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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a 12-year period, 46 children and adolescents with inflammatory bowel disease were followed from the time of diagnosis with regular biochemical tests of liver function. Thirty-four patients had ulcerative colitis and 12 had Crohn's disease. Mean age at the time of diagnosis was 10.2 years (range 7 months-17 years) and the mean follow-up period was 5.2 years (range 1-11 years). Pathological liver function tests were found in 60% of the 34 patients with ulcerative colitis: 9 of these 20 patients demonstrated more severe disturbance, usually at the time of diagnosis. Liver damage was most frequent in patients with total colitis. Liver biopsy was performed in eight patients, demonstrating "pericholangitis", fibrosis and in one case cirrhosis. Morphometry of electron microscopical pictures revealed a significantly increased number of lysosomes and dilated cisternae of the rough endoplasmic reticulum. ERCP was performed in two patients, verifying primary sclerosing cholangitis in one. Four of the 12 patients with Crohn's disease had mildly pathological liver function tests. No correlation was found to the extent, duration or treatment of bowel disease. In our series of juvenile inflammatory bowel disease, liver damage occurred frequently, especially in ulcerative colitis. The more severe changes tended to coincide with the onset of bowel disease.
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PMID:Liver damage in juvenile inflammatory bowel disease. 221 95

Gastrointestinal cryptococcosis is extremely rare, especially in patients with no involvement of the central nervous system. We describe a 63-yr-old man undergoing prednisone therapy for chronic hepatitis and cirrhosis who presented with peritonitis, colitis, and skin lesions. Pathological studies revealed necrosis and numerous cryptococcal organisms in the colon, omentum, and skin, and cultures yielded Cryptococcus neoformans. The patient died of multisystem organ failure following emergency exploratory surgery performed when he had onset of symptoms of a bowel perforation after an endoscopic biopsy. Clinicians should be aware that gastrointestinal cryptococcosis can occur in the absence of infection of the central nervous system or lungs, and that it may affect relatively healthy patients who are immunocompromised because of splenectomy, chronic liver disease, or steroid therapy.
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PMID:Disseminated, nonmeningeal gastrointestinal cryptococcal infection in an HIV-negative patient. 222 Jul 42

Hepatobiliary disorders are well known complications in patients with ulcerative colitis but it is not possible to predict those patients with ulcerative colitis who will eventually develop liver disease. In this study, liver biopsies from 74 patients with ulcerative colitis have been reevaluated. None of the patients showed clinical or biochemical signs of liver disease at the time of biopsy. Thirty seven (50%) had a completely normal liver biopsy. The others showed minimal portal inflammation or fatty infiltration. The biopsies of three patients displayed concentric, periductular fibrosis, or so called 'onion skin' lesions. None showed other signs of fibrosis or cirrhosis. The histological findings were unrelated to either activity or extent of colitis, except for the onion skin lesions which were seen exclusively in biopsies of patients with involvement of the total colon. Sixty eight of the 74 patients were reviewed after a mean interval of 18 years. The majority had no symptoms of hepatobiliary disorders and only two had developed liver disease; one suffered from cryptogenic cirrhosis, possibly due to non-A, non-B hepatitis and the other of an autoimmune liver disease and later developed a bile duct carcinoma. Both were women with total colonic involvement. At the time of the first liver biopsy one showed no histological abnormalities and the other only minor fatty infiltration. Thus, minor abnormalities in liver tissue are common in patients with ulcerative colitis without biochemical evidence of liver disease. The morphological changes are of little help in predicting the future risk of a patient with ulcerative colitis developing a clinically relevant hepatobiliary complication. The absence of biochemical parameters for liver disease during the early years of ulcerative colitis predict a favourable longterm diagnosis as regards hepatobiliary complications.
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PMID:Liver histology and follow up of 68 patients with ulcerative colitis and normal liver function tests. 233 76

Using the test of glucagon load and the test of galactose tolerance the usefulness was compared of both these carbohydrate tests in the clinical diagnosis of cirrhosis. The studied group comprised 30 patients with cirrhosis divided into two groups depending on the stage of the disease, and 21 women with spastic colitis serving as a control group. Both tests were found to be useful in the diagnosis of cirrhosis. The results of these tests were statistically significantly different from those in the control group which could be demonstrated as different shapes of blood glucose curves. Moreover, range values could be proposed for blood glucose levels characteristic of cirrhosis and criteria could be established using these tests for differentiating compensated against decompensated cirrhosis.
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PMID:[Comparison of the value of the glucagon test and galactose tolerance test in the clinical diagnosis of cirrhosis]. 236 89

