Background: Viral-associated trichodysplasia of immunosuppression is an increasingly recognized entity characterized by follicular-based papules, primarily in the central part of the face, that produce variable degrees of alopecia and dysmorphic features. It has been primarily described in transplant recipients but has recently been recognized in patients receiving chemotherapy for leukemia and lymphoma. It is associated with distinctive histologic features such as dilated anagen hair follicles, absent hair papillae, and abrupt cornification of the inner root sheath. Observations: A 5-year-old boy presented with spiny follicular papules that caused thickening of the skin of the face 1 year after cardiac transplantation. He had been exposed to several immunosuppressive agents, including mycophenolate mofetil, tacrolimus, intravenous immunoglobulin, rituximab, cylcophosphamide, and prednisone. Despite the failure of multiple topical treatments, our patient's eruption improved with systemic valganciclovir therapy. Conclusions: We describe the youngest patient (to our knowledge) with viral-associated trichodysplasia of immunosuppression and discuss the characteristic clinicopathologic features. Our report supports the theory that immunosuppression is the predisposing factor to a folliculotropic papovavirus that alters follicular maturation.

Interstitial pulmonary fibrosis is a common feature of scleroderma (systemic sclerosis) which may result in impairment of pulmonary function and may be a major determinant of morbidity and mortality. Clinicopathologic observations suggest that interstitial and alveolar inflammation may appear prior to fibrosis. Using the bronchoalveolar lavage (BAL) technique, we have characterized the nature of the inflammatory process in the lower respiratory tracts of 19 nonsmoking scleroderma patients. Eleven of 19 patients (58%) had increased percentages of neutrophils and/or eosinophils in BAL fluid. Five of 10 patients (50%) had elevations of IgG in BAL fluid. The presence of neutrophils was associated with a decreased lung diffusing capacity for carbon monoxide (P < 0.05) and with more advanced radiographic features of interstitial fibrosis in patients with disease of more than 1 year's duration. This study suggests that scleroderma lung involvement may be characterized by an inflammatory alveolitis and that the presence of such inflammation may relate to the severity of the pulmonary disease.

Interstitial lung disease is a common feature of scleroderma (systemic sclerosis), and it may be a major determinant of morbidity and mortality. Analysis of bronchoalveolar lavage fluid from patients with scleroderma has shown evidence of inflammation in the lower respiratory tract of many patients. We have analyzed sera and bronchoalveolar lavage fluid from scleroderma patients for the presence of immune complexes, which may play a role in the inflammatory process. Using a solid-phase C1q enzyme-linked immunosorbent assay, we detected immune complexes in the sera of 6 of 23 patients (26%) and in none of 32 controls (P less than 0.01). All 6 patients with serum immune complexes had inflammatory cells in bronchoalveolar lavage fluid, and the presence of serum immune complexes correlated with the percentage of neutrophils in lavage fluid (P less than 0.02). Immune complexes were detected in lavage fluid of 11 of 21 patients (52%) compared with 1 of 7 normal controls (14%). Subjects having immune complexes in lavage fluid had a lower forced vital capacity than did those without lavage fluid immune complexes (P less than 0.05). The levels of immune complexes in bronchoalveolar lavage fluid exceeded those in serum by a mean of 45-fold, suggesting either local formation or selective deposition of immune complexes in the lower respiratory tract of some scleroderma patients.

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