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PubMed1997

Autoantibodies to hair follicles in C3H/HeJ mice with alopecia areata-like hair loss.

We have previously described spontaneous but reversible hair loss that clinically and histologically resembles human alopecia areata in a colony of C3H/HeJ mice. Alopecia areata in humans is associated with antibodies to hair follicles. This study was conducted to determine whether C3H/HeJ mice with hair loss have a similar abnormal antibody response to hair follicles. Eighteen C3H/HeJ mice with alopecia, 12 unaffected littermates, and 15 control mice were examined for circulating antibodies to C3H/HeJ anagen hair follicles by indirect immunofluorescence and against extracts of isolated C3H/HeJ and human anagen hair follicles by immunoblotting. Using both procedures, antibodies to anagen hair follicles were present in all C3H/HeJ mice with alopecia but in none of the control mice. The antibodies were also present in some unaffected C3H/HeJ littermates but were absent in mice of an unrelated strain with inflammatory skin disease and alopecia, indicating that their appearance did not result from the hair loss. These antibodies reacted to hair follicle-specific antigens of 40-60 kDa present in murine and human anagen hair follicles. These antigens were also reactive with human alopecia areata antibodies. Some of the antibodies in both C3H/HeJ mice and humans with alopecia areata reacted to antigens of 44 and 46 kDa, which were identified as hair follicle-specific keratins. This study indicates that C3H/HeJ mice with hair loss have circulating antibodies to hair follicles similar to those present in humans with alopecia areata. These findings confirm that these mice are an appropriate model for human alopecia areata and support the hypothesis that alopecia areata results from an abnormal autoimmune response to hair follicles.

Alopecia Areata↗
PubMed1991

Immunohistologic and ultrastructural comparison of the dermal papilla and hair follicle bulb from "active" and "normal" areas of alopecia areata.

The "active" edges of patches of alopecia areata and normal areas from the same scalp (i.e., bearing normal terminal hair) from seven patients with alopecia areata were investigated immunohistologically. Similar areas from a further eight patients were examined using light and electronmicroscopy. "Active" and "normal" areas of alopecia areata scalps were immunohistologically similar and varied from normal controls in the number, distribution, and ratio for T4 and T8-positive cells. Similarly the ultrastructural changes seen in the "active" areas when compared to normal controls were also present in the "normal" areas of alopecia areata scalps. The most significant differences found between normal "control" follicles and both "active" and "normal" areas of alopecia areata scalps were the polymorphic nature of the dermal papilla cells and the loss of cellular organization within the dermal papillae taken from alopecia areata scalps. In addition, the junction between the dermal papilla and the bulb of the hair follicle, the dermo-epithelial junction of the hair follicle bulb, demonstrated critical changes in follicles taken from both "active" and "normal" areas of alopecia areata scalps. These results support the suggestion of a subclinical state of alopecia areata and indicate that further work on the etiology of alopecia areata should be directed towards the "normal" areas of alopecia areata scalps, in particular the cells of the dermal papilla and the dermo-epithelial junction of the hair follicle bulb.

Adult↗
PubMed2006

Male New Zealand Black/KN mice: a novel model for autoimmune-induced permanent alopecia?

