A 3-year-old girl had severe intractable diarrhea with trichorrhexis nodosa and cirrhosis. This patient was referred to the pediatric dermatology clinic for lifelong brittle hair. The brittle hair microscopically demonstrated trichorrhexis nodosa. The girl also had facial dysmorphism, with a prominent forehead and cheeks, broad flat nose, and hypertelorism. She had a history of severe intractable diarrhea since 2 weeks of age and failure to thrive requiring lifelong total parenteral nutrition (TPN). Hepatomegaly was noted and prompted liver biopsy which demonstrated cirrhosis. Mental retardation and developmental delay was also found upon examination. This child may be included in the syndrome of intractable infant diarrhea, an entity known in the gastroenterology literature but yet not reported in the dermatologic literature. Dermatologists should be aware of this syndrome in which trichorrhexis nodosa is commonly seen.

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We report two cases of bathtub suction-induced purpura. Two girls, ages 9 and 14 years, developed recurring purpura "spontaneously" in the same lower back location and in the same U-shaped distribution. The patients had similar histopathologic findings, with extravasated erythrocytes and a sparse superficial inflammatory infiltrate. After extensive evaluation, one patient eventually admitted to self-inducing her lesions by creating suction against a bathtub. The second patient denied self-inflicting her lesions; however, her purpura improved when she stopped taking baths.

Exposure of newborn BALB/c mice to murine leukemia virus (MLV) TR1.3 induces fusion of brain capillary endothelial cells (BCEC), loss of cerebral vessel integrity, hemorrhagic stroke, and death. Although TR1.3 infects endothelial cells in multiple organs, syncytia are only observed in BCEC. To determine if viral and cellular factors are responsible for selective syncytia formation, capillary endothelial cells (CEC) from multiple organs were assayed in vitro for MLV infection and cell fusion. Following incubation with virus, all CEC were infected to an equal extent as determined by expression of MLV envelope and infectious virus production; however, MLV-induced syncytia were only observed in TR1.3-infected BCEC cultures. These in vitro results mirror the in vivo pattern of TR1.3 MLV infection and neuropathology, and definitively show that selective fusion and pathology of BCEC by MLV is determined by properties unique to BCEC as contrasted to other endothelial cell types.