An immune pathological and ultrastructural skin analysis for rhododenol-induced leukoderma patients.

As reported in the mass media on July 2013, numerous consumers who had used the cosmetic ingredient containing rhododendrol (4-(4-hydroxyphenyl)-2-butanol, Trade name; rhododenol), which is a melanin inhibitor isolated from Acer nikoense Maxim, released from Kanebo Cosmetics Inc. (Tokyo, Japan) noticed leukoderma patches on their face, neck and hands. We have experienced 32 cases that developed leukoderma after using such cosmetics so far and skin biopsy samples in some cases were obtained from both leukoderma and pigmented lesions. A histopathological analysis for skin lesions obtained from such patients notably showed basal hypo-pigmentation, melanin incontinence, and remaining melanocytes in most patients which is not relevant in vitiligo vulgaris. Subsequently, we comprehensively carried out immunohistochemical analyses of immune-competent cells infiltration to assess the effect of the cellular immune response to inducible hypopigmentation. Furthermore, detailed morphological observations performed by electron-microscopy notably showed the presence of melanocytes with only a small number of melanosomes, dermal fibroblasts containing melanosome globules and melanophages whereas no damage associated with melanosome transfer and the basal layer apparatus. These findings provide a cue to diagnose as rhododenol-induced leukoderma differentiate from vitiligo vulgaris and for rhododendrol to induce local immunity in addition to melanocyte damage.

Bullous pyoderma gangrenosum: a case report and review of the published work.

Pyoderma gangrenosum (PG) is an ulcerative skin disorder characterized by neutrophilic infiltrations. PG is generally classified into four types: (i) ulcerative; (ii) pustular; (iii) bullous; and (iv) vegetative. Among them, bullous PG is known as a rare type. Herein, we report a case of bullous PG together with a summary of the 12 PG cases treated in our department over the previous 15 years, and we review 38 well-documented bullous PG cases (65.8% female; aged 18-80 years [mean ± standard deviation, 51.6 ± 16.8]) in the published work, including the present case, from 1972-2011. Although the disease most frequently associated with PG is inflammatory bowel disease, bullous PG is most commonly associated with hematological disorders (25/38, 65.8%), which indicates the characteristic pathophysiology specific to bullous PG.

Aberrant cytokeratin 7 expression of centrilobular hepatocytes: a clinicopathological study.

AIMS: This study has attempted to elucidate the clinicopathological features of aberrant cytokeratin 7 (CK7) expression by centrilobular hepatocytes. METHODS AND RESULTS: A total of 113 liver biopsy specimens from patients with common non-neoplastic liver diseases, including hepatitis B or C, non-alcoholic steatohepatitis, alcoholic liver disease and other diseases were examined. In 56 specimens (49.6%), CK7-positive centrilobular hepatocytes (CK7 + CHs) were identified and sometimes showed binuclear features. CK7 + CHs were associated with patients' older age (P = 0.004), higher serum levels of aspartate aminotransferase (P = 0.016) and γ-glutamyltransferase (P = 0.006), centrilobular fibrosis (P < 0.001), prominent thickening of hepatocytic plates (P < 0.001) and higher scores of total and periportal CK7-positive hepatocytes (both P < 0.001), but were not correlated with gender, steatosis, serum levels of total bilirubin or alanine aminotransferase. In 55 cases of hepatitis B and hepatitis C only, CK7 + CHs were related to a higher stage of fibrosis (P = 0.006). CONCLUSION: CK7 + CHs occur relatively frequently in non-neoplastic liver disease, associated with centrilobular scarring and the presence of CK7-positive periportal hepatocytes, and appear to be a non-specific phenomenon with respect aetiology of underlying disease. CK7 + CHs may represent age-dependent activation of hepatic progenitor cells or a regenerative phenomenon of hepatocytes themselves, both of which might contribute to liver regeneration.

Therapeutic effects of tacrolimus ointment for refractory ocular surface inflammatory diseases.

PURPOSE: To investigate the therapeutic effects of topical tacrolimus ointment on refractory ocular surface inflammatory diseases. DESIGN: Retrospective interventional consecutive case series. PARTICIPANTS: Ten consecutive patients with severe ocular surface inflammatory diseases who were suspected to be steroid responders (elevation of intraocular pressure [IOP]) or were refractory to standard steroid therapy were studied. One patient had peripheral ulcerative keratitis with impending corneal perforation, 1 had a Mooren's ulcer, 2 had scleroperikeratitis, 5 had atopic keratoconjunctivitis, and 1 had vernal keratoconjunctivitis. METHODS: The clinical findings and therapeutic responses after treatment with 0.02% topical tacrolimus ointment were determined by conventional ophthalmological examinations. MAIN OUTCOME MEASURES: Resolution of the ocular surface diseases (e.g., decrease of hyperemia, ulceration, size of papillae) and IOP. The necessity to use steroids was also assessed. RESULTS: In all cases, marked to moderate improvement was obtained, including suppression of the melting reaction of the inflamed cornea, remission of scleroperikeratitis, and reduction of a giant papilla and corneal epithelial defect in severe atopic keratoconjunctivitis. The elevated IOP was reduced in steroid responders after successful cessation of steroid therapy. No adverse side effect was noted for 2 to 26 months of continuous treatment. CONCLUSIONS: Topical tacrolimus ointment is effective in treating refractory ocular surface inflammatory diseases and should be considered as an alternative to higher doses, steroid supplementation, or surgical intervention.