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Introduction: Tocilizumab (TCZ), a recombinant humanized antihuman monoclonal antibody targeting interleukin-6 (IL-6) signaling, is often utilized in the management of autoimmune disease. Few reports have demonstrated hair growth changes in patients on TCZ. Case Presentation: Herein, we review the literature and report a 21-year-old woman with progressive alopecia areata (AA) presenting with AA improvement while on TCZ for concomitant posterior uveitis. Discussion: Our case demonstrates the potential ability of TCZ to disrupt IL-6 signaling involved in AA, leading to hair loss and regrowth.

Alopecia areata (AA) is a common autoimmune disease characterized by non-scarring hair loss. (1) Tofacitinib is an effective oral JAK 1/3 inhibitor that can block IL-2, IL-7 and IL-6 and is reported as an option for alopecia areata treatment.(2,3) Though some JAK inhibitors are possible new treatments for severe acute respiratory syndrome coronavirus disease, no treatment of Covid-19 with tofacitinib has been reported to date and the withdrawal of the drug in patients with alopecia areata that become infected with the virus, is controversial.

Intravenous corticosteroid pulse therapy (pulse therapy) has been reported to be effective for rapidly progressive alopecia areata (RP-AA). Mostly, a single 3-day administration of corticosteroid (methylprednisolone 500 mg/day) has been performed in Japan; however, to what extent additional administrations improve the outcome has not been fully elucidated. To assess the advantage of repeating the pulse therapy to RP-AA cases refractory to the initial intervention, retrospective clinicopathological analysis was performed. Detailed chronological analysis was conducted in eight cases (one man and seven women; average age, 38.3 ± 10.4 years) demonstrating total scalp hair loss 3 months after the first pulse therapy and treated with additional rounds of the pulse therapy. All cases manifested total hair loss, scalp edema, itch or pain on the scalp after the initial intervention. Histopathological analyses of affected lesions prior to additional pulse therapies revealed persisting dense perifollicular lymphocytic inflammation in all cases. Interestingly, such inflammatory change tended to be severer when compared with previously reported pulse therapy good responders. Extra pulse therapy resulted in partial regrowth of terminal hairs in three out of eight cases, but all of them experienced relapse in the long run. The literature review also suggested limited efficacy of repeating pulse therapy to severe AA cases. These findings suggested that the efficacy of currently conducted repetitive pulse therapy is limited in RP-AA cases with extensive perifollicular inflammation and resistant to the initial pulse therapy. Modulation of the dose and the interval of intervention, in combination with alternative approaches, may be required to achieve a successful outcome.

Alopecia in dogs occurs secondary to a variety of underlying inflammatory and noninflammatory conditions. Hair cycle arrest (alopecia X) is a noninflammatory alopecia that is frustrating to diagnose and treat due to lack of understanding of disease pathogenesis. A variety of therapies for hair cycle arrest have been described with inconsistent efficacy in different dog breeds and sexes; no definitive treatment is available. This report describes the use of a deslorelin acetate implant in two sexually intact adult male keeshonden, both diagnosed with hair cycle arrest. The dogs had progressive alopecia of the trunk that spared the head and distal limbs present for at least 2 yr. Diagnosis of hair cycle arrest was made based on clinical features, dermatohistopathology, and lack of systemic abnormalities. Treatment with a single subcutaneous 4.7 mg deslorelin acetate implant resulted in profuse hair regrowth within 3.5 mo that endured for at least 14 mo. Deslorelin implantation is a management option that is safe, affordable, and appears effective for sexually intact male keeshonden with hair cycle arrest.

Plica neuropathica (PN) is an uncommon scalp condition that usually presents as a compact mass of scalp hair. We report a case of a 55-year-old woman presenting with PN. She presented with a 40-year history of thick plaques of yellow scale afflicting the entire scalp, progressive alopecia, and seeming lack of care of her own condition. Histology showed epidermal nevus-like features and severe miniaturization. info:eu-repo/semantics/publishedVersion

Lupus erythematosus, especially the discoid form, and lichen planopilaris may be associated and can occur in different topographies (coexistence) or in the same lesion (lupus eythematosus/lichen planus overlap syndrome). Frontal fibrosing alopecia is considered a variant form of lichen planopilaris and is characterized by frontotemporal hairline and eyebrow involvement. Of the association with lupus erythematosus we have only a few descriptions. Hydroxychloroquine and chloroquine diphosphate are antimalarial drugs described as viable treatment options for both diseases, due to an antilymphocytic effect. The association between frontal fibrosing alopecia and lupus erythematosus (discoid or systemic) is reported in this article, showing a progressive alopecia in the frontotemporal hairline despite treatment with hydroxychloroquine.

Background Captive Andean bears (Tremarctos ornatus) develop a distinct alopecic syndrome of unknown aetiology. Hypothesis/objectives To describe the histological features of healthy Andean bear skin, to define the clinical and histopathological features of Andean bears with signs of alopecia, and to propose an aetiopathogenesis. Animals Eighteen healthy Andean bears housed in 12 European zoos and 13 Andean bears with mild to severe alopecia housed in nine European zoos. Methods Two surveys describing signalment and clinical features of affected bears; follicular density was measured in a single healthy bear using a dermatoscope; cytological samples were collected by tape stripping from two healthy and three alopecic bears; skin biopsies were collected for histological evaluation from healthy and alopecic bears; immunohistochemistry (CD3, AE1/AE3 cytokeratins) was performed when lymphocytic inflammation was observed. Results The syndrome is an acquired, slowly progressive alopecia. Bears are otherwise healthy. Histological features include a dermal inflammatory infiltrate composed of T lymphocytes and eosinophils; atrophy of hair follicles at the level of or below the isthmus, and lymphocytic infiltration of hair follicles and the epidermis. Multinucleated giant cells were present in the outer root sheaths of hair follicles in five bears. Conclusion and clinical importance Andean bear alopecia syndrome is an acquired, progressive alopecia with histological features consistent with a lymphocytic immune-mediated reaction directed against follicular sheaths and the epidermis. Trigger factors have not been identified. Further studies are indicated to define the features of this multifactorial syndrome.

