allele, a wool alopecia resistance gene, as AlpA. Alopecia will only be revealed in homozygotic Alpa/Alpa state, due to recessivity of alopecia gene, but heterozygotic AlpA/Alpa and homozygotic AlpA/AlpA sheep will have a normal wool coat. A new polymorphic trait is supposed to exist which is conditioned by simultaneous presence of two genetic alleles in a sheep population with descrete phenotypic manifestation.

Alleles↗

PubMed1982

[Treatment of alopecia areata totalis and maligna with Solvezink (author's transl)].

Treatment with Solvezink has been performed in 284 patients: 42 with alopecia areata, 106 with alopecia totalis (preserved axillar and pubic air as well as eyelashes and brows) and 136 with alopecia maligna. The duration of the treatment including maintenance therapy was up to 6 years. In patients with alopecia areata a state without relapse of 1 to 4 years was achieved in 42,8% of cases, in alopecia totalis and maligna a maintenance therapy was necessary to ensure a permanent regrowth of the hair. When applied correctly, Solvezink was well tolerated. The dosages and the treatment intervals of the treatment should be adjusted individually.

Administration, Oral↗

PubMedDate not supplied

[Drug-induced alopecia: review of the literature].

Drugs are capable of producing a wide spectrum of hair loss, ranging from barely detectable shedding to irreversible baldness. Drug-induced alopecia is usually described as a diffuse non-scarring alopecia which is reversible upon withdrawal of the drug. Only a few drugs (mainly antimitotic agents) routinely cause hair loss whereas many drugs may be the cause of isolated cases of alopecia. Some psychotropic drugs are likely to induce a drug-related alopecia. Case reports with tricyclic antidepressants rarely appear in the literature. It has been reported that 15 per cent of patients taking lithium developed hair thinning. Hair loss is reported secondary to some anticonvulsant agents mainly valproic acid. Among antihypertensive drugs, systemic or topic beta-adrenoceptor antagonists should be considered as possible causes of hair loss. Hair loss from salicylates or nonsteroidal analgesics occurs in a very small percentage of patients. All anticoagulant and antithyroid drugs can produce hair loss. Diffuse hair loss can also be associated with the use of oral contraceptives, while receiving the pill and after stopping the drug. There is a long list of drugs that on occasion have been cited as causing hair loss: cimetidine, retinoids, amphetamines, bromocriptine and levodopa. A few isolated cases have been reported with some hypocholesterolaemic or anti-infectious agents. Diagnosis of drug-induced alopecia remains difficult. The only way to confirm it is to see if an improvement occurs after cessation of the suspected drug. This side effect must be recognized because it may be a source of poor compliance in some patients.

Alopecia↗

PubMed1997

[Cicatricial alopecias: diagnosis and therapy].

The cicatricial alopecias often are both a diagnostic and therapeutic challenge to the practitioner. Where there is no obvious physical/chemical injury or acute infectious etiology, clinical differential diagnosis of scarring alopecia is often difficult. The loss of follicular orifices in an area of alopecia points to a permanent loss of hair. In all of these cases a scalp biopsy is indicated. Primary and secondary scarring alopecia are differentiated: While the former is due to preferential destruction of the follicle, the latter results from events outside the follicle, which eventually impinge upon and eradicate the follicle. These include infiltrative processes such as granulomatous inflammation or neoplastic disease. In the group of primary scarring alopecia, well-defined chronic-inflammatory diseases of the scalp amenable to specific therapies are differentiated microscopically on the basis of the pattern of inflammation and the type of inflammatory cell that predominates. Thus, accurate diagnosis based on histopathology is a prerequisite to any rational therapy. Management of the less well classified diseases is much more problematic. Where end-stage fibrosis is established, surgical treatment and/or prosthetic help are taken into consideration. With the expanding knowledge of the immunology and molecular biology of the hair follicle, there is hope for the feasibility of therapeutic interventions that interfere early in the course of the pathogenetic processes ultimately leading to the permanent loss of hair.

Alopecia↗

PubMed1999

Acquired scalp alopecia. Part II: A review.

The neutrophil-associated and infiltrative scarring alopecias are reviewed including folliculitis decalvans, tufted folliculitis, dissecting cellulitis of the scalp, acne keloidalis and follicular degeneration syndrome. The management of acquired scalp alopecia is also reviewed including newer, promising therapies. More specific agents targeting components of the androgen system will make the treatment of androgenetic alopecia more rewarding. Similarly new immunomodulatory therapies show great promise for the lymphocyte-associated alopecias and include a new generation of macrolide immunosuppressives (tacrolimus, SDZ ASM 981, and SDZ 281-240), some of which appear to have good transcutaneous absorption.

