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Notes: Granulomatous slack skin is a rare lymphoproliferative disorder characterized clinically by gradual development of pendulous folds of lax erythematous skin in flexural areas, and histologically by non-necrotizing granuloma, with numerous multinucleated giant cells, mononuclear histiocytes, and atypical lymphocytes associated with loss of elastic fibers. Although there are many reports describing the histological and immunophenotypic features of this disease, only a few have described the ultrastructural features.Methods: Here we report a case of granulomatous slack skin and describe the ultrastructural findings.〈section xml:id="abs1-2"〉〈title type="main"〉Results and conclusion:We could detect some previously not noted abnormal findings in multinucleated giant cells, histiocytes, and atypical lymphocytes.

Notes: A 48-year-old woman had suffered from gradual progression of skin pigmentation since 1987 and liver dysfunction since 1994, without having been treated by specialists. In September 1996, she suffered from acute development of morning stiffness of the hands and multiple arthralgias, especially of the fingers. In November 1996, her regular physician, who suspected she had rheumatoid arthritis, referred her to the Departments of Orthopedics, Rheumatology, and Internal Medicine of our hospital. Laboratory findings revealed elevation of titers of antinuclear antibody (× 320, homogeneous pattern), anti-smooth-muscle antibody (× 320), levels of immunoglobulin G (2.58 g/L; normal, 8.70–1.70 g/L), anti-DNA antibody (16 IU/mL; normal, 0–7 IU/mL), aspartate aminotransferase (97 U/L; normal, 0–35 U/L), and alanine aminotransferase (88 U/L; normal, 0–35 U/L). Results of tests for rheumatoid factor immunoglobulin M and G, hepatitis B surface antigen, hepatitis C virus antibody, lupus erythematosus cells, lupus erythematosus test, antimitochondrial antibody, anticentromere antibody, and anti-Sjögren syndrome A and B antibodies were all negative. Other laboratory findings were within normal ranges. Autoimmune hepatitis was suspected and liver biopsy was performed. A liver biopsy specimen revealed chronic nonsuppurative destructive cholangitis with dense lymphocytic infiltration around the portal veins, piecemeal/spotty necrosis, and periductal fibrosis. On the basis of these clinicopathologic findings, autoimmune cholangitis was diagnosed.Her skin pigmentation was examined at the Department of Dermatology of our hospital. On initial examination, reticular or ‘‘rippled,’' gray–brown pigmentation was found on the nape of the neck, upper back ( 〈link href="#f3-1"〉Fig. 1), and the extensor aspects of both arms ( 〈link href="#f3-2"〉Fig. 2). There was no Raynaud's phenomenon. No sclerodactylia or proximal scleroderma was found. She had no history of pre-existing dermatoses, such as atopic dermatitis, chronic eczema, or contact dermatitis. She denied the occurrence of excessive friction of the skin. A skin biopsy specimen revealed eosinophilic homogeneous masses in the papillary dermis and upper dermis. These homogeneous masses were positive to Dylon and Congo red staining ( 〈link href="#f3-3"〉Fig. 3). In the liver biopsy specimen, no materials positive to Dylon or Congo red staining were found. In addition, results of electrophoresis of urinary and blood protein were normal. The patient was therefore diagnosed with macular-type primary localized cutaneous amyloidosis.〈figure xml:id="f3-1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD047-4:IJD_047_f3-1"/〉Reticular or ‘‘rippled’' gray–brown pigmentation on the upper back〈figure xml:id="f3-2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD047-4:IJD_047_f3-2"/〉Skin pigmentation on the extensor aspects of both arms〈figure xml:id="f3-3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD047-4:IJD_047_f3-3"/〉Homogeneous masses, positive to Dylon staining, in the papillary dermis (Dylon staining; original magnification, × 300)Administration of prednisolone 30 mg daily improved liver function and arthralgia. The dosage of prednisolone was gradually decreased to 10 mg daily without exacerbation. Although no progression of skin lesions has occurred, skin pigmentation has persisted as of November 1999.

Notes: The patient, a 34-year-old Japanese woman who noticed worsening of her rash after using topical corticosteroid preparations on her neck, was patch tested for both commercial preparations and corticosteroids themselves. The patch lest results revealed that she had a contact allergy to gold, oxytetracycline, and 2 types of corticosteroid (acetonides and esters) in 7 compounds (betamethasone valerate and dipropionate, hydrocortisone butyrate and hydrocortisone butyrate propionate, ameinonide, budesonide, and fluocinonide).

Notes: Abstract Conflicting reports exist concerning ultraviolet-B (UVB) effects on keralinocyte (KC) interleukin-l (IL-1) expression. To clarify the modulatery effects of UVB on IL-1, the following study was undertaken. Normal human epidermal KCs cultured in a standard low Ca2+ and serum-free medium were irradiated in quiescent phase with UVB. In this study, we used semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to determine the mRNA level of interleukin-1α (IL-1α) and interleukin-1β (IL-β). After exposure to 100 or 300 J/m2 UVB, a transient increase in mRNA levels was observed within I hour for IL-1α and 3 to 6 h for IL-β Following this transient induction, mRNA levels for both IL-1α and IL-1β returned to steady-state levels after 100 J/m2. After 300 J/m2 irradiation, IL-1α and IL-1β levels were downregulated compared to unirradiated cultures at 24-h post-irradiation. The half-life for IL-1α and IL-1β was estimated using actinomycin D treatment. Both IL-1α and IL-1β mRNAs half-lives (t1/2) decreased faster in irradiated cells (t1/2 = 30 minutes for IL-1α and 2 h for IL-1β) compared to unirradiated cells (t1/2= 1 h and 4 h, respectively). These results suggest that IL-1α and IL-1β mRNA expression are differentially regulated by UVB. In contrast to down-regulation of mRNA levels, a significant increase in IL-1α protein levels, measured by ELISA. was observed in culture supernatant from 6 h to 24 h after 300 J/m2 UVB irradiation. Cycloheximide treatment did not abrogate this increase in IL-1α protein level. Since this dose of UVB irradiation decreased the stability of IL-1α and IL-1β mRNA, this suggests that the release of IL-1α after UVB irradiation was due to leakage from UVB-damaged cells and not from de novo protein synthesis.