Ryoji Tanei

Clinical and Histopathologic Analysis of the Relationship between Lichen Planus and Chronic Hepatitis C

A prospective clinical investigation of 45 patients with lichen planus (LP) demonstrated a significant association between LP and chronic hepatitis C. Anti‐hepatitis C virus (HCV) antibodies were found in 17 (37.8%) of the 45 LP patients. This was significantly higher than in the controls. This higher prevalence of anti‐HCV antibodies was found equally in both male and female patients in the three types of LP; cutaneous only type, mucous only type, and both cutaneous and mucous type. Most of the patients with positive anti‐HCV antibodies had abnormal values of transaminase enzymes and/or a past history of chronic hepatitis. Histological and immunohistological investigations of three cases with LP and chronic hepatitis C demonstrated some morphologic similarities between these two diseases. Histopathologic findings of both LP and chronic hepatitis C were based on a T lymphocytic infiltrate with keratinocyte or hepatocyte damage. The degrees of infiltrating cells positive to UCHL‐1, MX‐panB, Leu‐7, and human leukocyte antigen (HLA)‐DR antibodies in the chronic hepatitis C lesions seemed to be similar to those in the LP lesions. These results may support a possible relationship between LP and chronic hepatitis C and the hypothesis that LP may be associated with chronic liver diseases as a result of a cytotoxic attack on the hepatocytes.

Induction of Eczematous Skin Reaction in Experimentally Induced Hyperplastic Skin of Balb/C Mice by Monoclonal Anti-DNP IgE Antibody: Possible Implications for Skin Lesion Formation in Atopic Dermatitis

Biphasic skin reaction with peak response at 1 and 24 h with prominent mast cell degranulation was induced by intravenous application of a monoclonal anti-DNP IgE antibody and subsequent skin test. This reaction was hapten-specific and mast-cell-dependent because no reaction was observed when oxasolone was used as an elicitation antigen or skin test was elicited in genetically mast-cell-deficient mice (W/Wvv). A partial spongiotic reaction and mononuclear cell infiltration into the epidermis were observed in mice with hyperplastic epidermis induced by topical retinoic acid. Cotransfer of DNFB-sensitized lymph node cells with anti-DNP IgE antibodies failed to enhance the skin test reaction in unsensitized mice. These results suggest that, to some degree, IgE antibody may play some role in the development of eczematous skin lesions in the rodent system without the involvement of cellular hypersensitivity.

Clinical analyses of atopic dermatitis in the aged

The aim of the present study was to analyze the characteristics of atopic dermatitis (AD) in the senile phase. Subjects were comprised of 16 patients investigated for clinical features, serum immunoglobulin (Ig)E levels and skin manifestations. Mean age was 76.9 ± 6.2 years (range, 68–87), with a man : woman ratio of 3:1. Mean age at onset was 67.7 ± 15.7 years. Eight patients (50%) had personal histories of chronic eczema until the young adult phase and three patients (18.8%) showed the classic course of child AD. Eczematous erythroderma in 10 patients (62.5%) and unclassified chronic eczema in five patients (31.3%) were the predominant clinical presentations. Mean total IgE level in sera of the 16 patients was 8810 ± 13 511 IU/mL (range, 5–53 605). Fourteen patients showed positive results for antigen‐specific IgE antibodies, and the mean total IgE level for these patients was 10 056 ± 14 044 IU/mL. Specific IgE to the main antigen, Dermatophagoides farinae, was observed in 12 patients (85.7%), representing the principal antibody in eight patients (57.1%). Eczematous dermatitis manifested predominantly in the face and neck, trunk and extensor and flexure sites of extremities, and less commonly in the antecubital and popliteal areas. Other stigmata of AD were observed as follows: red face in 10 patients (62.5%); Hertoghes sign in six (37.5%); goose‐skin in four (25%); facial pallor in three (18.8%); and dirty neck in one (6.3%). These results indicate that senile‐type AD represents a characteristic subgroup of AD that appears in the last stage of life in AD patients.

Lichen Planus and Sjögren‐type Sicca Syndrome in a Patient with Chronic Hepatitis C

We report a 54‐year‐old Japanese male with lichen planus and Sjögren‐type sicca syndrome, accompanied by the latent complication of chronic hepatitis C. The patient first showed erythematous and erosive lesions with white irregular striae in the buccal mucous membrane, and blepharitis and hyperemia of conjunctiva in his eyes. He later had two small erosions on the glans penis, and flat‐topped violaceous papules on the dorsa manus and nape. A biopsy specimen of the lower lip lesion demonstrated a lichenoid tissue reaction at the basement membrane zone, and lymphocytic focal accumulations in the salivary glands. Immunohistochemical study of this specimen revealed CD45RO+ (T) cells associated with the expression of HLA‐DR antigens predominantly in both the lichenoid tissue reaction and the lymphocytic sialadenitis. Objective keratoconjunctivitis sicca was confirmed by the Schirmer and Rose‐Bengal tests. Anti‐DNA antibody was positive; however anti‐SS‐A, and anti‐SS‐B antibodies were negative. Increased levels of transaminase enzymes, TTT, ZTT, and IgG were observed in first laboratory examinations; thereafter, anti‐hepatitis C virus (HCV) antibodies and HCV‐RNA were detected. The high serum amylase level, in which salivary amylase predominated, was normalized by etretinate therapy in parallel with the clinical improvement of the oral LP lesions. Our case is considered to support the hypothesis that an etiologic association may be present among lichen planus, Sjögrens syndrome, and chronic hepatitis C.

Characterization of infiltrating T cells in human scalp explants from alopecia areata to SCID nude mice: possible role of the disappearance of CD8+ T lymphocytes in the process of hair regrowth.

