Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sera from patients with ulcerative colitis or Crohn's disease had elevated titers to colon antigen from germ-free rats significantly more often than sera from patients with gastroenteritis, irritable colon, non-gastrointestinal diseases, and healthy controls. Elevated anticolon titers in significant frequency were also found in patients with liver cirrhosis, urinary tract infections, and in polyposis coli and their relatives. Females with ulcerative colitis had, on an average, higher titers than men especially in the age group 30 years and over. In Crohn's disease the antibody titers often increased with time--as opposed to those in ulcerative colitis and non-gastrointestinal diseases. In conjunction with results published earlier, the present work supports the assumption that the antibodies in ulcerative colitis patients react with antigenic determinants distinct from those recognized by the colon antibodies present in other groups, including patients with Crohn's disease and polyposis.
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PMID:Immunological studies in ulcerative colitis. VIII. Antibodies to colon antigen in patients with ulcerative colitis, Crohn's disease, and other diseases. 7 16

A 29 year old patient with Crohn's disease and posthepatitic HBsAg-positive cirrhosis developed zinc deficiency in the course of complete parenteral nutrition. Zinc deficiency was proven by a low plasma zinc level of 12 microgram/dl. The daily input of zinc was 0.5 mg as calculated from the zinc concentration of infusion solutions used in parenteral nutrition during 3 1/2 months of treatment. The clinical picutre was that of acrodermatitis enteropathica. Cirrhosis of the liver and Crohn's disease were contributory causes of zinc deficiency. 6 bolus injections of 12-36 mg of zinc (total amount 144 mg) were given during 13 days. The plasma zinc level increased to 60-80 microgram/dl. 52% of the total amount of zinc injected were excreted by urine. The plasma half-life times of zinc were independent from basic zinc concentrations and averaged 1.55 +/- 0.22 h. It is concluded that severe signs of zinc deficiency will develop during parenteral nutrition in the presence of conditions leading to a negative zinc balance. In the case of long-term complete parenteral nutrition zinc should be substituted from the beginning of the treatment on.
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PMID:[Zinc deficiency syndrome during long-term parenteral nutrition in a patient with Crohn's disease and cirrhosis of the liver. Casuistry and zinc-pharmacokinetic (author's transl)]. 11 3

Total lymphocyte counts, B-, T-, C'3 receptor-bearing lymphocytes, and K-cell activity were studied in peripheral blood in patients with Crohn's disease and inflammatory liver disease. Patients with active untreated Crohn's disease and acute virus B hepatitis exhibited a markedly increased K-cell activity measured in a plaque assay when compared with normal controls (P less than 0.01). Patients with immunosuppressive treated Crohn's disease, HBsAg-positive chronic active hepatitis, and cirrhosis of the liver showed only a slight increase of K-cell activity (P less than 0.01). In the postacute phase of hepatitis (four to 12 weeks from onset) K-cell activity fell to normal levels. The number of B-lymphocytes showed a relative and absolute decrease in all groups of patients. With the exception of patients with acute HBsAg-positive hepatitis and the post-acute phase of hepatitis all the other groups showed statistically decreased absolute numbers for C'3 receptor-bearing lymphocytes. The significant decrease in K-cell activity and the number of T-lymphocytes in Crohn's disease treated with immunosuppressive drugs was interpreted as an effect of azathioprine and prednisone on these lymphocyte subpopulations.
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PMID:K-lymphocytes (killer-cells) in Crohn's disease and acute virus B-hepatitis. 30 25

Exocrine pancreatic function was determined by oral administration of N-benzoyl-L-tyrosyl-p-aminobenzoic acid (peptic-PABA-test) in 120 controls, 74 patients with chronic pancreatitis, 35 patients with acute pancreatitis 2--6 weeks after recovery, 201 patients with a variety of gastro-intestinal diseases and in 10 patients with anorexia nervosa. In the control group, 70% +/- 18% of the oral administered dose of PABA was found within 6 hours in the urine. In contrast the group of chronic pancreatic patients excreted only 40% +/- 13% over the same period. "False negative" PABA excretion was found in 11 (9%) of the 120 persons with no pancreas disease. "False positive" PABA excretion was found in 13 (17,5%) of the 74 patients with chronic pancreatitis. The test was not influenced by age or sex. After stomach resection or cholecystectomy and in patients with ulcus duodeni, chronic hepatitis, functional diarrhea, Crohn's disease, colitis ulcerosa and acute pancreatitis 2--6 weeks after recovery the peptide-PABA-test was not distored. Diminished PABA excretion was encountered in some patients with toxic liver disease, inflammatory disease of the small intensine like M. Whipple, celiac disease and unspecific enteritis and in a few patients with cholelithiasis. Low PABA excretion was found in early all patients with partial small intestinal resection, terminal liver cirrhosis or liver metastasis with ascites and in all patients with anorexia nervosa.
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PMID:[The specificity of peptide-PABA-test (author's transl)]. 31 33

In 45 patients with inflammatory bowel disease (9 with Crohn's disease and 36 with ulcerative colitis) and associated liver disorders, increased liver copper content (above 100 microgram/g dry weight) was found in 14 (31%). These patients represented about 50% of the patients with either biliary cirrhosis or pericholangitis. Four of the patients had levels regarded as compatible with hepatolenticular degeneration (greater than 250 microgram/g dry weight). In patients with chronic active hepatitis or non-specific changes in liver tissue, normal levels were found. The patients with Crohn's disease also had normal levels. Plasma ceruloplasmin was normal or increased in all. Determination of urinary copper output gave little diagnostic information. Alkaline phosphatases were markedly increased in most of the patients with increased liver copper concentration. In patients with ulcerative colitis and enhanced alkaline phosphatases, elevated liver copper content should be suspected and chelation therapy should be considered.
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PMID:Liver copper content in patients with inflammatory bowel disease and associated liver disorders. 53 3

