Scot W. Hutton

A histopathologic study of gastric and small intestinal graft-versus-host disease following allogeneic bone marrow transplantation

Twenty-two stomach and 14 small intestinal biopsy specimens from 24 allogeneic bone marrow transplant recipients were reviewed to evaluate the histopathologic changes of graft-versus-host disease (GVHD) in these organs. Associations between these results and clinical symptoms and other biopsy results were sought. In both organs, single epithelial cell necrosis was found to correlate with GVHD. Gastric GVHD was diagnosed in eight patients and small intestinal GVHD in four. Gastric GVHD was characterized by nausea, vomiting, and upper abdominal pain without diarrhea (the latter being present in only two patients), while all four of the patients with small intestinal GVHD had upper gastrointestinal symptoms and diarrhea. These symptoms correlated with concurrent rectal biopsy findings; pathologic alterations were seen in only one of six specimens from patients with gastric GVHD but in three of four with small intestinal GVHD. These findings suggest that stomach biopsy may be necessary to diagnose GVHD in patients with upper gastrointestinal symptoms but no diarrhea and normal rectal biopsy specimens. Diagnostic problems may arise in the early posttransplantation period, when the effects of cytoreductive therapy may simulate GVHD, and in patients with gastrointestinal cytomegalovirus infection, which may also produce changes identical to those of GVHD.

Cytomegalovirus infection of the liver in transplant recipients

Thirty-two transplant recipients with cytomegalovirus (CMV) infection documented by positive culture of blood and/or organs other than the liver were evaluated for hepatic involvement. Thirteen of the 32 (41%) had evidence of hepatic involvement with CMV. Inclusions alone were present in three patients; liver cultures alone were positive for CMV in three; and both were present in seven. Although the presence of CMV inclusions was the only histological feature that clearly separated the groups with and without hepatic involvement, two items helpful in finding inclusions were lobular aggregates of polymorphonuclear cells and portal karyorrhexic debris. The presence of liver involvement had a significant correlation with multiple organ infection, indicating it is a good marker of widely disseminated disease. This study indicates that liver histology and culture are useful and complementary methods for documentation of hepatic involvement (hence, tissue invasion) in immunocompromised patients with CMV infection.

Thyrotropin-releasing hormone suppressed gastric acid output in patients with Zollinger-Ellison syndrome and systemic mastocytosis

Abstract Thyrotropin-releasing hormone administered intravenously was found to be as potent an inhibitor of gastric acid secretion as a conventional dose of oral cimetidine in two patients with Zollinger-Ellison syndrome and one patient with systemic mastocytosis.

Platelet function in scurvy and experimental human vitamin C deficiency

Abstract A consistent clinical feature of human scurvy is mucocutaneous hemorrhage which has been attributed to abnormal blood vessel structure secondary to deficient collagen synthesis. Quantitative and qualitative platelet abnormalities have also been implicated in the pathogenesis of scorbutic bleeding in some studies; however, the presence of other nutritional deficiencies has clouded interpretation of these results. To further evaluate the effect of vitamin C deficiency on platelet number and function, we studied one patient with typical perifollicular hemorrhagic manifestations of scurvy and five normal subjects fed a diet deficient only in ascorbic acid. Markedly decreased plasma (0.07 mg/dl) and leukocyte (4.92 μg/10 8 cells) ascorbic acid was found in the scurvy patient, and similar levels developed in the normal subjects fed the ascorbic acid deficient diet (mean plasma level 0.12 mg/dl; mean leukocyte level 8.1 μg/10 8 cells). Platelet number; glass bead column retention; aggregation in response to ADP, collagen, epinephrine, sodium arachidonate and ristocetin; serotonin release; bleeding time and platelet retention during bleeding were all normal in the patient with scurvy. Platelet retention during bleeding decreased in all five normal subjects when they became vitamin C deficient, but none became abnormal. The bleeding time remained normal in all five subjects. Slight thrombocytopenia developed in one subject, but otherwise platelet number and all of the above platelet functions were normal in the ascorbic acid deficient control subjects. We conclude that mucocutaneous hemorrhage in scurvy is not a consequence of impaired platelet function. Previously reported abnormal platelet function in scurvy is probably not the result of vitamin C deficiency per se, but may be the consequence of other coexisting nutritional deficiencies.