Immunoglobulin light-chain (AL) amyloidosis is a form of systemic amyloidosis in which the fibrils are derived from monoclonal light chains. We report a case of a 66-year-old woman presenting with nail changes, parchment-like hand changes, progressive alopecia and sicca syndrome. Histopathological studies of biopsy specimens of the scalp, the nail, minor labial salivary glands and abdominal skin revealed deposits of AL κ-type amyloid. Urine protein electrophoresis exhibited a weak band of κ-type light chains. Based on this striking case, we here review the characteristic nail and hair manifestations associated with systemic amyloidosis. Knowledge of these signs is important for an early diagnosis of systemic amyloidosis, identification of the underlying disease and patient management.

A 1-year-old female cat was presented for progressive alopecia, gait abnormalities, and stiffness. Radiography demonstrated multiple calcified lesions within the soft tissues of the cervical and thoracic spine, shoulder, and limbs. Postmortem computed tomography provided more detailed information on the distribution, pattern, and extension of lesions. In addition, computed tomography helped guide sample selection for histopathology. The final diagnosis was fibrodysplasia ossificans progressiva. This is a rare disorder of unknown etiology, characterized by fibrosis and heterotopic bone formation in connective tissues. To the authors' knowledge, this is the first report describing this disease in a European cat.

BACKGROUND: Dermoscopic studies evaluating noninflammatory, nonpruritic progressive alopecia attributable to pattern alopecia are currently unavailable. HYPOTHESIS/OBJECTIVES: To evaluate the dermoscopic features observed in healthy skin of short coated dogs and compare these findings with those observed in dogs affected by pattern alopecia diagnosed by clinical and dermatopathological examination. ANIMALS: Thirty male and female, healthy, breed matched, young adult, short coated dogs (controls) and 30 male and female, young adult, short coated dogs affected by pattern alopecia. METHODS: Dermoscopy was performed with a Fotofinder II videodermoscope equipped with software that allowed the measurement of structures visualized in magnified images (20×-40×-70×). Skin biopsy samples were obtained from the thorax and evaluated dermoscopically for dermoscopic-histological correlation in affected dogs. RESULTS: Dermoscopic findings in canine pattern alopecia were hair shaft thinning, circle hairs and follicular keratin plugs; in the affected sun exposed areas there was a honeycomb-like pattern of pigmentation. Arborizing red lines reflecting vascularization were classified as a nonspecific finding because they were also common in healthy dogs. Dermoscopic features correlated with histology for selected hair follicle abnormalities. CONCLUSIONS AND CLINICAL IMPORTANCE: Although canine pattern alopecia is a visually striking disease, this study supports the value of dermoscopy for clinical examination and also opens promising perspectives for the identification of diagnostic dermoscopic patterns that may be useful for other skin disorders.

Congenital dyserythropoietic anaemia (CDA) is a heterogeneous group of rare genetic disorders that in humans is characterised by ineffective haematopoiesis with morphological abnormalities in erythroid precursor cells and secondary iron overload. In the 1990s, a syndrome of CDA with dyskeratosis and progressive alopecia was reported in Poll Hereford calves in Canada and the USA. We report the clinical and pathological findings in two Poll Hereford calves with this syndrome from separate properties in South Australia. The animals had a variably severe anaemia, associated with abnormal nucleated red blood cells in peripheral blood, and large numbers of rubricytes and metarubricytes with a characteristic nuclear ultrastructure in the bone marrow. Both calves were born with a wiry hair coat and a progressively 'dirty-faced' appearance associated with hyperkeratosis and dyskeratosis (apoptosis).

Of the world population, 1.7% is suffering from alopecia areata at some point in their lives. The exact etiology of this disease is still unknown, and the course of the disease is unpredictable. Effective treatments, especially for severe multifocal alopecia areata, alopecia areata totalis, and alopecia areata universalis, are lacking. The present article will discuss side effects and relapse rates of different systemic agents for treatment of severe and rapid progressive alopecia areata.

Hyperoestrogenism causing progressive alopecia in neutered ferrets may be induced by ovarian remnant syndrome (ORS) and nodular hyperplasia of the adrenocortex (hyperadrenocorticism, NHA). The objec - tive of the study was to determine whether a slow-release implant of a gonadotropin releasing hormone (GnRH) analogue, deslorelin, has any value in therapy of hyperoestrogenism of adrenocortical origin (NHA). Three sup- posed cases of NHA with alopecia and other clinical signs of hyperoestrogenism (n = 2 spayed females in oestrous and n = 1 castrated male) were treated with a subcutaneous implant of 4.7 mg deslorelin acetate. Blood samples were collected, and plasma levels of estradiol (E 2 ) were determined just before, and some weeks after treatment. For realistic monitoring, blood samples for E 2 determination were also taken from intact, healthy (untreated control) females after the beginning of heat (n = 5), or 9-21 days after, with hCG induced ovulation (n = 6), or

Frontal fibrosing alopecia (FFA), is an acquired clinical entity characterized by a scarring, slowly progressive alopecia of the frontoparietal hairline. It is commonly accompanied by thinning or complete loss of eyebrows. Although there are only 117 cases reported, it is likely that FFA is more frequent than it has been thought as it is often misdiagnosed or not diagnosed at all. Epidemiologic data show that the disease, in the vast majority of cases, primarily affects women older than 60 years of age. The histology of FFA is indistinguishable from that of lichen planopilaris and Lassueur-Graham-Little-Piccardi syndrome, and the diagnosis depends mainly on the clinicopathologic correlation. Lymphocytic infiltration surrounding the upper portion of hair follicles confirms FFA. Treatment modalities are not efficacious. In cases where the disorder is rapidly progressive, short courses of oral prednisone or chloroquine may temporarily stabilize the disease; however, further progression after the withdrawal o...