In a review of 906 consecutive liver biopsies, sinusoidal dilatation, unrelated to passive congestion of the liver, sinusoidal infiltration, or cirrhosis, was found in 26 cases (2.9%). In 21 of them the final diagnosis was a neoplastic or granulomatous disease (tuberculosis, brucellosis, Crohn's disease), but in only half of them was there evidence of neoplastic or granulomatous infiltration of the liver. In the remaining cases, sinusoidal dilatation was either the only histological abnormality or it was associated with nonspecific changes. Although the pathogenesis of sinusoidal ectasia is not known, our findings indicate a definite relationship to the presence of tumor or granulomatous disease in the liver or elsewhere in the body. It is concluded that the finding of sinusoidal dilatation as an isolated histological change in a liver biopsy specimen should prompt the search for a tumor or a disease associated with granulomas.
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PMID:Incidence and clinical significance of sinusoidal dilatation in liver biopsies. 68 May 4

Excretion of oxalic acid in urine was measured in 28 healthy and 97 patients with gastrointestinal diseases. We found significantly higher values in the following groups: patients after resection of parts of the small intestine, patients with sprue and other diseases with malabsorption, patients with M. Crohn of the small intestine, colitis ulcerosa and granulomatosa, patients with chronical diseases of the pancreas gland and patients with cirrhosis of the liver. In 4 patients after resection of parts of the small intestine or pancreas urolithiasis could be verified. Reduction of fat and food without ballast reduced the excretion of oxalic acid in urine. Hyperoxaluria correlied significantly with the following parameters: excretion of fat in feces, exhalation of 14CO2 in the glykocholate breath test, resorption of vit. B12 and the length of resected small intestine. This form of hyperoxaluria is caused by hyperresorption of oxalic acid from food. The mechanism of this hyperresorption is not clarified yet, an important factor seems to be ill resorption of fat.
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PMID:[Hyperoxaluria in intestinal and liver diseases]. 83 13

The relation between malabsorption of bile acids, the bile lipid composition, and biliary stones was examined in 8 patients subjected to ileal resection (particularly for Crohn's disease), 6 with ileal bypass for morbid obesity, and 10 healthy controls. The 1-14C-cholylglycine breath test was employed to detect of the absorption and deconjugation of bile acids. Bile lipid composition was expressed according with Metzger's saturation index. Healthy subjects gave normal findings in all respects, whereas ileal resection was accompanied by malabsorption, increased deconjugation, and faecal loss of 14C. These changes, particularly malabsorption, were more evident after ileal bypass. Preoperative saturation values rose to more than 1 in all cases, especially after resection. Liver disease (steatosis and cirrhosis) 6 months after bypass, together with cholesterol lithiasis in 2/6 patients.
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PMID:[Correlation of malabsorption of bile acids, bile lipid composition and calculi]. 90 52

The protein content in serum and peritoneal fluid has been determined and analysed electrophoretically in patients with Crohn's disease and ulcerative colitis and the data obtained compared with previously published data on serum and ascites content in liver cirrhosis, heart failure and intestinal tuberculosis. Ascites fluid in liver cirrhosis and heart failure, representing a true transudate, had a comparatively low protein content while the ascites fluid in inflammatory bowel diseases including Crohn's disease had high protein content. There was no difference in ascites protein content or ascites/serum protein ratio between patients with Crohn's disease and patients with ulcerative colitis. An exudative nature of both these inflammatory bowel conditions appears to be the main cause to the peritoneal fluid often observed at laparotomy. It cannot be excluded, however, that a lymphatic stasis, which is thought to be involved in Crohn's disease, might at least partly contribute to the development when larger quantities of ascitic fluid are at hand in this disease.
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PMID:Protein patterns in serum and peritoneal fluid in Crohn's disease and ulcerative colitis. 93 40

Patients with ulcerative colitis showed in 71-93%, patients with cirrhosis of the liver in 64-91%, cellular immunity against Common Antigen (CA) and human fetal intestinal antigens as measured by the leucocyte migration test (LMIT). Patients with Crohn's disease exhibited cellular immune reactions to a lesser degree - from these only patients without immunosuppressive therapy differed significantly from normal controls (p less than 0.05). Approximately 30% of patients with Crohn's disease and ulcerative colitis had elevated antibody titers against intestinal antigens and CA. A high percentage of patients in both diseases showed a reciprocal relationship between cellular and humoral immunity. It was concluded that Crohn's disease and ulcerative colitis can be separated in most cases using intestinal antigens and CA in the LMIT. The occurrence of cellular immunity against these antigens cannot be interpreted as being the only pathogenetic principle in these two diseases. It is also concluded that there appears to be only a weak immune tolerance against intestinal antigens. The high percentage of cellular immune reactions in patients with cirrhosis of the liver demonstrates that this group may have an impairment of the physiological elimination of antigens by the liver.
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PMID:Cellular immune reactions against common antigen, small intestine, and colon antigen in patients with Crohn's disease, ulcerative colitis, and cirrhosis of the liver. 125 Nov 32


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