Notes: A 75-year-old woman was referred for treatment of multiple keratoacanthomas and hypertrophic lichen planus. Surgical excision was considered but was not possible given the multiplicity of the lesions. Etretinate, potent topical corticosteroids and gradient support stockings were initiated. Complete resolution was achieved in four months and oral and topical therapy was discontinued. Four months after discontinuation of all therapy there has been no recurrence.

Notes: Background:  Microtubule associated protein 2 (MAP-2) is one of a group of polypeptides that are an integral component of the microtubular cytoskeletal structure of the central and peripheral nervous system. During the course of another investigation that utilized immunohistochemistry, MAP-2 expression was observed in the hair follicle, almost exclusively in the innermost layer of the outer root sheath of the anagen follicle. This innermost layer, the so-called companion layer, has unique properties that clearly distinguish it from the rest of the outer root sheath. Among these are diminished glycogenation and an intimate association with the Henle's layer, which it directly apposes. Numerous intercellular connections exist between the companion layer and Henle's layer and, in fact, the companion layer accompanies Henle's layer during its vertical ascent in the follicle. Circumferentially oriented keratin filaments have also been demonstrated between the companion layer and Henle's layer, apparently providing structural support to the inner root sheath. Experimentally, disturbances in the keratin filaments of the companion layer in animals ultimately results in destruction of the hair follicle and an alopecia.Methods:  Immunohistochemical studies for MAP-2 were performed on 25 additional paraffin-embedded scalp specimens using standard techniques. Because of the parallels between the follicle and nail, MAP-2 expression in the nail unit was also investigated in three specimens.Results:  The presence of MAP-2 in the companion layer was confirmed in all cases. Intense MAP-2 expression in the companion layer begins at the B-fringe (the start of the keratogenous zone with cornification of the Henle's layer of the inner sheath) and extends to the level of the isthmus where the inner root sheath exfoliates. MAP-2 is also expressed in the upper layers of the nail matrix.Conclusion: The expression of MAP-2 almost exclusively in the companion layer is probably related to the unique cytoskeletal structure of this microanatomic layer. Since experimental evidence has shown that the cell cytoskeleton is important to the integrity of the hair follicle, it is probable that MAP-2 expression is also important and disturbances in its expression could play a role in the pathogenesis of some alopecias. MAP-2 may play a similar role in the nail matrix.

Notes: In cases of solid organ or bone marrow transplantation, up to 2 to 10% of patients may develop lymphoproliferative disorders (LPD), often induced by Epstein-Barr virus (EBV). Despite a morphology mimicking malignant lymphoma, in some cases the lesions will disappear completely after the degree of immunosuppression is lowered. Lately, similar processes have been described in non-transplant, immunosuppressed patients. A SNOMED search was performed on the database of three hospitals between 1990 and 1997, to identify patients with immunosuppression-relaied lymphoproliferative disorders (IR-EPD) involving primarily the skin. Two patients were identified. One was 2 years after kidney transplantation, and the other was being treated with methotrexate for dermatomyositis. In both biopsies, there was a diffuse perivascular proliferation of large lymphocytes with ample cytoplasm and pleomorphic nuclei, associated with extensive dermal and subcutaneous necrosis. Immunohistochemical studies revealed expression of CD20, CD45RO, CD43, CD30, EBV-LMP1, and EBV-NA2 by the atypical lymphocytes in both cases and, in one case, of the EBV-transcriptional replication activation protein. In both cases the lesions completely disappeared and have not recurred. Primary involvement of the skin by IR-LPD is very rare. Based on our results, it is possible that some of these cases in the skin contain EBV and co-express CD30 and T- and B-ccll markers. The diagnosis of IR-LPD should be considered in cutaneous lymphoid proliferations in immunosuppressed patients. Belore rendering an unequivocal diagnosis of malignant lymphoma, reduction of immunosuppression and follow-up of 4-8 weeks should be considered.

Notes: Calcifying aponeurotic fibroma (CAP) is an unusual but well-characterized soft tissue neoplasm that typically involves the digits of children and frequently recurs locally. This report describes a case from the subcutis of the lumbosacral region. A 26-year-old man initially presented at age 3 and developed three recurrences over a 23-year period each at approximately 8-year intervals (ages 10, 18, and 26). The microscopic findings in all recurrences showed a lobulated, poorly circumscribed proliferation of dense fibrous tissue containing epithelioid-like fibro-blasts, multinucleated cells, and islands of metaplastic chon-droid differentiation with focal calcification. Despite origin from an unusual anatomic site, this case reported herein demonstrates the classical morphologic features and clinical history of CAT which showed little in the way of morphologic evolution despite 23 years of persistence. The clinical and histologic features helpful in distinguishing CAP from infantile fibromatosis and soft tissue chondroma are discussed.