BACKGROUND: Irreversible, permanent and scarring alopecia is associated with several autoimmune diseases, including all autoimmune connective tissue disorders. The pathogenesis of autoimmune-induced permanent alopecia (APA) is still poorly understood, and instructive, simple mouse models for the study of APA are needed urgently. During the course of our studies in a well-established mouse model for chronic rheumatoid arthritis, the New Zealand Black/KN (NZB/KN) mouse, we noticed that ageing male NZB/KN mice developed spontaneous APA. OBJECTIVES: To study whether alopecia seen in ageing male NZB/KN mice displays key features of human APA and may, thus, be a useful new mouse model for clinically relevant APA research. METHODS: NZB/KN, the F1 hybrid of NZW/N Slc x NZB/KN (W/BKN F1), the F1 hybrid of NZB/KN x NZW/N Slc (BKN/W F1), and the F2 hybrid of W/BKN F1 x W/BKN F1 mice were employed in this study, in order to check which strain carries the highest risk of alopecia development. Besides routine histology, CD3, CD4 and CD8 expression as well as immunoglobulin (Ig) G and IgM deposition in hair follicles were investigated by immunohistology/immunofluorescence. Mast cell distribution/degranulation and Ki-67 (proliferation)/TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling) (apoptosis) positive cells were also analysed. RESULTS: Only F2 male NZB/KN mice were prone to develop alopecia, suggesting that Y chromosome-associated gene(s) are involved in the pathogenesis of APA, which incidence rises with increasing age. The lesional alopecia skin in 12-month-old male NZB/KN mice showed a sharp decline in hair follicle density, thus meeting a key criterion of permanent alopecia. Both macroscopically and histologically, the alopecia seen in these mice resembled in many respects different stages of clinical APA, such as alopecia associated with chronic discoid lupus erythematosus (DLE) in humans. Lesional APA hair follicles in mice displayed intrafollicular and perifollicular mononuclear cell infiltrates, as well as an increased number of activated (degranulated) perifollicular mast cells. In the fully developed lesion, many CD4+ cells were seen in perifollicular locations, including the epithelial stem cell region (bulge), and also contained a few CD8+ T cells. IgM deposits were found in the follicular basement membrane zone (BMZ). Both in the bulge and the hair matrix region of the affected anagen hair follicles, there were signs of massive keratinocyte apoptosis. CONCLUSIONS: Our currently available data suggest that male but not female NZB/KN mice may indeed represent a suitable mouse model for APA, with some similarities to the permanent alopecia seen in human DLE patients, although additional and confirmatory investigations are needed before this mouse strain can be accepted as a murine equivalent of APA in humans.

Aging↗
PubMed1995

Busulfan concentration in relation to permanent alopecia in recipients of bone marrow transplants.

Alopecia is an important long-term complication after bone marrow transplantation (BMT). The aim of this study was to analyze the influence of busulfan concentration on the development of permanent alopecia. Sixty five patients who survived for at least 6 months after BMT were studied. The median follow-up was 2.1 years (range 0.5-5.7 years). Thirty one patients (47%) had some degree of alopecia and 19 of these patients had extensive alopecia. The mean minimum busulfan concentration was 656 +/- 222 ng/ml in patients who developed alopecia compared with 507 +/- 224 ng/ml in those who did not (P = 0.005). Patients with more extensive alopecia had higher busulfan concentrations than patients with less significant abnormalities. In multivariate analysis, alopecia was associated with busulfan concentrations higher than the median (OR 3.43; 95% CI 3.04-3.88), allogeneic transplantation (OR 2.56; 95% CI 2.28-2.88) and female sex (OR 1.96; 95% CI 1.73-2.88). There was no association between alopecia and chronic graft-versus-host disease. High busulfan concentrations may contribute to the development of permanent alopecia and the risk for alopecia should be considered when choosing the conditioning regimen before BMT.

Adolescent↗
PubMed1996

Pulsed administration of corticosteroids in the treatment of alopecia areata.

BACKGROUND: Widespread alopecia areata (AA) is difficult to treat and modalities such as topical and systemic steroids, topical sensitizers (e.g., squaric acid dibutylester and diphencyprone), psoralen-ultraviolet A (PUVA) therapy, minoxidil, and immunomodulators have been tried. METHODS: Patients with widespread alopecia (> 40% scalp involvement), including alopecia totalis (AT) and universalis (AU), were treated with 300 mg oral prednisolone pulses at 4-week intervals, for a minimum of 4 doses or until cosmetically acceptable hair growth was obtained. Response to therapy was monitored by serial photographs and patients were examined monthly for side effects of steroids. A 1000 mg oral prednisolone pulse was administered to five patients with alopecia totalis/universalis and to three failures of the 300 mg-pulse treatment. RESULTS: Thirty-two patients (24 men, 8 women) with a mean age of 29 years were recruited. They had alopecia for a mean period of 2.8 years. Twenty-seven patients (21 alopecia areata, 5 alopecia universalis, 1 alopecia totalis) received 300 mg pulse therapy and eight patients received 1000 mg prednisolone pulses. Fourteen (58.3%) patients (13 AA, 1 AT) out of 24 evaluated treated with 300 mg pulse therapy showed complete or cosmetically acceptable hair growth. Response was evident on average after 2.4 months and was cosmetically acceptable at 4 months. Three (AA, AT, AU-one each) out of seven patients assessed for the 1000-mg pulse had cosmetically acceptable hair growth at 6-9 month. CONCLUSIONS: An oral monthly pulse of prednisolone 300 mg is effective, safe, and can be administered on an outpatient basis. It is recommended as one of the modalities for the treatment of widespread alopecia areata.