Keratosis follicularis spinulosa decalvans (KFSD) is an X-linked condition characterized by keratotic follicular papules and progressive alopecia, which is caused by mutations in the MBTPS2 gene. We carried out a genetic study on a child who was suspected clinically to have KFSD. Sanger sequencing was performed to detect mutations in the entire coding region of MBTPS2. A novel missense mutation (c.599C>T) was identified in the patient, confirming a diagnosis of KFSD. We reviewed related cases with MBTPS2 mutations for evidence of genotype-phenotype correlations.

A 33-year-old woman presented with a 3-year history of progressive alopecia of the scalp. Past treatment with hydroxicloroquine did not show improvement. Physical examination revealed multiple areas of alopecia with atrophic aspect of the scalp, and axillary and pubic hypotrichosis. Dermoscopy showed hyperkeratosis and accentuation of follicular ostia. Anatomopathological examination revealed decrease in the number of hair follicles, upper perifollicular infiltrate and areas with fibrosis. The Piccardi-Lassueur-Graham-Little syndrome is a rare disorder, characterized by the triad of multifocal scarring alopecia of the scalp, keratotic follicular eruption and hypotrichosis of axillary and pubic regions. Management is a challenge and many medications tried have controversial results. We report a case of this rare syndrome which improved with corticoids.

This study evaluated the clinical and histopathological features and results of light and electron scanning microscopy assessments of follicular dysplasia in five Weimar Pointers. The data were compared with those obtained in three normal Weimaraners. In our study, this dermatosis affected young adults that showed progressive alopecia of the trunk (head and limbs were spared) associated with recurrent folliculitis/furunculosis. Exclusion of other dermatoses and the presence of histopathological lesions and hair shafts abnormalities seen in light and/or scanning electron microscopy similar to colour dilution alopecia led to the diagnosis of follicular dysplasia. The lesions we observed are the same as those described previously in colour dilution alopecia, but they were less pronounced in all our samples.

Alopecia areata is a common chronic inflammatory disease, which is probably mediated by lymphocytes. The predisposition to alopecia areata is polygenic in nature but environmental factors may trigger episodes of the disease. The diagnosis is usually not difficult and this presentation will concentrate mainly on patient management. An explanation of alopecia areata, including discussion of the nature and course of the disease and the available treatments, is an important part of management. Overall, there is a high rate of spontaneous remission but almost all sufferers will experience more than one episode of alopecia and patients presenting to dermatologists tend to be affected more severely. Poor prognostic indicators include onset in childhood, failure of recovery within 1 year and extensive hair loss. The decision to treat alopecia areata actively should not be taken lightly. Treatment can be uncomfortable for the patient, time consuming and potentially toxic. Some patients find it difficult to cope with relapse following or during initially successful treatment and they should be forewarned of this possibility. On the other hand, some patients are appreciative that something has been tried, even if it does not work. A number of treatments can induce hair growth in alopecia areata, but none has been shown to alter the natural history and few have been subjected to randomized controlled trials. Simple topical treatments include topical steroids, minoxidil lotion and dithranol although there is little evidence that the results are superior to placebo. Intra-lesional steroids stimulate hair growth in a high proportion of patients and can be helpful where hair loss is limited in extent or for certain sites such as the eyebrows. Several uncontrolled studies have suggested that pulsed high-dose systemic steroids are effective in some patients and this approach is possibly useful in rapidly progressive alopecia. The most effective treatment in severe alopecia is contact immunotherapy. However, the long-term response rate in this group of patients is low (15–20%), it is available in only a few centres and there are significant safety considerations for patients and carers. Following sympathetic counselling no treatment is an active option for many patients with alopecia areata. Prescription of a wig can make the difference between social isolation and leading a normal life for patients with extensive hair loss. Finally, we have a responsibility to deter patients from indulging in a succession of useless and inevitably expensive ‘cures’.

The management of progressive alopecia areata (AA) is often challenging. Recently, i.v. corticosteroid pulse therapy has been reported to be effective for acute and severe AA, however, inclusion criteria have not been sufficiently precise, leaving a chance that its efficacy could be further improved by optimizing therapeutic indications. In our attempts to delineate the factors that correlate with favorable outcomes, we minutely evaluated the clinicopathological findings and the prognoses of single-round steroid pulse-treated progressive AA cases with full sets of image and pathology records during the course. Almost complete hair regrowth has been achieved and maintained up to 2 years in five out of seven AA patients with varying degrees of clinical severity. Interestingly, the worst clinical presentation observed during the course correlated with the size of the area where hairs with dystrophic roots were pulled rather than the extent of visible hair loss on the first visit. Dermoscopy detected disease spread but contributed little in assessing prognoses. Dense perifollicular cell infiltration was detected in all cases treated within 4 weeks of onset and those treated later but with excellent response. Importantly, the cases with poor or incomplete hair regrowth were treated 6-8 weeks of onset and showed moderate inflammatory change with high telogen conversion rate. These findings mandate global dermoscopy and hair pull test for judging the treatment indication and suggest that early administration of high-dose corticosteroid, ideally within 4 weeks of onset, enable efficient suppression of active inflammation and maximize the effectiveness of the remedy.

