1/22. Unilateral Schamberg disease in a 14-year-old Japanese boy.We report a 14-year-old Japanese boy who has had asymptomatic, multiple, reddish-brown macules and petechiae distributed segmentally only in the right lower extremity for the last 6 months. Histological examination showed a perivascular lymphohistiocytic infiltrate in the papillary dermis, extravasation of red blood cells, and hemosiderin deposition. Treatment with tranilast and topical corticosteroid was dramatically effective. Although the histological findings were compatible with those of Schamberg disease, this case was unusual because the patient was very young and only one extremity was affected.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
2/22. A case of prurigo and lichenified plaques successfully treated with proton pump inhibitor.A case of prurigo and lichenified plaques successfully treated with proton pump inhibitor is presented. She presented with pruritic eruptions, which showed marked lichenification and prurigo nodules, on her trunk and extremities. She had been treated with steroid ointment and H1-histamine receptor antagonist without success. Laboratory examinations revealed increased eosiophils and elevated lactate dehydrogenase. The skin biopsy specimen showed moderate acanthosis with spongiosis and lymphocytic and eosinophilic infiltration into the upper dermis. Because of vomiting and epigastralgia, endoscopical examination was performed, and an ulcer was found at the angle of her ventricle. A biopsy specimen disclosed a benign gastric mucosa with moderate inflammation within the lamina propria, and organisms consistent with helicobacter pylori. Treatment for gastric ulcer with proton pump inhibitor (omeprazole) and aluminium hydroxide gel improved her eruptions and her pruritus resolved. She was discharged with complete cure of her eruption and ventricular ulcer. Our case indicates that gastric lesions induced by helicobacter pylori infection may play an important role in dermatological diseases. proton pump inhibitors including omeprazole are one of the choices for the treatment of some dermatological diseases including prurigo and lichenified plaques.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
3/22. Lichen amyloidosus: a bullous variant.INTRODUCTION: Lichen amyloidosus is a common skin disease seen among Asian patients. CLINICAL PICTURE: Typical features range from macular hyperpigmentation to pruritic, lichenified, hyperpigmented papules. However, in this rare bullous variant of lichen amyloidosus, bullae and vesicles are present. Histopathologically, deposits of amyloid were seen in the papillary dermis, associated with an intraepidermal or subepidermal blister. TREATMENT AND OUTCOME: No good treatment so far, but pruritus can be relieved by topical steroid. CONCLUSION: It is important to screen for systemic amyloidosis with the relevant investigations as it can present similarly with blistering eruptions, in which the prognosis would be grave.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
4/22. Gianotti-Crosti syndrome presenting as lichenoid dermatitis.Papular acrodermatitis of childhood (Gianotti-Crosti syndrome) is an uncommon, self-limited disease characterized by an erythematous papular eruption symmetrically distributed on the face and limbs and mild lymphadenopathy, thought to be of viral origin. The histopathologic findings are nonspecific and include focal parakeratosis, mild spongiosis, superficial perivascular infiltrate, papillary dermal edema, and extravasated red blood cells. Interface changes with some basal vacuolization may be present, but are not a conspicuous feature. We present a 2 1/2-year-old boy with multiple papules and plaques on the face and extremities and cervical lymphadenopathy. Histopathologic analysis showed compact orthokeratosis, focal parakeratosis, hypergranulosis, psoriasiform epidermal hyperplasia, and a dense lichenoid lymphohistiocytic infiltrate with extensive exocytosis of mononuclear cells. Immunoperoxidase staining with CD 1 a revealed clusters of langerhans cells in the epidermis and in the papillary dermis. In view of the clinical findings, a diagnosis of Gianotti-Crosti syndrome was made. Although there are a few reports describing a lichenoid pattern of infiltration in Gianotti-Crosti syndrome, this histologic pattern is not widely known. This case is presented to illustrate the fact that Gianotti-Crosti syndrome can present as lichenoid dermatitis, and, especially in children, should be added to the differential diagnoses of lichenoid infiltrates.- - - - - - - - - - ranking = 2keywords = dermis (Clic here for more details about this article) |
5/22. Giant cell lichenoid dermatitis within herpes zoster scars in a bone marrow recipient.Cutaneous lesions arising in herpes zoster (HZ) scars are rare. We report a 34-year-old woman with acute lymphoblastic leukemia underwent allogenic bone marrow transplant (BMT). Ten days after the BMT, she developed clusters of vesicles over the right neck, scapula, shoulder and chest. She was treated with intravenous acyclovir and foscarnet. One month after the vesiculous episode of HZ she showed 5 mm to 2 cm clustered flat violaceous lichenoid papules and confluent plaques within the HZ scars. Histopathologic examination revealed a inflammatory infiltrate present in the papillary dermis with granulomatous aggregated formed by histiocytes, multinucleated giant cells and lymphocytes. She was treated with topic steroids with significant improvement. Pathologic findings are similar to those of an unusual lichenoid reaction named "giant cell lichenoid dermatitis". We present the first reported case of giant cell lichenoid dermatitis at the sites of HZ scars.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
