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)

Zinc is essential for many metabolic and enzymatic functions in man. Deficiency of zinc in man has now been recognized to occur not only as a result of nutritional factors, but also in various disease states, including malabsorption syndromes, acrodermatitis enteropathica, Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency state in human subjects exists as a spectrum extending from mild to severe degree. The clinical manifestations of mild zinc deficiency include oligospermia, weight loss and hyperammonaemia. Moderate zinc deficiency is characterized clinically by growth retardation, hypogonadism in males, skin changes, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In severe zinc deficiency states, bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorders, weight loss, intercurrent infections, hypogonadism in males and, if unrecognized, death have been observed. Zinc is needed for the functions of over 100 enzymes. It is essential for DNA, RNA and protein synthesis and, as such, is important for cell division. Zinc is an inducer of mRNA of metallothionein, a protein which may have an important role in the regulation of intestinal zinc absorption. Zinc has a specific effect on testes in animals and man. Recent reports indicate that in human subjects thymopoietin may be zinc dependent and in animal studies somatomedin may be affected adversely due to dietary zinc restriction. Zinc plays an important role in the protection of cell membrane integrity and may be protective against free radical injury. Zinc is known to compete with cadmium, lead, copper, iron and calcium for similar binding sites. In the future, a potential use of zinc may be to alleviate toxic effects of cadmium and lead in human subjects. Recent evidence suggests that thymic-dependent lymphocytes (T cells are zinc dependent. T-helper and suppressor cells, T-effector cells and T-natural killer cells appear to be zinc dependent. Zinc is also essential for some of the neutrophil functions. Thus, it appears that zinc may play an important role in immunity. One may suggest that some of the clinical features of cirrhosis of the liver, such as testicular atrophy, loss of body hair, night blindness, poor wound healing, poor appetite, susceptibility to infections and enhanced sensitivity to drugs, may be related to conditioned deficiency of zinc, future studies are required to determine whether or not zinc supplementation is beneficial to these patients.
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PMID:The role of zinc in gastrointestinal and liver disease. 661 39

To evaluate the results of jejunoileal bypass for morbid obesity, we studied 100 patients with intact bypasses an average of more than five years after surgery. Mean weight loss at five years was 102.7 lb (46.6 kg) (33 per cent). Although nearly half the patients regained some weight between one and five years after surgery, only 17 per cent regained 20 lb (9 kg) or more. Medical benefits (such as improved glucose tolerance and lowered blood pressure) were maintained at five years, but side effects and complications continued to occur in the late postoperative period. Diarrhea (more than three stools per day) persisted in 58 per cent of the patients, and electrolyte disturbances occurred in over a third. Diminished levels of B12 or folate or both were present in 88 per cent. Twenty-one per cent of the patients had nephrolithiasis, and 20 per cent of those who were at risk required cholecystectomy. Progressive hepatic structural abnormalities occurred in 29 per cent of the patients, and there was a 7 per cent incidence of cirrhosis. Although 81 per cent of the patients had satisfactory results at five years, side effects and complications continued to occur, mandating careful follow-up indefinitely. The risk-to-benefit ratio at five years after surgery seems acceptable, but the continued untoward effects of the bypass in the late postoperative period have led us to abandon this procedure in favor of gastric bypass. Only continued longitudinal follow-up will determine whether on balance jejunoileal bypass represents such a serious long-term health hazard that prophylactic restoration of intestinal continuity is indicated.
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PMID:Jejunoileal bypass for morbid obesity. Late follow-up in 100 cases. 683 18

Recent evidence suggests that the cirrhosis of alpha-1-antitrypsin deficiency is not invariably fatal as it was previously thought. Portal hypertension is often the major determinant of survival. The few reports of porta-systemic venous anastomosis in this disorder have shown poor results or uncertain outcome. Thus, doubts exist as to whether porta-systemic shunts should be performed in alpha-1-antitrypsin deficiency. Two patients with alpha-1-antitrypsin deficiency (PiZZ) and associated portal hypertension, cirrhosis, and hypersplenism underwent splenorenal shunt and splenectomy 8 yr ago, and both have done well. One of the patients has chronic severe headaches, diarrhea, exudative enteropathy, sinusitis, and hematuria, all uncommon in alpha-1-antitrypsin deficiency but possibly related to the antienzyme deficiency. She also has a higher trypsin inhibitory capacity than is generally reported in ZZ individuals. Based on the experience with these 2 patients, it appears that alpha-1-antitrypsin deficiency with cirrhosis is not a valid contraindication to the performance of a portasystemic shunt.
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PMID:Successful spleno-renal shunt and splenectomy in two patients with alpha-1-antitrypsin deficiency. 697 26