Administration, Oral↗
PubMed2003

Histopathologic features of alopecia areata: a new look.

BACKGROUND: A peribulbar lymphocytic infiltrate is the expected histologic feature of alopecia areata, but it is absent in many scalp biopsy specimens. Other diagnostic criteria are needed. OBJECTIVE: To establish the histologic features of alopecia areata in scalp biopsy specimens taken from different types of alopecia areata, using follicular counts to relate biopsy findings to stages of the disease. METHODS: Fifty consecutive new patients with alopecia areata were studied. Four-millimeter punch biopsy specimens were taken from the scalp in areas of recent, active hair loss; old, inactive hair loss; or recent hair regrowth. Specimens were sectioned horizontally. Terminal and vellus-like hairs were counted. Inflammation and fibrosis around lower and upper follicles were rated. RESULTS: The histopathologic features of alopecia areata were not significantly affected by the sex, age, and race of the patient or by the type, percentage of hair loss, total duration, or regression of alopecia areata. The major factor affecting the histopathologic features was the duration of the current episode of alopecia areata. In the acute stage, bulbar lymphocytes surrounded terminal hairs in early episodes and miniaturized hairs in repeated episodes. In the subacute stage, decreased anagen and increased catagen and telogen hairs were characteristic. In the chronic stage, decreased terminal and increased miniaturized hairs were found, with variable inflammation. During recovery, increasing numbers of terminal anagen hairs from regrowth of miniaturized hairs and a lack of inflammation were noted. CONCLUSIONS: The histopathologic features of alopecia areata depend on the stage of the current episode. Alopecia areata should be suspected when high percentages of telogen hairs or miniaturized hairs are present, even in the absence of a peribulbar lymphocytic infiltrate.

Adult↗
PubMed2006

Alopecia associated with treatment with selective serotonin reuptake inhibitors (SSRIs).

PURPOSE: To study the association between alopecia and selective serotonin reuptake inhibitors (SSRIs) by estimating reporting rates and by making association comparisons within databases of adverse drug reactions (ADRs). METHODS: All reports of alopecia with marketed SSRIs until the end of 2004 were identified in SWEDIS, the national Swedish database for spontaneously reported ADRs, and in Vigibase, the international ADR database of the World Health Organization. Total SSRI sales volumes in Sweden until the end of 2004 were obtained from the National Corporation of Swedish Pharmacies. The Bayes' Confidence Propagation Neural Network (BCPNN) method was used to estimate associations between alopecia and each of the SSRIs within the two databases. RESULTS: A total of 27 reports of alopecia were identified in SWEDIS. As two reports concerned the use of two SSRIs, there was a total of 29 drug-ADR combinations. All except three reports concerned women (88.9%). The reporting rate of alopecia in Sweden was significantly higher with sertraline compared with citalopram; 20.1 (95%CI 10.7-34.4) reports per million patient-years versus 4.5 (95%CI 1.8-9.3) reports per million patient-years. No significant differences in reporting rates were noted for the remaining SSRIs. Sertraline also showed a statistically significant association with alopecia in both SWEDIS and Vigibase. Citalopram was significantly associated with alopecia in Vigibase, but not in SWEDIS. No statistically significant associations were found for any of the other SSRIs. CONCLUSIONS: Alopecia appears to be a rare ADR to SSRIs. The risk of alopecia seems to vary between the different SSRIs, and might be higher in women than in men.

Adult↗
PubMed2001

Scarring alopecia and the dermatopathologist.

BACKGROUND: The evaluation of patients with cicatricial alopecia is particularly challenging, and dermatopathologists receive little training in the interpretation of scalp biopsy specimens. Accurate interpretation of specimens from patients with hair disease requires both qualitative (morphology of follicles, inflammation, fibrosis, etc.) and quantitative (size, number, follicular phase) information. Much of this data can only be obtained from transverse sections. In most cases, good clinical/pathologic correlation is required, and so clinicians should be expected to provide demographic information as well as a brief description of the pattern of hair loss and a clinical differential diagnosis. RESULTS: The criteria used to classify the various forms of cicatricial alopecia are relatively imprecise, and so classification is controversial and in a state of evolution. There are five fairly distinctive forms of cicatricial alopecia: 1) chronic, cutaneous lupus erythematosus (discoid LE); 2) lichen planopilaris; 3) dissecting cellulitis (perifolliculitis abscedens et suffodiens); 4) acne keloidalis; and 5) central, centrifugal scarring alopecia (follicular degeneration syndrome, folliculitis decalvans, pseudopelade). Not all patients with cicatricial alopecia can be confidently assigned to one of these five entities, and "cicatricial alopecia, unclassified" would be an appropriate label for such cases. CONCLUSION: The histologic features of five forms of cicatricial alopecia are reviewed. Dermatopathologists can utilize a "checklist" to catalog the diagnostic features of scalp biopsy specimens. In many, but not all, cases the information thus acquired will "match" the clinical and histologic characteristics of a form of cicatricial alopecia. However, because of histologic and clinical overlap between the forms of cicatricial alopecia, a definitive diagnosis cannot always be rendered.