A 27-year-old woman presented with a progressive alopecia, persisting since two years. Examination revealed an area of cicatricial alopecia parieto-occipital, 12 × 10 cm in diameter. Histopathological examination revealed multiple hair tufts emerging from dilated follicle openings surrounded by a mixed inflammatory infiltrate and fibrosis. Results of bacteriologic examination of pus extruding from the dilated follicular ostia revealed Staphylococcus aureus. The patient was treated with a systemic antibiotic therapy, whose effects still have to be awaited. Tufted hair folliculitis is a rare folliculitis with irregular areas of scarring alopecia within which numerous hair tufts emerge from dilated openings. Its pathogenesis is not fully understood. Bacterial infections seem to play an important causative role although bacterial infections cannot always be detected. For this reason, antibiotics administered systemically are a promising treatment option.

A recent report suggests that elastic fibers appear in scars in a time-dependent fashion. This observation prompted our investigation, because we have found elastic tissue stains helpful in determining the pattern of scarring in cases of permanent alopecia. We carried out this investigation to determine if the Verhoeff-Van Gieson (VVG) elastic stain can reliably differentiate scarred from non-scarred dermis and to test our hypothesis that elastic stained sections are helpful in distinguishing lichen planopilaris (LPP) from lupus erythematosus (LE), central progressive alopecia in black females ("follicular degeneration syndrome" and "hot comb alopecia" are other terms used to describe this condition) and classic ivory white idiopathic pseudopelade. We studied histological sections from surgical scars of known duration, stained with the VVG elastic stain and VVG-stained sections of scalp biopsies from patients with established lesions of permanent alopecia. In most cases, both vertical and transverse sections were examined. In every case, the VVG stain clearly differentiated scar from the normal surrounding dermis. Distinct patterns of elastic tissue allowed for correct classification in most of the well-established cases of permanent alopecia studied. We determined that the Verhoeff-Van Gieson stain is an excellent stain to evaluate the pattern of scarring in cases of permanent alopecia and elastic tissue stains may be helpful in the histological evaluation of alopecia.

BACKGROUND: Chronic progressive generalized alopecia in dairy cattle has been anecdotally discussed in veterinary forums. OBJECTIVE: To describe subclinical changes in an otherwise apparently healthy animal with chronic progressive generalized alopecia. ANIMALS: One 10-month-old Jersey heifer. METHODS: Case report. RESULTS: A heifer was presented for chronic progressive alopecia. The skin was hyperpigmented and very thin (2.4 ± 0.0 mm, compared with 8.1 ± 0.3 mm measured in four contemporaneous Jersey heifers). Histopathological examination of the skin revealed severe epidermal hyperplasia, orthokeratotic hyperkeratosis and diffuse follicular atrophy. Clinicopathological changes included hypocalcaemia that did not respond to calcium therapy. Serum parathyroid hormone (PTH) was not detected, compared with 1.38 ± 0.78 pmol/L in four contemporaneous Jersey heifers. A diagnosis of hypoparathyroidism was made based on hypocalcaemia and low PTH in the presence of normal magnesium levels. The heifer was otherwise healthy and was allowed to continue normal life. A spontaneous abortion occurred at 5.5 months of pregnancy and this was likely due to the presence of twin fetuses. Despite targeted therapy of the ensuing retained placenta, the heifer declined in health and had to be euthanized. From the time of diagnosis with hypoparathyroidism until euthanasia (29 months of age), blood levels of calcium, phosphorus and PTH were regularly monitored. Calcium and phosphorus levels varied widely. Serum PTH was consistently undetectable. At postmortem examination, the parathyroid glands could not be located. CONCLUSIONS AND CLINICAL IMPORTANCE: To our knowledge, this is the first report of naturally occurring hypoparathyroidism in cattle and with a clinical presentation of alopecia.

We report on 2 sibs with consanguineous parents, and an identical progressive extrapyramidal movement disorder with onset in adolescence and associated with progressive alopecia and primary hypogonadism. To our knowledge, this syndrome has not been reported, and probably represents a newly recognized autosomal recessive condition.

Frontal fibrosing alopecia (FFA) and fibrosing alopecia in a pattern distribution (FAPD) as originally reported by Kossard in 1994 and by Zinkernagel and Trüeb in 2000, respectively, represent two distinct patterns of cicatricial pattern hair loss. Both share a patterned distribution and histological evidence of a lichenoid follicular inflammation with fibrosis. FFA is characterized by a marginal alopecia along the frontotemporal hairline, and FAPD by a progressive alopecia of the centroparietal scalp. Since the original reports, evidence has accumulated that there exists considerable clinical overlap among FFA, FAPD, and lichen planopilaris, with coexistence of features of the three conditions within the same individual. Moreover, familial cases of FFA have been reported, pointing to a possible genetic background to the condition. Our observation of familial occurrence of FFA and FAPD in daughter and mother, respectively, further underscore a nosologic relationship between the two conditions with respect to both an androgenetic background and the (lichenoid) inflammatory reaction pattern.

Adult onset progressive alopecia and leukotrichia developed in 2 registered black Angus cows, aged 6 and 7 years. Histopathologic findings in skin were prominent melanin clumping and degeneration of matrix cells with formation of giant multinucleate cells within hair bulbs, accompanied by peribulbar melanin incontinence and fibrosis and dystrophic hair shafts. Intrabulbar and peribulbar lymphocytes were cluster of differentiation (CD)3-positive T cells. Findings were characteristic of alopecia areata.