Alopecia↗

PubMed1984

Ophthalmologic oncology: alopecia of the eyelashes.

The variety of lesions that can cause alopecia of the eyelashes (Table 1) demonstrates the need for accurate diagnosis. A full-thickness biopsy of lid margin with appropriate three-suture closure can leave an imperceptible defect and may provide invaluable information. Although a partial-thickness lid biopsy is certainly appropriate for many common eyelid tumors such as basal-cell carcinomas or nevi, we feel strongly that a full-thickness lid biopsy is indicated when discussing chronic eyelid lesions that cause alopecia. The information gathered from a full-thickness biopsy is far superior especially in those lesions which cause chronic blepharitis or especially in a case of a recurrent chalazion where the conjunctival surface and skin surface are both equally significant. The high mortality associated with sebaceous-cell carcinomas makes a good pathologic specimen allowing for accurate diagnosis essential. Partial-thickness eyelid biopsies, especially in cases of sebaceous carcinoma, may lead the pathologist to an erroneous, more benign, diagnosis and the clinician to a false sense of security. While many of the nonscarring alopecias may be diagnosed on their clinical characteristics alone, the scarring alopecias will frequently need a lid biopsy to ascertain diagnosis and gauge treatment.

Alopecia↗

PubMed1983

Diphencyprone in the treatment of alopecia areata.

27 patients suffering from either extensive alopecia areata (n = 5) or alopecia totalis (n = 22) were treated topically with diphencyprone, a new potent contact allergen. The duration of treatment ranged from 4 to 17 months. Unilateral induction of hair growth after unilateral treatment was observed in 23 patients. A continuous response after continuous treatment has been observed so far in 18 of these patients. Thus, diphencyprone was found to be as effective as DNCB or squaric acid dibutylester in the treatment of alopecia areata. Unlike DNCB, diphencyprone is not mutagenic in the Ames test. Compared with squaric acid dibutylester, diphencyprone is more stable and thus more suitable for storage when dissolved in acetone. Further investigative evaluation of diphencyprone may show whether this drug is suitable for a more general use in the treatment of severe forms of alopecia areata.

Adolescent↗

PubMed1992

Alopecia areata. A review of therapy, efficacy, safety, and mechanism.

Although it is clear from the foregoing that some of the drugs and chemicals used to treat severe alopecia areata are efficacious to some degree, it is impossible to draw any meaningful comparisons among the data outlined in Tables 1 and 2. Virtually all of the studies were designed differently. Differences in chronicity and extent of disease as well as history of previous treatment resistance may significantly affect efficacy data even as two investigators compare the same drug. Drug-induced hair regrowth in alopecia areata may be very slow; a cosmetic response may take 1 to 2 years to achieve. Efficacy determinations made at shorter intervals may, therefore, not reflect true therapeutic potential. Efficacy end points vary significantly and need to be standardized. From a practical standpoint, scalp hair coverage that is deemed by the patient to be cosmetically acceptable seems to be a reasonable efficacy end point to report. Maintenance of cosmetic effect with continued treatment and/or following discontinuation of treatment also is useful to document. Table 3 outlines my approach to therapy of alopecia areata. Topical treatments often must be used for as long as 3 months before evidence of regrowth can be seen. In my experience with severe disease, if topical treatments cannot control a flare or induce regrowth, then the patient will often require either lengthy or frequent courses of systemic steroids. In my experience, prednisone doses as low as 20 mg/d may be associated with aseptic neurosis of the hip or severe gastrointestinal bleeding. Severe alopecia areata is a disease for which all therapies are, at best, palliative and, at worst, potentially harmful to patients who are usually otherwise very healthy. The psychosocial significance of this disease is enormous. The insights shared by a long-time sufferer of the disease mirror those expressed by the many patients with whom I have worked during the past 12 years. Three key elements to effectively treat the patient are (1) to help the patient understand the disease; (2) to encourage the patient to share his or her feelings with the physician, family, friends, and other sufferers of the disease; and (3) to help the patient to maintain a sense of hope for future scientific knowledge and treatment of the disease. With a thorough knowledge of the potential benefits and risks of each treatment or combination treatment, the physician with the patient's understanding and cooperation may then embark on what may be in severe cases a lengthy and sometimes unproductive therapeutic process.