Alopecia↗
PubMed1998

Reappraisal of Ikeda's classification of alopecia areata: analysis of 356 cases from Chandigarh, India.

Three hundred and fifty six patients (234 males, 122 females) with alopecia areata were classified according to Ikeda's classification. The common type of alopecia areata was most frequently seen in 239 (67.13%) patients, followed by atopic in 60 (16.85%), prehypertensive in 48 (13.4%), and autoimmune/endocrine in 9 (2.52%) patients. Severe alopecia did not occur with a higher frequency in atopic or endocrine/autoimmune alopecia areata than in the common type (p > 0.05). Prehypertensive alopecia areata had the lowest frequency of severe alopecia in the present study. The odds for developing severe alopecia were highest (2.6) when onset was before 16 years of age, followed by female sex (2.12), atopy (0.86), autoimmune/endocrine (0.53), and prehypertensive (0.28) types. Alopecia areata should be broadly classified as childhood (< 16 years) and adult onset with subtypes of atopic, autoimmune/endocrine, and common type under both. The prehypertensive type should be combined with the common type of alopecia areata.

Adolescent↗
PubMed1998

Acquired scalp alopecia. Part I: A review.

In this two-part series we review the acquired scalp alopecias. A broad spectrum of diseases result in alopecia. In this first part we provide a framework for the assessment and diagnosis of scalp hair loss, and begin covering the individual conditions. The non-scarring alopecias covered include effluvium, androgenetic alopecia, alopecia areata, trichotillomania, and loose anagen syndrome. The scarring alopecias cause permanent pilosebaceous follicle loss; the lymphocyte-associated scarring alopecia described encompasses lichen planopilaris, discoid lupus erythematosus, pseudopelade, and follicular mucinosis. Part II will cover the neutrophil-associated and infiltrative processes causing scarring alopecia followed by the medical management of alopecia. There is particular reference to newly described conditions and progress in the understanding of older conditions. More recently characterized conditions include the loose anagen syndrome, chronic telogen effluvium, and the frontal fibrosing variant of lichen planopilaris.

Alopecia↗
PubMedDate not supplied

A clinical study of childhood alopecia areata in Chandigarh, India.

All new cases of alopecia areata (AA) were studied during the years 1983-1993. Eight hundred forty-one cases were recorded, including 201 (23.9%) children less than 16 years of age. The female:male ratio was 1.4:1 (117 girls, 84 boys) for childhood AA. Alopecia was severe, that is, total, universal, or extensive, in 34 (16.9%) children. Onset occurred in 77 (38.3%) children between ages 6 and 10 years, in 67 (33.3%) before 5 years of age, and in 57 (28.4%) between 11 and 16 years. Onset before 5 years of age was more often associated with severe alopecia than onset at ages 11 to 16 years (p < 0.01). Onset before 2 years of age was commonly associated with severe alopecia, seen in 6 (55.5%) of 11 children. Twenty-five (12.4%) children had one or more family members with AA. Definite evidence of atopy was obtained in 35 (17.5%) children. Association of atopy with severe alopecia was not statistically significant at initial presentation (16% vs 23.5% for circumscribed and severe alopecia, respectively; p > 0.05). Nail changes were found in 60 (30%) children and were more frequent in severe alopecia (53%) than in circumscribed alopecia (25.2%, p < 0.001). Associated vitiligo was found in seven (3.5%) children, and one child was hypothyroid. Childhood AA in Chandigarh, India, is remarkably similar to that seen in Western countries, except that an association of atopy with younger age at onset and severe alopecia was not confirmed.

Adolescent↗
PubMedDate not supplied

Failure of two TNF-alpha blockers to influence the course of alopecia areata.