Androgenetic alopecia (AGA) is the most common hair loss disorder in men and is largely determined by genetic factors and the peripheral action of androgens which produce a gradual conversion of terminal hairs to vellus hairs. AGA is an aged- dependent disease characterized by non-scarring progressive alopecia due to follicular miniaturization with a characteristic pattern distribution. Others mechanisms such as chronic inflammation and several hormones or vitamins like aldosterone, insulin or vitamin D have been implicated in the pathogenesis of AGA. The diagnosis of AGA is made by clinical history and clinical examination, other complementary studies are: dermoscopy, trichoscan, trichograms and laboratory tests. Histopathology is not usually necessary in men with androgenetic alopecia unless an atypical pattern is present. Minoxidil and finasteride are the main two drugs approved for the treatment of AGA. The precise mechanism of action of minoxidil is not well-known, one hypothesis is based on vasodilatory properties and the increase of blood flow. Finasteride is an inhibitor of type II 5-α-reductase; this enzyme converts testosterone to dihydrotestosterone. Although AGA poses no direct consequences to physical health it can be a marker of others diseases (cardiovascular risk factors or benign prostatic hyperplasia) or lead to significant psychosocial morbidity.

Background Alopecia areata (AA) is a common acquired hair disorder showing variable hair loss. Although various prognostic factors have been reported, no evident factors for determining prognosis and appropriate treatment are known. Objective To identify prognostic factors in AA patients, especially those with positive results for the hair-pull test on the first visit or with a history of rapidly progressive AA (RPAA) within 6 months prior to the first visit. Methods One thousand thirty (1030) patients diagnosed with AA at Tokyo Medical University Hospital were retrospectively examined for 3 years, and their prognosis was assessed on the basis of various indices using multivariate analysis. Results Patients with regenerated vellus hairs showed a significantly higher improvement or cure rate regardless of severity. Early onset and lengthy duration were significantly associated with lower cure, and higher relapse, rates. RPAA patients tended to show a good prognosis regardless of the treatment employed. Limitations The present study is retrospective, and treatment modalities were chosen according to clinical and social circumstances. Conclusion RPAA patients tend to show a favorable prognosis regardless of treatment modality. Furthermore, the presence of regenerated vellus hairs may indicate a good prognosis.

Primary cicatricial alopecias (PCAs) are a group of permanent hair loss disorders, of which the pathogenesis is still poorly understood. The alopecia and excoriation ( AE ) mouse strain is a dominant mutant generated from ethyl nitrosourea mutagenesis. AE mice exhibit a progressive alopecia phenotype similar to that seen in PCAs, resulting from a point mutation in the gasdermin A3 gene. Mutant mice begin to show alopecia on the head from postnatal day 22 and experience complete hair loss by the age of 6 months, along with hyperkeratosis and catagen delay. The results of a histological examination showed that bulge stem cells in AE skin are gradually depleted, as indicated by decreased keratin 15 and CD34 expression, and reduced bromodeoxyuridine label–retaining cells in the AE bulge. In addition, AE mice display an inflammatory condition in the skin from postnatal day 7, including elevated tumor necrosis factor-α and monocyte chemotactic protein-1 mRNA levels and significantly increased macrophages and dendritic cell number. Immune privilege in the bulge was also compromised in AE skin. Consistently, after treatment with the immunosuppressive agent, cyclosporine A, immune privilege collapse, stem cell destruction, and alopecia phenotype of AE mice were all rescued. Collectively, our data demonstrate that immune-mediated destruction of bulge stem cells plays a crucial role in the pathogenesis of alopecia in AE mice, and this strain might be an interesting model for PCAs, especially for lichen planopilaris.

Hair transplantation is a permanent treatment option for androgenetic alopecia in suitable male and female patients. The best long-term outcome is achieved in medically or spontaneously stabilized hair loss. In these cases, the redistributed hair increases density and scalp coverage. Realistic expectations, a good donor-to-recipient area ratio, careful personal planning, and a skillful surgical team are essential. Follicular unit transplantation is the standard, involving dense placement of very large numbers of natural bundles of 1–4 hairs into recipient sites of appropriate size, angle, distribution, and direction. These transplanted hairs are virtually undetectable from the original hair. Thus, progressive alopecia is no longer a contraindication per se, if sufficient donor hair is available. The grafts are harvested with local anesthesia through strip excision with trichophytic closure to keep the scar minimal and/or by follicular unit extraction. Both harvesting methods have individual indications. Stereomicroscopic dissection with backlighting and the use of loupes for recipient site creation greatly reduce transection rates and temporary effluvium of preexisting hair. The hairline is created based on individual characteristics with micro- and macroirregularities, including a frontal transition zone of single hair units. More quantitative evidence from controlled trials is necessary to evaluate special techniques for each component of the procedure.

A 6-year-old intact male New Zealand Huntaway dog had slowly progressive alopecia that was first observed at 12 weeks of age.Patchy alopecia was confined to the black-haired areas of the body, and was most evident on the head and dorsum of the body; tan-haired areas of skin appeared normal. Histological examination of black-haired skin revealed distended melanocytes and large aggregates of melanin within, and surrounding, the hair follicles and the epidermis. Macrophages distended with melanin were also visible within the peri-follicular and superficial dermis, and follicular lumina were often plugged by keratin that contained aggregates of melanin. The follicles were dysplastic and few hair shafts were visible emerging from follicular infundibula within the sections.The clinical and histological findings were consistent with black-hair follicular dysplasia (BHFD).This is the first report of BHFD in a dog in New Zealand, and is the first report in a Huntaway. The most significant effect of BHFD is a predisposition to follicular plugging and secondary bacterial skin infections. Due to the hereditary nature of the follicular dysplasias, breeding from affected dogs should be discouraged. Histological examination of the skin is required to differentiate between the different follicular dysplasias as well as differentiating between follicular dysplasia and follicular atrophy due to endocrinopathy.

The authors report a 48-year-old Chinese woman who presented with acute peripheral neuritis with progressive alopecia. Laboratory examinations disclosed a high blood concentration of thallium (97 microg/L) versus a normal value (0.9 microg/L), and she was diagnosed as having acute thallotoxicosis. After her hospitalization, the cutantest of dimercaptopropansulfonate sodium was positive and the patient refused to take Prussian blue because it caused constipation. She rapidly entered remission after assistance via double-filtration plasmapheresis (DFPP), suggesting the potential efficacy of DFPP for thallotoxicosis.