Alopecia Areata↗

PubMed1995

Congenital generalized follicular hamartoma associated with alopecia and cystic fibrosis in three siblings.

BACKGROUND: Generalized follicular hamartoma is a rare condition that has been described in association with alopecia, myasthenia gravis, and circulating autoantibodies. To date, all reported cases have appeared in female individuals. We report a kindred in which three siblings were affected by this condition in association with alopecia and cystic fibrosis. OBSERVATIONS: Three children of two consanguineous patients were affected by cystic fibrosis. They also had the same phenotype characterized by senilized facies, partial alopecia, and hypohidrosis, severe retardation of physical growth, and hyperelasticity of the skin. In all three children, skin biopsy specimens revealed the presence of basaloid proliferations at the level of the hair follicles that could not be demonstrated in their healthy parents. Myasthenia gravis did not appear during the clinical course of our patients, and circulating autoantibodies were not detected. All three patients died during childhood due to complications of cystic fibrosis. CONCLUSIONS: Generalized follicular hamartoma is a rare condition previously reported in association with alopecia, myasthenia gravis, and/or circulating autoantibodies (antinuclear and antiacetylcholine receptor antibodies). These are the first congenital cases of generalized follicular hamartoma described, and it is also the first time that an association with cystic fibrosis is reported. The striking association of generalized follicular hamartoma with cystic fibrosis in these three siblings suggests that there may be a genetic linkage between the two conditions.

Alopecia↗

PubMed1997

Morphological analysis of hair follicles in alopecia areata.

This study characterizes hair follicles from early alopecia areata lesions at both the light and electron microscopic levels and describes how affected hair follicles differ from normal hair growth. The study focuses on acute and active lesions where hair follicles show greatest divergence from the normal growth pattern and are most likely to display features of primary pathology. Morphologic analysis revealed regressive changes in the hair bulbs of anagen hair follicles in alopecia areata. While tissue injury did not appear to be cell type specific, pre-cortical keratinocytes and hair bulb melanocytes were primarily affected. Three distinct patterns of cell degeneration, of variable frequency, are described including "dark cell" transformation, apoptosis, and necrosis. Abnormal melanogenesis was a common finding in this study, which may explain some of the associated pigmentary anomalies seen clinically in acute alopecia areata. Tissue damage, which was not always associated with a mononuclear cell infiltrate, may explain the premature involution of suboptimal anagen hair follicles into an early resting phase in alopecia areata. Finally, scanning electron microscopic, light microscopic, and transmission electron microscopic studies describe defective cortex differentiation in characteristic "exclamation-mark" hair shafts. These hairs may result from a transient phase of cell degeneration among pre-cortical keratinocytes.

Adolescent↗

PubMed1992

Alopecia and mood stabilizers: two case reports.

Two cases of alopecia observed during treatment with lithium and valproate are described, and the recent literature on this subject is reviewed. Our clinical observations confirm earlier reports. These toxic alopecias are characterized by a diffuse but rarely total hair loss. After stopping medication, the hair grows back generally and completely. Two cases of toxic alopecia are presented where hair grew back following a substitution of lithium by valproate in the first case and after stopping valproate in the second. The evaluation and therapeutic attitude in the presence of alopecia in patients needing mood stabilizers are also discussed.

Adult↗

PubMed1995

[Scarring psoriatic alopecia].

Temporary hair loss is well accepted as a possible result of psoriatic plaques. On the other hand, it is still a controversial issue whether psoriasis can cause scarring alopecia. The following report presents a 38-year-old woman who had been suffering from progressive hair loss from chronic psoriatic plaques of the scalp for some years. Clinical examination revealed an area of scarring alopecia in association with typical features of psoriasis. Histology showed a cord-like fibrosis replacing former hair follicles, a perivascular lymphohistiocytic infiltrate in the upper dermis occasionally invading the follicular epithelium, and characteristic features of psoriasis of the scalp. The clinical course and the lack of evidence for any other causes of scarring alopecia suggest an aetiopathogenetic link between psoriasis and scarring alopecia. Knowledge of this relationship appears to be of practical significance, since efficient antipsoriatic therapy can stop hair loss and thus may be able to prevent scarring.

Adult↗