Alopecia areata is a form of hair loss believed to be due to an anti-hair-bulb autoimmune process in which CD4 and CD8 lymphocytes affect the peribulb area. Alopecia universalis is the most severe form of alopecia areata and manifests itself as a complete loss of all body hair. The authors present the case of a 44-year-old psoriasis patient with a 20-year history of alopecia universalis who failed to respond to etanercept in terms of skin psoriasis and alopecia universalis, while reporting improvement in arthropathy. While tumor necrosis factor-alpha inhibitors succeeded in the treatment of some autoimmune disorders, reports of alopecia areata failures and this one of alopecia universalis demonstrate resistance to such treatment. Tumor necrosis factor-alpha inhibitors seem to not represent an effective treatment modality for alopecia universalis. The understanding gained from this experience should redirect the aims of alopecia areata therapy toward alternate mechanistic interventions.

Adult↗
PubMed2003

Prevalence of polycystic ovaries in women with androgenic alopecia.

OBJECTIVE: Although androgenic alopecia is recognised to be a symptom of polycystic ovary syndrome (PCOS), it is not known whether polycystic ovaries (PCO) and associated endocrine abnormalities are present in patients who present with alopecia as a primary complaint. We therefore set out to determine the strength of the association between androgenic alopecia and PCO. We examined the prevalence of ultrasound-based polycystic ovarian morphology and associated clinical and biochemical features in a large multiethnic group of women whose presenting complaint was of alopecia, and in a control group. SUBJECTS AND METHODS: We studied 89 women of mixed ethnic origin with androgenic alopecia and compared them to 73 control women. A detailed history was taken, anthropometry was performed and assessment of body-hair distribution was made. The presence of PCO was established by pelvic ultrasound scan. Serum gonadotrophins, testosterone, androstenedione, dihydrotestosterone and sex hormone binding globulin concentrations were measured. RESULTS: Women with alopecia had a higher prevalence of PCO and hirsutism than the control population (PCO: 67% vs 27%, P<0.00001; hirsutism: 21% vs 4%, P=0.003). Women with alopecia (with or without PCO) had higher testosterone, androstenedione and free androgen index than controls, even though few had frankly abnormal androgens. CONCLUSIONS: These findings confirm an association between androgenic alopecia and PCO, and other symptoms of hyperandrogenaemia. Thus most women who present with androgenic alopecia as their primary complaint also have PCO and have indices of abnormal androgen production. Since PCO is a well known risk factor for development of type 2 diabetes, this association has important implications for long-term management.

Adult↗
PubMed2006

Review of scalp alopecia due to a clinically unapparent or minimally apparent neoplasm (SACUMAN).

Neoplastic cells, both malignant and benign, local occurring and metastatic, can cause alopecia of the scalp. However, the infiltration of neoplastic cells is sometimes not florid; a condition known as "scalp alopecia due to a clinically unapparent or minimally apparent neoplasm" (SACUMAN). Neoplastic cells can nevertheless destroy hair follicles by inducing fibroplasias via inflammatory mediators, attracting inflammatory cells and/or replacing normal cellular populations. The infiltrative nature of such an alopecia can be unapparent or only minimally apparent. The most common neoplasm in which an uncomplicated, minimally or unapparent scalp alopecia occurs and no infiltrate of cancer is suspected is metastatic breast carcinoma. Other causes include squamous and basal cell carcinomas, angiosarcoma, gastric carcinoma, placental site tromphoblastic tumor, and mycosis fungoides. Syringoma-like proliferations can underlie alopecia. It is unclear whether these proliferations are true syringomas or normal findings. In conclusion, neoplasms causing cicatricial alopecia of the scalp are very rare, so generalizations from the limited number of case reports are of uncertain importance. Moreover, it is likely that many cases of neoplasms causing cicatricial alopecia of the scalp are diagnosed as inflammatory alopecia and not neoplasms, thus depriving us of a full accounting and understanding of this entity. Dermatologists must be aware that in rare cases a bland scalp alopecia can represent a new or recurring, local or metastatic neoplasm.

Alopecia↗
PubMed2004

Permanent alopecia after cranial irradiation: dose-response relationship.

