Histologic, ultrastructural, chemical, and statistical methods were used to study liver biopsy and autopsy specimens from 43 patients who had primary sclerosing cholangitis (PSC), with or without chronic ulcerative colitis (CUC), and from 19 patients who had CUC without PSC. In all study groups, essentially the same abnormalities were found in the hepatic parenchyma outside the major bile ducts, although nondiagnostic tissue samples were observed also. Specimens from patients with extrahepatic PSC were indistinguishable from those patients with combined extra- and intrahepatic PSC. Common findings included periductal fibrosis and inflammation, portal edema and fibrosis, focal proliferation of bile ducts and ductules, focal bile duct obliteration and loss of bile ducts, copper deposition, and cholestasis. Proliferation of bile ducts in some portal tracts and obliteration or absence of bile duct in others were the most characteristic changes. In most specimens, inflammatory changes appeared mild, yet biliary cirrhosis had developed in 34% of the patients. Specimens from patients with PSC, with or without CUC, more often contained bile and strikingly increased stainable copper (Grades 2 and 3) than did specimens from patients with CUC without PSC. Hepatic copper contents, measured by atomic absorption spectrophotometry, also were higher in specimens from patients with PSC. Study of PCS specimens by transmission electron microscopy and by energy-dispersive X-ray microanalysis revealed that most copper was sequestered in lipolysosomes. The recognition of strikingly similar morphologic features in many liver specimens from patients with either PSC or CUC or both suggests that the causes of these conditions are closely related.

Cholangitis↗

PubMedDate not supplied

Selenium status in patients receiving home parenteral nutrition.

Selenium (Se) status was evaluated in patients with intestinal failure requiring home parenteral nutrition (HPN). Ninety-two percent of patients (11 of 12) studied just prior to starting HPN had low serum Se values, and the mean value was 42 ng/ml, significantly less than mean values in disease controls with Crohn's disease not on HPN (76 ng/ml) and healthy controls (88 ng/ml). Eighty-five percent of patients (22 of 26) already on HPN for 2 to 109 months when studied had low serum Se levels (mean 38.4 ng/ml). The mean 24-hr urinary Se values were 3.7 micrograms in patients on HPN who did not have Crohn's disease, 10.9 micrograms in HPN patients with Crohn's, and 17.9 micrograms in healthy controls. In patients with Crohn's disease on HPN, a significant direct correlation existed between serum Se and the activity of whole blood glutathione peroxidase, a selenoprotein ; and a significant inverse correlation was found between serum Se and months of HPN. This study confirms that Se deficiency is very common in patients before starting and during HPN. These data and recent reports of cardiomyopathies associated with Se deficiencies in patients on HPN increase the importance of proper Se replacement and maintenance.

Crohn Disease↗

PubMedDate not supplied

Implications of tract metals in human diseases.

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Body Fluids↗