Background Postmenopausal frontal fibrosing alopecia (PFFA) was described by Kossard et al. as a progressive recession of the frontal hairline affecting particularly postmenopausal women. Further cases of PFFA have been reported to date, all of them considering it as a variant of lichen planopilaris on the basis of its clinical, histological and immunohistochemical features. Objective To describe clinical features, and response to treatment of 16 cases of frontal fibrosing alopecia diagnosed at our department in the last 6 years. Methods In addition to clinical data, biopsies and laboratory tests (antinuclear antibodies, sex hormones, thyroid hormones) were performed in order to rule out other causes of scarring alopecia. Patients were treated with intralesional corticosteroids, finasteride, and minoxidil, depending on the stage of the disease and association to androgenetic alopecia. Results All patients presented progressive alopecia localized to the frontal and temporal hairlines. Eight patients (50%) had loss of eyebrows, and six patients (37.5%) had axillar alopecia. Ages ranged from 45 to 79. Three of these women were premenopausal. Androgenetic alopecia was evident in seven patients (43.8%). All patients biopsied showed perifollicular lymphocitic infiltrate with lamelar fibrosis limited to the upper portions of the follicle. The progression of the condition stopped in most patients after a variable period on treatment. When treatment was abandoned the alopecia progressed to ‘clown alopecia’ appearance. Discussion Cases of Kossard's type scarring alopecia affecting premenopausal women made us consider that this condition is not exclusive of postmenopausal women. Differential diagnosis should take into account conditions like female androgenetic alopecia, fibrosing alopecia in a pattern distribution, alopecia areata, and chronic lupus erythematosus. Except for the pattern of alopecia, lichen planopilaris and frontal fibrosing alopecia are indistinguishable, thus the latter is included as a variant of lichen planopilaris. Although the disease tends to spontaneous stabilization, intralesional and topical corticosteroids, and anti-androgens may stop the progression of the disease and improve the female androgenetic alopecia that usually is associated to FFA.

Alopecia areata has been reported to be accompanied by abnormal autoimmune dysfunction. We examined the expression of cutaneous lymphocyte-associated antigen (CLA), which is a skin-specific lymphocyte homing receptor, in the peripheral blood lymphocytes and skin of patients with alopecia areata. In the patients' peripheral blood, the percentage of CLA-positive CD4 + or CD8 + lymphocytes, was significantly higher than that of normal controls. The patients with severe or progressive alopecia areata showed a much higher CLA-positivity compared to patients recovering from the disease. A chronological study showed that the percentage of CLA-positive peripheral blood lymphocytes, CD4+ or CD8+ lymphocytes decreased in parallel with the patients' good clinical course. The CLA-positivity in peripheral blood lymphocytes, CD4+ or CD8+ lymphocytes of patients with alopecia areata who did not respond to oral corticosteroid therapy remained higher than in those who responded well to the treatment. In the affected scalp skin, many infiltrating lymphocytes around the hair follicles, which were CD4 + or CD8 + lymphocytes, expressed CLA. These findings suggest that the CLA-positivity correlates with clinical activity and that CLA-positive CD4+ or CD8+ lymphocytes may play an important role in alopecia areata.

RXRα is the most abundant of the three retinoid X receptors (RXRs) in the epidermis. In this study, we have used Cre-mediated recombination to selectively disrupt the mouse gene for RXRα in epidermal and hair follicle keratinocytes. We show that RXRα is apparently dispensable for prenatal epidermal development, while it is involved in postnatal skin maturation. After the first hair pelage, mutant mice develop a progressive alopecia, histologically characterised by the destruction of hair follicle architecture and the formation of utriculi and dermal cysts in adult mice. Our results demonstrate that RXRα plays a key role in anagen initiation during the hair follicle cycle. In addition, RXRα ablation results in epidermal interfollicular hyperplasia with keratinocyte hyperproliferation and aberrant terminal differentiation, accompanied by an inflammatory reaction of the skin. Our data not only provide genetic evidence that RXRα/VDR heterodimers play a major role in controlling hair cycling, but also suggest that additional signalling pathways mediated by RXRα heterodimerised with other nuclear receptors are involved in postnatal hair follicle growth, and homeostasis of proliferation/differentiation of epidermal keratinocytes and of the skin’s immune system.

Relata-se o caso de um canino, Poodle, fêmea de 12 anos, apresentando poliúria, polidipsia, polifagia, alopecia progressiva e cegueira. Ao exame clínico, observou-se caquexia, alopecia simétrica bilateral em tronco, dorso, membros e abdômen, pele hiperpigmentada, adelgaçada e hipotônica, associados à seborréia, ceratoconjuntivite seca, piodermite interdigital e catarata bilateral. Na avaliação laboratorial, constatou-se hiperglicemia, glicosúria e anemia, configurando-se inicialmente um quadro de diabetes mellitus. Para investigação de um provável hiperadrenocorticismo como doença primária, foi realizada a avaliação da função da adrenal, utilizando-se o teste de supressão com dexametasona na dose de 0,01mg/kg/IV, cujos resultados (basal=3,4mig/dl e 8 horas após dexametasona = 1,5mig/dl) mostraram-se normais. Após instituição da terapia com insulina observou-se diminuição da poliúria/polidipsia, aumento de peso corpóreo e total recobertura pilosa após três meses de tratamento. Conclui-se que o quadro dermatológico foi decorrente das alterações metabólicas relacionadas à deficiência de insulina, fato este raro segundo a bibliografia compilada. A 12 year-old female toy Poodle was presented with polyria, polydipsia, polyphagya, progressive alopecia and blindness. The animal was cachetic, with simmetric bilateral alopecia of the torso, abdomen and limbs. The skin was hyperpigmented, thin and hypotonic with seborhea and interdigital pioderma. The dog also had keratoconjuntivitis sicca and bilateral cataracts. Hyperglicemia, glicosuria and anemia were confirmed by laboratory exams and a working diagnosis of Diabetes meilitus was established. A low-dose dexamethasone (0,01mg/kg/IV) supression test was performed to rule out hyperadrenocorticism and was normal (basal value = 3.4mu/dl and 8 hours post-dexamethasone = 1.5,mug/dl). Insulin therapy was initiated and resulted in remission of all clinical signs, with body weight recovery, polyuria and polydipsia resolution and complete hair coat regrowth within 3 months. We concluded that the dermatosis in this case was associated to metabolic alteration related to insulin deficiency.

