Fluid transport in the rabbit gallbladder. A combined physiological and electron microscopic study.

The fine structure of the rabbit gallbladder has been studied in specimens whose functional state was undetermined, which were fixed either in situ or directly after removal from the animal; in specimens whose rate of fluid absorption was determined, either in vivo or in vitro, immediately prior to fixation; and in specimens from bladders whose absorptive function was experimentally altered in vitro. Considerable variation was found in the width of the epithelial intercellular spaces in the bladders whose functional state was undefined. In bladders known to be transporting fluid, either in vivo or in vitro, the intercellular spaces were always distended, as were the subepithelial capillaries. This distension was greatest in bladders which had been functioning in vitro. When either Na(+) or Cl(-) was omitted from the bathing media, there was no fluid transport across the wall of the gallbladder studied in vitro. The epithelial intercellular spaces of biopsies taken from several bladders under these conditions were of approximately 200 A width except for minor distension at the crests of mucosal folds. The addition of the missing ion rapidly led to the reestablishment of fluid transport and the distension of the intercellular spaces throughout most of the epithelium of these bladders. Studies of sodium localization (by fixation with a pyroantimonate-OsO(4) mixture) showed high concentrations of this ion in the distended intercellular spaces. Histochemical studies of ATPase activity showed that this enzyme was localized along the lateral plasma membrane of the epithelial cells. The analogy is drawn between the structure of the gallbladder mucosa and a serial membrane model proposed by Curran to account for coupled solute-solvent transport across epithelia. It is concluded that the intercellular compartment fulfills the conditions for the middle compartment of the Curran model and that active transport of solute across the lateral plasma membrane into the intercellular space may be responsible for fluid absorption by the gall bladder.

Changes in protoporphyrin distribution dynamics during liver failure and recovery in a patient with protoporphyria and Epstein-Barr viral hepatitis.

Acute liver failure with cholestasis, histologic and serologic evidence of Epstein-Barr viral infection, and associated autoimmune hemolytic anemia occurred in a patient with lifelong protoporphyria. Changes in previously established baseline protoporphyrin distribution dynamics in erythrocyte, plasma, and fecal excretion compartments were observed during the period of severe hepatic dysfunction and recovery. These changes were consistent with predictions of a previously described conceptual model for human protoporphyria.

Hepatic Hodgkin's disease simulating cholestatic hepatitis with liver failure.

Fulminant liver failure is an unusual complication that may be seen in patients with hepatic infiltration by non-Hodgkin's lymphomas and leukemias. In such cases, hepatomegaly, marked abnormalities of serum liver function tests, and lactic acidosis may simulate severe viral, alcoholic, or drug hepatitis. We describe the clinical presentation of severe cholestatic hepatitis with liver failure in a patient who was found to have widespread liver involvement by Hodgkin's disease at autopsy. The major histologic findings included extensive portal and periportal Hodgkin's infiltrates, associated loss of periportal liver cells, and variable damage to small bile ducts.

Pneumatosis and cystoides intestinalis. Report of a case with colonoscopic findings of inflammatory bowel disease.

A patient with pneumatosis cystoides intestinalis noted on barium enema performed for evaluation of rectal bleeding was found on fiberoptic colonoscopy to have evidence of inflammatory bowel disease, consistent with granulomatous colitis, the sigmoid colon element of which responded to topical steroid therapy as documented by repeat colonoscopy three months later.

Addisonian crisis while taking high-dose glucocorticoids. An unusual presentation of primary adrenal failure in two patients with underlying inflammatory diseases.

The diagnosis of acute hypoadrenalism seldom is considered in patients without known adrenal insufficiency who are taking supraphysiologic amounts of glucocorticoids. We report two patients who presented in acute addisonian crisis on more than one occasion while taking high doses of glucocorticoids (30 to 40 mg of prednisone daily) for underlying inflammatory disease (recurrent pleuropericarditis and sarcoidosis). Evidence of severe mineralocorticoid deficiency was present in each patient, and the conditions of both improved remarkably when mineralocorticoid was added to their regimens. The cause of primary adrenal failure and its acute presentation was unclear in both patients but is presumed to be related to the underlying inflammatory disease.

Serum lysozyme, serum proteins, and immunoglobulin determinations in nonspecific inflammatory bowel disease.

The serum levels of lysozyme, serum electrophoresis, and serum immunoglobulins were determined prospectively in 101 patients with ulcerative colitis, ulcerative proctitis, Crohn's disease, or nonclassifiable nonspecific inflammatory bowel disease. Although the mean serum lysozyme concentration of patients with Crohn's disease (10.5 +/- 6.8 microgram/ml) and ulcerative colitis (9.6 +/- 4.1 microgram/ml) performed by a standardized lysoplate method was significantly greater than normal controls (6.0 +/- 1.5 microgram/ml), the results did not correlate with the diagnosis nor with the degree of disease activity. Individually separated protein fractions and serum immunoglobulins also did not correlate with the serum lysozyme levels. This study indicates that measurement of the level of serum lysozyme in individual patients is not helpful in determining the cause or degree of activity of nonspecific inflammatory bowel disease.