Notes: An active 62-year-old man with noninsulin-dependent diabetes and chronic tinea pedis and tinea unguium developed a painless neurotrophic foot ulcer. His medical history was significant for mild hypercholesterolemia, chronic obstructive pulmonary disease, and long-term tobacco and alcohol use. Oral medications were Glyburide, Glucophage, Zestoretic, gemfibrozil, and aspirin, all of which had been administered daily for at least 8 months. There was no personal or family history of skin disease.After the ulcer failed to respond to conventional therapy, including wound care, debridement, and oral antibiotics, oral terbinafine was prescribed, 250 mg/day, for dermatophytosis-impaired wound healing. After 44 days of terbinafine therapy, the patient developed a generalized, erythematous, maculopapular, pruritic eruption accompanied by fatigue and chills. He denied cough, arthralgias, dizziness, hematuria, or exposure to anyone ill. Despite instructions to stop taking the medication, the patient erroneously continued to take terbinafine. One week later, he was referred to our institution.Physical examination revealed a nontoxic appearing middle-aged man with diffuse, confluent, erythematous plaques studded with pustules, lakes of pus, and crusted erosions and a fever of 38.9 °C ( 〈link href="#f1 #f2"/〉). Palms, soles, and mucous membranes were unaffected, and the groin was relatively spared. Toenails exhibited yellow–white discoloration, subungual debris, and onychauxis. Fingernails were normal. Lymphadenopathy was absent. A 1.3 cm by 1.7 cm superficial, painless ulcer without significant undermining was present on the left sole over the first metatarsophalangeal joint. There was decreased sensation from the toes to the midleg. Pedal pulses were palpable.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD669:IJD_669_f1"/〉Extensive pustular eruption of acute onset involving the trunk and extremities〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD669:IJD_669_f2"/〉Erythematous plaques, pustules, lakes of pus, and crusted erosionsLaboratory analyses revealed elevated white blood cell count (10.7 × 103 μL) with 11% eosinophils. Electrolytes, renal, thyroid, and liver function tests, urinalysis, and sedimentation rate were normal.A skin biopsy specimen showed an intraepidermal, spongiotic, vesiculopustular dermatitis with a superficial, perivascular, mixed inflammatory cell infiltrate of lymphocytes, neutrophils, and scattered eosinophils ( 〈link href="#f3 #f4"/〉). A periodic acid–Schiff stain was negative for fungi.〈figure xml:id="f3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD669:IJD_669_f3"/〉Vesiculopustular dermatitis with diffuse superficial perivascular infiltrate (original magnification, ×10)〈figure xml:id="f4"〉4〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD669:IJD_669_f4"/〉Subcorneal neutrophilic pustule, perivascular infiltrate of mononuclear cells, neutrophils, and occasional eosinophils (original magnification, ×40)Terbinafine was stopped, but all other medications were continued. Hydrotherapy, twice-daily triamcinolone ointment, and a prednisone taper from 60 mg to 0 mg over 3 weeks were initiated. In 4 days, there was complete resolution of the fever and pustulosis and a significant reduction of the erythema. At 40 days, mildly pruritic, erythematous plaques persisted on the trunk and extremities.The temporal relationship strongly suggested terbinafine as the inciting agent in this patient. Oral provocation test was not performed due to unacceptable patient risk.

Notes: The list of entities comprising a proliferation of CD34 (+) spindle cells continues to grow. Described, herein, is a patient who had an indolent eruption of scattered papules composed of CD34 (+) spindle cells, beginning in adolescence.An 18-year-old female patient presented with asymptomatic, tan/brown papules over the neck, chest, and proximal extremities. They appeared 6 years previously and had slowly increased in number. Biopsy from the neck showed a proliferation of plump spindle cells, associated with delicate collagen, in the upper reticular dermis. No atypia nor mitotic figures were present. The spindle cells were negative for S-100, muscle actins, and Factor XIIIa, but stained intensely with CD34. This unusual mesenchymal proliferation of CD34 (+) apparent dermal dendrocytes did not have the storiform pattern, short fascicles, nor mitotic figures of DFSP. The completely negative muscle markers helped to exclude dermatomyofibroma, and no morphological evidence of vasoformative differentiation was seen. The clinical picture militated against solitary fibrous tumor. These eruptive tumors are benign and thought to represent a distinctive fibroma produced by proliferated CD34 (+) stromal cells.

Notes: Abstract The development of an cellular inflammatory response secondary to mechanical wounding has not been observed previously in the fetus. The effect of amniotic fluid exclusion on the inflammatory response in fetal rabbits subjected to full-thickness dorsal excisional wounds on day 25 of gestation (term=31–32) was examined. The fetuses were either returned immediately to the uterus; a silicone cover was sutured over the wound; or a silicone cover with a centrally located hole was sutured over the wound. Seventy-two hours after wounding, uncovered wounds (19 live fetuses) exhibited only occasional inflammatory cells. Covered wounds (14 live fetuses) showed a pronounced cellular inflammatory response. Partially covered wounds (six live fetuses) showed a peripheral, intermediate response. The findings suggest that amniotic fluid contains factors inhibitory to inflammation, which the cover effectively excludes.