HUTCHINSON-GILFORD syndrome, or progeria, is a rare precocious senility disorder in which progressive alopecia, adipose atrophy and deficient growth produce an appearance of old age during childhood. The complications of atherosclerosis lead to premature death, usually before the age of 30 years.

Background. Pseudopelade is a rare idiopathic progressive alopecia that has no initial inflammatory phase. Even so, pseudopelade has been classified as a scarring alopecia with postinflammatory alopecias. Atrophy rather than true scarring is the cardinal feature of pseudopelade. Materials and Methods. A review of reported cases of pseudopelade, especially those with a family history, was undertaken. The discovery of a young man and his mother, who had pseudopelade, plus two other familial cases prompted this study. Results. Examination of the clinical and pathologic material shows pseudopelade to be a disease separate from other alopecias. The striking familial association in these cases demonstrates a plausible etiology. Conclusions. Pseudopelade is an autosomal dominant disorder of the scalp marked by atrophic loss of hair follicles.

Successful immunotherapy of established B16 melanoma metastases in C57BL/6 mice can be achieved by antibody-targeted interleukin-2 administration. This therapeutic effect is accompanied in approximately 20% of the animals by induction of a population of lymphocytes that migrates to and substantially disrupts the cytoarchitecture of the skin, which results in progressive alopecia. The histologic changes associated with the hair loss, i.e., peri-, and intrafollicular inflammatory infiltrates consisting of both activated CD4+ and CD8+ T cells, as well as expression of major histocompatibility complex class I antigens on subinfundibular follicle epithelium, are similar to those observed in human alopecia areata. Furthermore, the alopecic phenotype can be transmitted horizontally by passive transfer of lymphocytes from treated animals to naïve mice. Since lymphocytes from treated animals either lacking or displaying signs of alopecia are able to transmit these phenotypic changes to a similar percentage of naïve animals, the initiation of alopecia seems to be dependent on the coincidence of at least two different events: the presence of specific lymphocyte populations as well as specific features of the skin disclosing a target for these cells.

Background: To properly assess the progression and treatment response of alopecia, one must measure the changes in hair mass, which is influenced by both the density and diameter of hair. Unfortunately, a convenient device for hair mass evaluation had not been available to dermatologists until the recent introduction of the cross-section trichometer, which directly measures the cross-sectional area of an isolated bundle of hair. Objective: We sought to evaluate the accuracy and sensitivity of the HairCheck® device, a commercial product derived from the original cross-section trichometer. Materials and Methods: Bundles of surgical silk and human hair were used to evaluate the ability of the HairCheck® device to detect and measure small changes in the number and diameter of strands, and bundle weight. Results: Strong correlations were observed between the bundle's cross-sectional area, displayed as the numeric Hair Mass Index (HMI), the number of strands, the silk/hair diameter, and the bundle dry weight. Conclusion: HMI strongly correlated with the number and diameter of silk/hair, and the weight of the bundle, suggesting that it can serve as a valid indicator of hair mass. We have given the name cross-section trichometry (CST) to the methodology of obtaining the HMI using the HairCheck® system. CST is a simple modality for the quantification of hair mass, and may be used as a convenient and useful tool to clinically assess changes in hair mass caused by thinning, shedding, breakage, or growth in males and females with progressive alopecia or those receiving alopecia treatment.

Ultrastructural evidence of dyserythropoiesis was found in ten calves (ages 1 to 16 months) previously diagnosed as having congenital anemia, dyskeratosis, and progressive alopecia. Morphologic abnormalities found in erythroid precursors of all calves were associated with the nucleus. Rubriblast nuclei were irregular with numerous blebs, indentations, and deep clefts. Elongated blebs appeared as satellite nuclei in some sections. Nuclear membranes had numerous defects or gaps, which were frequently present in, but not limited to, recently divided cells. Cytoplasmic material could be found within these gaps and extending into the nucleus. Rubricytes had chromatin that was abnormally condensed and hyperosmiophilic, with numerous translucent vacuoles present. Binucleate rubricytes occurred frequently in affected calves. These changes resemble those of type I congenital dyserythropoiesis in human beings, and we suggest congenital anemia, dyskeratosis, and progressive alopecia of Polled Hereford calves as the appropriate diagnostic terms to describe this disease.

A new syndrome of anemia, alopecia, and dyskeratosis was identified in Polled Hereford calves in this study. Cutaneous changes included hyperkeratosis and hair loss around the muzzle and ear margins, which progressed to a generalized alopecia and hyperkeratotic dermatitis. Histologically, orthokeratotic hyperkeratosis with dyskeratosis of epidermal and follicular keratinocytes was present. Alopecia was correlated with dyskeratosis of Huxley's layer and an increasing proportion of follicles in the telogen phase of the hair cycle. Dermatitis was characterized by a mild dermal mononuclear cell infiltrate and mild lymphocytic perivascular dermatitis. The anemia present at birth was nonprogressive and was classified as normochromic and normocytic to macrocytic. Reticulocytosis was absent, but bone marrow was markedly hyperplastic. Nuclear cytoplasmic asynchrony of the rubricyte and metarubricyte stages occurred in the bone marrow. Abnormal rubricyte nuclei and maturation arrest at the late rubricyte stage were common. Cytologic features of the erythroid series are similar to those of type I congenital dyserythropoietic anemia of human beings. Genealogic features suggest that this is a primary hereditary defect. The mode of inheritance, however, remains to be determined.