Endoscopic retrograde pancreatograms were examined in a consecutive series of patients with cholestatic disease caused either by primary biliary cirrhosis (PBC) (35 patients) or by sclerosing cholangitis (SC) (38 patients). The pancreatic ducts were abnormal in three of the patients with PBC but in none with SC. Gallstone disease occurred concomitantly in the two patients with most advanced pancreatic involvement. The liver disease was classified as advanced PBC in 11 of the 35 patients. Symptoms of hepatobiliary disease were scarce in most SC patients. Eight of the 38 patients had histologically verified biliary cirrhosis. SC was associated with extensive, but most often inactive or mild, colitis in 97% (ulcerative colitis in 34 and Crohn's disease in 3 patients). Three of these patients had concomitant cholangiocarcinoma.
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PMID:The pancreatic ducts in primary biliary cirrhosis and sclerosing cholangitis. 385 33

Four patients with a long history of colitis, splenomegaly, hypersplenism and portal hypertension were examined with angiography, both with contrast medium and isotopes, liver-spleen scintigraphy and recording of portal pressure. At angiography hyperkinetic splenic and portal blood flow was demonstrated. The increased flow causes increased portal pressure, which probably gives rise to changes in the liver often considered as slight cirrhosis at microscopy. The scintigraphic findings differed from Laennec cirrhosis. The liver uptake was homogeneous and no activity in the skeleton was recorded. Splenectomy cures both the hypersplenism and portal hypertension.
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PMID:Splenomegaly, hyperkinetic splenic flow and portal hypertension in colitis. 745 87

We describe a case of phlegmonous colitis occurring in a 70-year-old man with liver cirrhosis, hepatocellular carcinoma and acute promyelocytic leukemia. He developed an acute abdominal emergency and died during the first day of admission. Autopsy revealed a colon lesion characterized by suppurative inflammation associated with marked edema and hemorrhage in the submucosa. These findings were identical both macroscopically and microscopically to those of phlegmonous colitis.
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PMID:Phlegmonous colitis in a patient with liver cirrhosis, hepatocellular carcinoma and acute promyelocytic leukemia. 754 39

Long-term treatment with triethylene tetramine dihydrochloride, (trientine, TETA) was evaluated in 19 patients with Wilson's disease (WD). Two were given the drug as first choice and 17 after treatment with penicillamine. The change was made because of side-effects, lack of improvement or worsening of neurological symptoms. All penicillamine-induced side-effects reverted. Thirteen patients still receive trientine, and the mean total observation time on this treatment is 8.5 years/patient. Seven of the 13 are free from symptoms related to WD, five have mild to moderate neurological symptoms, mainly dysarthria. One patient with neurological symptoms who received trientine from the start of treatment deteriorated rapidly and is now severely dystonic. The symptoms initially worsened and later improved in one patient. All other patients improved during trientine treatment. Three patients died: two from a multifocal cancer including the liver and one non-complier from a ruptured spleen. Two patients underwent liver transplantation for progressive liver failure: one non-complier and one with liver cirrhosis whose liver function deteriorated despite treatment; both are now free from symptoms. Unexpectedly, two patients developed a serious colitis, one with duodenitis as well, that improved after withdrawal of the drug. No other unfavourable effects of trientine were recorded.
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PMID:Long-term treatment of Wilson's disease with triethylene tetramine dihydrochloride (trientine). 758 74

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.
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PMID:Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy. 799 80

We report on eight children with severe diarrhea beginning in the first 6 months of life (< 1 month in six cases), who had a number of features in common. All were small for gestational age and had an abnormal phenotype, including facial dysmorphism, hypertelorism, and woolly, easily removable hair with trichorhexis nodosa. Two were products of consanguineous marriages. Severe secretory diarrhea persisted despite bowel rest (n = 7). Jejunal biopsy specimens showed total or subtotal villous atrophy with crypt necrosis, and inconstant T-cell activation in some cases (n = 3). Colon biopsy specimens showed moderate nonspecific colitis. All the patients had defective antibody responses despite normal serum immunoglobulin levels, and defective antigen-specific skin tests despite positive proliferative responses in vitro. Three had monoclonal hyper-immunoglobulinemia A. The course was marked by diffuse erythroderma in two cases and mental retardation in three. Treatment included bowel rest, intravenous administration of immune globulins, administration of corticosteroids (n = 6) and cyclosporine (n = 2), and bone marrow transplantation (n = 1). Five patients died between the ages of 2 and 5 years (of sepsis or cirrhosis), two are being fed enterally, and one continues to receive total parenteral nutrition. The cause of the combined low birth weight, dysmorphism, severe diarrhea, trichorrhexis, and immunodeficiency is unclear. These features may constitute a specific syndrome within the group of intractable diarrheas of infancy.
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PMID:Intractable infant diarrhea associated with phenotypic abnormalities and immunodeficiency. 802 82


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