We saw two newborn infants with striated muscle hamartoma. One patient had numerous associated congenital anomalies. The clinical appearance of both lesions was that of a soft fibroma. Histologically, striated muscle fibers and nerve bundles were seen in the central core and also at the periphery of the lesion, below the epidermis. A marked number of sebaceous glands, vellus hair follicles, and eccrine glands were also present. We propose the term striated muscle hamartoma, which points out the most remarkable feature of these lesions.
The amniotic band syndrome (ABS) refers to the infrequent occurrence of congenital deformities presumably due to fetal entanglement in strands of ruptured amniotic sac. The most commonly associated anomalies include amputations, constriction bands, syndactyly, craniofacial defects, club feet, and cleft lip. We present a typical case and short literature review of ABS. The infant reported also had a connective tissue nevus and a cutaneous striated muscle hamartoma.
A 46-year-old man was diagnosed as having pyoderma gangrenosum after special stains and cultures from a skin biopsy specimen were reported as negative. Cutaneous sporotrichosis is usually diagnosed with relative ease on the basis of clinicopathologic features and prompt growth of the fungus in culture, although organisms are difficult to detect in tissue even with special stains. Identification of Sporothrix schenckii was delayed for three months in this patient because of unusual growth characteristics noted in the culture. The report of this patient's clinical course illustrates both the need to frequently reassess the diagnosis of pyoderma gangrenosum in treatment-resistant patients and the fact that S schenckii may be difficult to diagnose clinically and mycologically if the growth characteristics of the fungus are unusual.
We describe a child who began developing subepidermal blisters in the recipient sites of split-thickness skin grafts; this process has continued for almost a year and continues to spare nongrafted skin. Routine histologic and immunofluorescence mapping studies demonstrated this disorder to be a relatively noninflammatory one characterized by sub-lamina densa blister formation. Results of direct immunofluorescence were negative. By electron microscopy, anchoring fibrils were sparse in number and in some areas appeared malformed; otherwise, the basement membrane zone was morphologically unremarkable. Bullous pemphigoid antigen, laminin, type IV collagen, epidermolysis bullosa acquisita antigen, and LDA-1 were all normally expressed along the dermoepidermal junction. In contrast, KF-1 antigen was absent. These findings suggest a disease process confined to skin graft recipient sites with features identical to those previously described with recessive dystrophic or immunofluorescence-negative acquired epidermolysis bullosa.
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