In a selected group of 8 patients with progressive alopecia areata (AA) leading to AA universalis, immunological aspects (in the peripheral blood and the tissue) were studied during the period of the initial attack of the disease. The peripheral T-cell helper/suppressor ratio appeared not to be a reliable parameter for the disease activity. The intrabulbar and peribulbar distribution of T-cells, Langerhans cells and of HLA-DR expression in and around the anagen hair follicles in the progressive areas of the disease (region of exclamation-mark hairs) may suggest a T-cell-mediated injury primarily in the peribulbar regions of the follicles. The data presented tend to support the possibility that in the early development of AA, the dermal pailla (capillary network?) may be the prime target of immunologic injury.

SUMMARYMice homozygous for the asebia mutation (ab/ab) are char1acterized by defective sebaceous glands, a short sparse hair coat from 7 days and progressive alopecia. In addition, we have found that the initial hair follicle rudiments in the skin of these mice are able to differentiate into relatively normal anagen follicles which are often excessive in length and have minor abnormalities of the inner and outer root sheath components. The inner root sheath fails to form the typical transverse corrugations at the level of the sebaceous glands and its cells apparently remain, partially undegraded, plugging the hair canal and adhering to emerging hair shafts. Defects noted in the outer root sheath may be responsible for the failure of inner root sheath degradation. With increasing age, irregularities in hair cycle duration, loss of the originally parallel arrangement of hair follicles and further abnormalities of the individual follicular components are increasingly evident. Follicles in asebic mice have a tendency to form buds and branches which occasionally begin typical follicular differentiation. The consistent failure of the asebic follicles to pass normally through the catagen stage to the telogen stage results in long twisted follicles with abnormal and often loosely anchored hair clubs. The dermal papillae are often abnormal or absent from telogen follicles, while typical germ cells are not formed. Thus the lack of multiple hair follicles, the disorganization of follicles and the progressive alopecia observed in the asebic mice are accounted for. It is suggested that the altered dermal environment and outer root sheath abnormalities may be responsible for many of the follicular defects.

It has previously been shown that, in patients with untreated progressive alopecia areata (AA), the peribulbar T4/T8 ratio is about 4:1. In the present study, the immunohistochemical findings obtained in untreated AA patients were compared to those obtained in patients who had received topical immunotherapy with diphencyprone. The untreated group consisted of 5 patients with progressive AA and 5 patients with inactive AA. The treated group consisted of 5 patients with a good response to diphencyprone and 5 patients with little or no hair regrowth after treatment. In untreated patients with progressive AA, the mean peribulbar T4/T8 ratio was 4:1, whereas in untreated patients with stable AA, the ratio was 2:1. In the treated patients with a good response to diphencyprone, the mean T4/T8 ratio was 1:1, while in the patients with poor or no response to treatment, the ratio was 0.7. In conclusion, topical immunotherapy considerably alters the peribulbar T4/T8 ratio in AA. The results are consistent with, but do not prove, the concept of topical immunomodulation.

Reduced coat 3 (Rco3) is a new spontaneous autosomal recessive mutation with defects in hair structure and progressive alopecia. Here we describe chromosomal mapping and molecular identification of the Rco3 mutation. The murine Rco3 locus maps to a 2-Mb interval on chromosome 15 encompassing the keratin type II gene cluster. Recently, mK6irs1 was described as a type II keratin expressed in Henle's and Huxley's layer of the murine inner root sheath. Genomic sequencing revealed a 10-bp deletion in exon 1 of mK6irs1 resulting in a frameshift after 58 amino acid residues and, therefore, the absence of 422 carboxy-terminal amino acid residues containing the complete α-helical rod domain. Henle's and Huxley's layers show no immunoreactivity with mK6irs1-specific antibodies and the absence of intermediate filament formation in electron microscopic images. These results indicate that the expression of functional mK6irs1 is indispensable for intermediate filament formation in the inner root sheath and highlights the importance of the keratinization of the inner root sheath in the normal formation of the hair shaft.

HAIR transplantation has become an increasingly popular procedure for the treatment of male-pattern alopecia.1 2 3 4 5 An unusual complication of this procedure prompted the presentation of the following ease. Case Report JA. (J.H.M.H.C. 13–98–13), a 35-year-old man, had experienced progressive alopecia prematura since the age of 29. After his 9th transplantation procedure, during each of which 30 to 60 hair-bearing skin plugs were transplanted from the posterior scalp to the anterior bald scalp, a throbbing left-frontal head pain associated with bleeding from the scalp developed. The bleeding vessel was not sutured because ice packs and a pressure bandage controlled the bleeding. However, . . .

REPORT OF A CASE A 55-year-old woman presented with a four-year history of arthritis of the hands and a cutaneous eruption of the face and scalp that was accompanied by progressive alopecia. She gave a history of Raynaud's phenomenon and photosensitivity. There was no history of serositis, and there were no complaints referable to the renal, cardiac, pulmonary, or central nervous systems. The patient's medical history was notable for hypothyroidism and hypertension. Physical examination of the skin revealed a large area of scarring alopecia present over the crown of the head (Fig 1). Erythematous, telangiectatic, atrophic, scarred plaques with pigment change and scale were present on the forehead and cheeks (Fig 2). There was striking involvement of the concha of both ears, as well as mild palmar erythema and periungual telangiectasia. A biopsy specimen was obtained from a scalp lesion (Figs 3 and 4). Laboratory data obtained over the years