PURPOSE: To develop a dose-response relationship for the occurrence of permanent alopecia after cranial irradiation and to analyze potential confounding variables that may contribute to this unwanted and often unavoidable complication of treatment. METHODS AND MATERIALS: Twenty-six patients were enrolled in this study. Three reviewers independently assessed 61 scalp regions and assigned a score for the degree of alopecia in each region using a 4-point scale. Patient and treatment data were collected using a patient questionnaire and outpatient medical chart review. The hair follicle dose was calculated for each scalp region and correlated with the alopecia score for that region. A dose-response relationship was established using the data from these correlations. RESULTS: Permanent alopecia correlated significantly with the follicle dose only (p < 0.001). A personal history of alopecia and the use of chemotherapy correlated with permanent alopecia with borderline statistical significance (p = 0.059 and p = 0.068, respectively). Patient age, family history of baldness, gender, tobacco use, diabetes, and beam energy did not correlate with alopecia. CONCLUSION: We report the first human dose-response relationship describing the effect of the follicle dose on the subsequent development of permanent scalp alopecia after cranial irradiation. This information will assist the radiation oncologist, physicist, and dosimetrist in designing a treatment plan that might minimize the risk of this untoward side effect of cranial irradiation.

Adult↗
PubMed2005

Lipedematous alopecia: an unusual sequela of discoid lupus, or other co-conspirators at work?

BACKGROUND: Lipedematous alopecia is a rare entity of uncertain origin characterized by a boggy scalp and varying alopecia. Of 11 cases in the literature, 7 occurred in African American women. Classic histopathologic findings include increased subcutaneous tissue, varying inflammation, and an absence of mucin. Some have sought to distinguish this disorder from lipedematous scalp, a condition with similar tactile features, but without alopecia. OBSERVATION: We describe a case of lipedematous alopecia in an African American woman who also had findings of discoid lupus erythematosus. Such an observation has not been made previously, and may provide insight into the cause of lipedematous alopecia. This case is contrasted with a case of lipedematous scalp. CONCLUSION: Some cases of lipedematous alopecia may represent an unusual consequence of discoid lupus erythematosus. Alternatively, it is possible that lipedematous scalp is a benign condition observed in some patients, and that a second insult results in alopecia. Finally, lipedematous alopecia might share some histopathologic and/or clinical findings with discoid lupus erythematosus, or it may represent a nonspecific reaction pattern to chronic injury.

Black or African American↗
PubMed2005

Etanercept does not effectively treat moderate to severe alopecia areata: an open-label study.

In this prospective, open-label pilot study, we evaluated the safety and efficacy of etanercept, a TNF-alpha inhibitor, in the treatment of moderate to severe alopecia areata, alopecia totalis, or alopecia universalis. Seventeen otherwise healthy adults with moderate to severe alopecia areata were enrolled. The primary outcome measure was the extent of hair regrowth during and after the end of treatment as evaluated by the Severity of Alopecia Tool (the SALT score). After between 8 and 24 weeks of continuous treatment with etanercept 50 mg given subcutaneously twice weekly, significant regrowth of hair was not shown in any of the subjects treated. Based on these results, etanercept appears to be ineffective in treating subjects with treatment-refractory, moderate to severe alopecia areata, alopecia totalis, or alopecia universalis.

Adult↗
PubMed2005

Orally administered FPRL1 receptor agonist peptide MMK-1 inhibits etoposide-induced alopecia by a mechanism different from intraperitoneally administered MMK-1.

Oral administration for 6 days of 100 mg/kg MMK-1, an agonist peptide selective for the FPRL1 receptor, suppressed alopecia induced by the anticancer drug etoposide in neonatal rats. The anti-alopecia effect of orally administered MMK-1 was not inhibited by pyrilamine or cimetidine, antagonists for histamine H1 and H2 receptors, respectively, which blocked the anti-alopecia effect of intraperitoneally administered MMK-1 at a dose of 10 mg/kg for 4 days. However, the anti-alopecia effect of orally administered MMK-1 was inhibited by indomethacin, an inhibitor of cyclooxygenase (COX), or AH-23848B, an antagonist of the EP4 receptor for prostaglandin (PG) E2, suggesting involvement of PGE2 release and the EP4 receptor in the oral MMK-1 anti-alopecia mechanism. The anti-alopecia effect of orally administered MMK-1 was also blocked by an inhibitor of nuclear factor-kappaB (NF-kappaB), pyrrolidine dithiocarbamate, suggesting that the oral anti-alopecia effect of MMK-1 may be mediated by activation of NF-kappaB. These results suggest that MMK-1 bound to FPRL1 receptor might suppress etoposide-induced apoptosis of hair follicle cells and alopecia by way of PGE2 release and NF-kappaB activation.

Administration, Oral↗