6/22. Lichenoid nail changes as sole external manifestation of graft vs. host disease.A 56-year-old-man who had refractory anemia with an excess of blasts underwent an allogeneic peripheral blood stem cell transplantation (PBSCT) from his brother after preparation with melphalan and fludarabin. He received GvHD (graft-vs.-host disease) prophylaxis with cyclosporine from day -1 at a daily dose of 5 mg/kg of body weight. The daily dosage was tapered gradually from day 20. On post-PBSCT day 68 he developed acute cutaneous GvHD grade 3 and acute gastrointestinal GvHD grade 2-3, which was resolved with a daily dose of 1 mg/kg of body weight of prednisone. The patient was discharged in good clinical condition and without signs of GvHD, and he started tapering his immunosuppressive treatment. By day 160 he developed oral lichen planus-like changes, with several reticulate white lesions on the oral mucosa. A biopsy specimen was microscopically consistent with lichenoid GvHD (Fig. 1). By day 150 after PBSCT, when he was being treated with CsA 100 mg once daily and prednisone 10 mg once daily, his fingernails started to grow abnormally and gradually became dystrophic and painful. Two months later his toenails became similarly affected. Although affecting all finger and toe nails, the lesions were especially important in both thumbs. physical examination revealed multiple findings on his nails (Fig. 2): thickening, fragility, onycholysis, longitudinal striations, and even pterygium. The micological cultures were negative. A biopsy specimen showed an sparse papillary dermis lymphoid infiltrate with focal exocytosis and presence of isolated multiple necrotic keratinocytes (Fig. 3). These findings were interpreted as a lichenoid GvHD with oral and nail involvement. The patient did not have other associated cutaneous lesions. He did not develop signs or symptoms consistent with hepatic GvHD. In May 2000 thalidomide was added to the immunosuppressive therapy, at a daily dose from 100 to 300 mg according to tolerance (constipation, sedation, ...). The lesions on the oral mucous showed a substantial improvement, but the nail changes remained more or less stable. thalidomide was discontinued after 7 months because the patient displayed numbness and tingling in the hands and feet consistent with a peripheral neuropathy. Twenty days later he stopped taking thalidomide and the oral lichenoid lesions worsened, resulting in difficulty in eating. He also developed periungueal erythema, swelling and intense pain after minimal trauma. The daily dose of prednisone increased to 20-30 mg with moderate improvement. However, the dose could not be increased because of the secondary immunosuppressive effects. Twenty-three months post-PBSCT the patient remains with intense oral and nail lichenoid lesions.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
7/22. Heparan sulphate proteoglycan in scleromyxedema promotes FGF-2 activity.The cause of progressive dermal sclerosis, proliferation of fibroblasts, and collagen deposition in scleromyxedema is unknown. We analyzed the heparan sulphate proteoglycans (HSPG) in cutaneous nodules from a patient with scleromyxedema in order to ascertain their role in the binding of fibroblast growth factor (FGF) and promoting signaling complex assembly. Total heparan sulphate (HS) was detected with a monoclonal antibody to HSPG on paraffin sections. Binding of FGF to HS was assessed using FGF-2 followed by anti-FGF-2 antibody. The formation of HS-mediated signaling complex was studied using soluble FR1-AP, which contains the extracellular domain of FGF receptor-1 linked to alkaline phosphatase (AP) and monoclonal anti-AP-antibody. Anti FGF-2 and anti-AP antibodies were visualized using the DAKO Envision Plus system. The dermal nodule of scleromyxedema contained ample HS and these bound FGF-2 and FR1-AP. Specificity was confirmed by prior incubation with heparitinase (no staining) and omission of FGF-2 (no staining). Increased amounts of HSPG were present in the dermal nodules of scleromyxedema compared to adjacent normal dermis and these bound FGF-2, immobilized the soluble receptor protein FGFR-1 and, therefore, formed a ternary complex composed of HSPG, FGF-2 and FGFR-1 in vitro. Since this complex resembles the signaling complex formed on live cells, HSPG in the nodules of scleromyxedema are in a configuration that promotes FGF activity.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
8/22. Colloid degeneration of the skin--a case report.A patient with multiple nodules on the chin and scalp is presented. Histologically, the nodules were composed of amorphous materials which also completely filled up the whole dermis. Histochemical observation indicated that the amorphous material in the nodule was a kind of glycoprotein. Electron microscopic examination revealed that the material consists of short wavy fibrils, 60 to 100 A in diameter, and of a low electron-dense amorphous substance. Biochemical examination supported the view that the amorphous material is so-called sialomucoid. The nodules were finally diagnosed as colloid degeneration of the skin (nodular type).- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
9/22. Localized longitudinal erythronychia: diagnostic significance and physical explanation.BACKGROUND: Longitudinal erythronychia (LE) is a term for red streaks in the nail. We describe the range of diseases manifested by localized (single or bifid) LE and explain the underlying physical changes. OBSERVATIONS: Longitudinal erythronychia can be multiple or localized. Multiple lesions typically indicate an inflammatory disease such as lichen planus. When localized, they may be a single or bifid streak arising through a benign or malignant neoplasm, scarring of the dermis or epidermis, or the first stage of an inflammatory process that may evolve into multiple LE. Excision of a localized LE may provide a diagnosis and cure. Incisional matrix biopsy of multiple LE may provide a diagnosis. Clinical manifestation of LE arises through reduced compression of the nail bed due to loss of bulk of the nail plate with a groove on the undersurface. A streak of thinned nail then allows an enhanced view of a corresponding streak of engorged nail bed. The reduction in nail thickness renders it more fragile with a tendency to split distally. CONCLUSIONS: Understanding LE can assist in diagnosis and explanation to the patient. Localized LE may represent a focal tumor or dysplastic process.- - - - - - - - - - ranking = 2keywords = dermis (Clic here for more details about this article) |
10/22. Discrete papular mucinosis on the back.A rare case of papular mucinosis on the back of a 78-year old man is described. The patient developed approximately 20 discrete papules on the upper back. His serum glucose concentration was borderline elevated, but no other systemic symptoms or signs were apparent. A biopsy revealed mucin deposits only in the upper reticular dermis. The papules were distinctly different from lichen myxedematosus in clinical and histochemical appearance. The present case may represent very early-stage lichen myxedematosus complicated by borderline diabetes mellitus.- - - - - - - - - - ranking = 1keywords = dermis (Clic here for more details about this article) |
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