ABSTRACT
A term newborn suffered disseminated herpes simplex virus (HSV) type II infection five days after cesarean section delivery for fetal distress. The mother had no history or evidence of herpetic lesions; the father had a history of genital herpetic lesions. The infant's terminal course was dominated by disseminated intravascular coagulation (DIC) with hepatic and renal failure. Microscopic examination revealed a necrotizing vasculitis of small and medium-sized lung and peripancreatic arteries. Nuclear inclusions characteristic of HSV were found in these arteries, as well as in the adrenal parenchyma, spleen, and lymph node; electron microscopy confirmed replication of virus within the arterial endothelial cells. The mechanism of arterial damage in severe herpetic infection contrasts with the immune-complex mechanism postulated for other viral vasculitides. Direct, virally induced arterial damage resulting in exposure of collagen may set the stage of DiC, a commonly fatal complication of this disease.
Subject(s)
Herpes Simplex/pathology , Infant, Newborn, Diseases/pathology , Vasculitis/pathology , Arteries/ultrastructure , Disseminated Intravascular Coagulation/etiology , Female , Herpes Simplex/complications , Humans , Infant, Newborn , Pancreas/blood supply , Vasculitis/etiologyABSTRACT
We studied the clinical, roentgenographic, and pathologic features of what is, to our knowledge, the seventh reported case of cholangiocarcinoma associated with Caroli's disease. Review of the literature reveals that the incidence of carcinoma in patients with this condition is higher than that previously reported for other forms of biliary-tract ectasia. Bile stasis, cholangitis, and the presence of carcinogens and promoters in bile may combine to produce the high incidence of carcinoma in these patients.