T cells may play a role in the pathogenesis of alopecia areata (AA). We attempted to elucidate the linkage between infiltrating T cells and hair regrowth processes by grafting scalp skin from the affected region of patients with AA onto severe combined immune deficiency (SCID) nude mice.

Transfusion-Associated Graft-versus-Host Disease: An in situ Hybridization Analysis of the Infiltrating Donor-Derived Cells in the Cutaneous Lesion

Background: Acute graft-versus-host disease (GVHD) can occur after a blood transfusion. Objective: In order to elucidate the pathomechanisms responsible for transfusion-associated GVHD, infiltrating donor-derived cells in a cutaneous lesion were analyzed. Methods: A skin sample obtained from a 69-year-old woman who developed fatal GVHD after blood transfusions from male donors was studied by performing in situ hybridization (ISH) with a Y-chromosome-specific probe. Results: The cell infiltrates comprised mainly CD3+ T lymphocytes. Immunohistochemistry and ISH in combination demonstrated that 99% (182/184) of the Y-body-positive cells were CD3+. Y bodies were observed in 80% of the CD8+ cells in the epidermis and dermoepidermal junction and in 77 and 45% of the CD8+ and CD4+ cells, respectively, in the dermis. Conclusion: These findings suggest that both CD4+ and CD8+ cells of donor origin were involved in the development of cutaneous GVHD.

Dermatitis herpetiformis in a Japanese patient with anaplastic large cell lymphoma.

We report a 73‐year‐old Japanese man with dermatitis herpetiformis which developed after diagnosis of anaplastic large cell lymphoma. The patient suffered fever, sweating, shivering, and multiple enlarged cervical lymph nodes. The diagnosis of anaplastic large cell lymphoma was confirmed by the histologic features of a biopsied cervical lymph node. The patient underwent combination chemotherapy. However, one month after the initial therapy, pruritic erythematous skin lesions with peripheral vesicles appeared on his buttocks. A skin biopsy showed subepidermal blister formation associated with polymorphonuclear and mononuclear cell infiltrates. Direct immunofluorescence examination of the area adjacent to the lesion showed granular deposits of IgA at the dermoepidermal junction. While it is well‐known that dermatitis herpetiformis can develop into lymphoma, there have been only a few reports of its appearance after a diagnosis of lymphoma. This case suggests that dermatitis herpetiformis may be induced by anaplastic large cell lymphoma.

Microchimerism Seems Uninvolved in the Pathogenesis of Idiopathic Lichen planus

The pathogenesis of lichen planus (LP) is believed to be caused by a T-cell-mediated immune response against an unknown antigen in the epidermis. It has been considered that the immunopathomechanisms of LP may be similar to graft-versus-host-reaction since LP-like lesions commonly occur in chronic graft-versus-host-disease (GVHD). Because sclerodermatous lesions are observed in later chronic GVHD, scleroderma has also been thought to be another dermatologic disorder for which GVHD may serve as a biological model. Interestingly, two recent reports [1, 2] suggest that microchimerism caused by pregnancy may be involved in the pathogenesis of scleroderma. Therefore, we analyzed whether microchimerism might also be involved in the pathogenesis of LP. An enzymatic detection in situ hybridization (ISH) analysis was performed on sections from a paraffin-embedded skin biopsy specimen with a Y-chromosome-specific DNA probe (DYZ1, DYZ3; P5062-DG.5, Oncor, Gaithersburg, D.C., USA), as described previously [3]. Ten female patients with cutaneous or mucosal LP (mean age 68 B 7 years; range 58–83) were studied. Eight patients had given birth to males and 3 of the 8 patients had sons only. Seven patients had a history of nonirradiated blood transfusion between 1963 and 1988. Eight of the 10 patients were serologically positive for antihepatitis C virus (HCV) antibodies. The characteristics of patients and the results are summarized in table 1. In all of the 10 patients, no Y-body-positive cells were observed in any cell infiltrate of the LP.

Scaling Lichenoid Eruptions and Sjögren‐like Syndrome: Manifestations of Nonfatal Postoperative Transfusion‐Associated Graft‐versus‐Host Disease?

We report a case of an 81‐year‐old woman in whom lichenoid eruptions and Sjögren‐like sicca syndrome developed 45 days after cholecystectomy. During surgery, one unit (130 ml) of unirradiated packed red blood cells from a male donor was transfused. The lichenoid eruptions cleared up with exfoliation; however, sicca symptoms remained during the follow‐up period of four years. Histological examinations of both skin and lip biopsy specimens were in agreement with those of graft‐versus‐host disease (GVHD). A Y‐chromosomal body was identified in the lymphocytes in the skin lesion by staining with quinacrine dihydrochloride and in the lip lesion by a method with in situ hybridization. The findings suggest that this case demonstrated the manifestations of non‐fatal transfusion‐associated GVHD.

Angiotropic B-Cell Lymphoma with Telangiectasia, Accompanied by Panniculitic Formation

A 67‐year‐old female presented with diffuse edema, generalized telangiectasia, and indurated skin plaques. Histopathological findings of the skin lesion included CD45+/CD79+/CD20+ large lymphoma cells that filled the vascular lumina and infiltrated the subcutaneous tissues with panniculitic formations. Three cycles of a CHOP (cyclophosphamide, adriamycin, vincristine, and prednisolone) chemotherapy regimen resolved the skin manifestations. After five cycles of CHOP, however, she developed dementia‐like symptoms. Three cycles of additional intrathecal chemotherapy (methotrexate, cytarabine and prednisolone) did not improve the neurological symptoms.