A three year old child with cirrhosis of the liver and ascites caused by alpha-1-antitrypsin deficiency, developed severe abdominal pain with diarrhea and fever. Spontaneous bacterial peritonitis was diagnosed by demonstrating a purulent ascitic fluid with gram-positive cocci in the smear which were identified as pneumococci in the bacterial culture. The peritonitis subsided under antibiotic treatment without complications. Spontaneous bacterial peritonitis in children with cirrhosis of the liver is mentioned in the literature, but up to now, however, only three cases were reported in detail. In order to establish the diagnosis, abdominal tap should be tried rather than explorative laparotomy, the demonstration of gram-positive cocci is diagnostic of spontaneous bacterial peritonitis. With early antibiotic therapy, prognosis of the disease is favourable. Newborns and children with nephrotic syndrome, however, are particularly at risk.
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PMID:[Spontaneous bacterial peritonitis in cirrhosis of the liver caused by alpha-1-antitrypsin deficiency (author's transl)]. 698 Oct 63

Eighteen mixed-breed beef cattle died as the result of consuming "tacky lithium grease" discarded from a rubber reclaiming plant. Four experimental groups of mature cattle were given oral doses of a lithium salt at levels of 0, 20, 500, and 700 mg/kg body weight. Although all animals in the 250 mg/kg group showed signs of intoxication, the signs were mild and transient. Doses of 500 and 700 mg/kg proved toxic and fatal. Signs, serum levels, and tissue-organ deposition were dose and time-related. Signs of intoxication were salivation, depression, anorexia, hypodipsia, anuria, and diarrhea. The high dose group also showed severe depression and ataxia. The highest mean lithium serum values were 19, 40, and 54 ppm for the 250, 500, and 700 mg/kg groups, respectively. Postmortem and histopathologic examinations revealed dose-related gastroenteritis, slight interstitial nephritis, and hepatic cirrhosis. Tissue residues of lithium were in striated muscle (86.8 ppm), heart (79.3 ppm), liver (68.7 ppm), kidney (67.1 ppm) , and brain (51.8 ppm), in the high dose group. Since serum levels of cattle consuming the "tacky lithium grease" were 0.49 ppm of lithium, we believe other contaminants in this discarded grease may have caused or enhanced the toxic effect of lithium.
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PMID:Lithium toxicity in cattle. 740 86

Vibrio parahemolyticus has been well documented to cause outbreaks of infectious diarrhea, usually related to poor food handling; only rarely has it been reported to cause fetal septicemia. In contrast, Vibrio vulnificus is a well-known cause of septicemia, especially in patients with cirrhosis. A 31-year-old woman with cirrhosis who developed fatal V. parahemolyticus sepsis after ingesting raw seafood is described. We review the clinical syndromes associated with sepsis caused by these two organisms. Leg pain and bullous skin lesions may be a clue to the diagnosis. Febrile patients with cirrhosis should be questioned regarding recent seafood ingestion, and appropriate antibiotics chosen if this history is obtained. Physicians should inform patients at risk to avoid raw seafood in an attempt to prevent this potentially lethal syndrome.
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PMID:Fatal Vibrio parahemolyticus septicemia in a patient with cirrhosis. A case report and review of the literature. 778 43

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

Two 2-year-old Salers cattle from different herds raised on pasture were evaluated for retarded growth and diarrhea. Increase of liver enzyme activities and prolonged sulfobromophothalein (BSP) half life (T1/2) indicated liver disease with impaired liver function. Histopathologic examination of liver biopsies revealed a micronodular cirrhosis with marked deposition of hemosiderin in hepatocytes, Kupffer cells, and arterioles. Transferrin saturation (TS) and liver iron content were markedly increased, consistent with a diagnosis of hemochromatosis. Both animals were euthanatized due to deterioration in their condition. Necropsy findings included hepatomegaly and hemosiderin accumulation in the liver, lymph nodes, pancreas, spleen, thyroid, kidney, brain and other glandular tissue. Continued surveillance of the second herd (serum iron, total iron binding capacity [TIBC], unsaturated iron binding capacity [UIBC], and TS), identified a heifer as a hemochromatosis suspect in a subsequent generation. Liver biopsies from that animal revealed the same histopathologic changes as the previous 2 animals, and similar increases in liver iron content (8,700 ppm, normal range 45 to 300 ppm). The 3 affected cattle were all products of line breeding programs and shared a common ancestor. The absence of dietary iron loading in conjunction with the histopathologic and metabolic findings were consistent with a diagnosis of primary hemochromatosis. The reported disease is similar to idiopathic hemochromatosis in human beings in which there is a hereditary defect in iron metabolism.
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PMID:Hemochromatosis in Salers cattle. 804 72

Five new cases of peritonitis caused by Aeromonas species are reported, and 29 others described in the literature are reviewed. Males predominated (71%), and the mean age was 56.9 years. Acquisition was nosocomial in 20% of the cases. All patients except one (3%) had significant underlying diseases; 73% had chronic hepatic disease, 15% had chronic renal failure (treated with chronic ambulatory peritoneal dialysis [CAPD]), and 9% had an intestinal perforation. Symptoms were similar to those of peritonitis caused by other pathogens, with the exception of diarrhea, which occurred in 25% of cases. Blood cultures were positive in 74% of the cases. The species isolated were Aeromonas hydrophila (27), Aeromonas sobria (5), and Aeromonas caviae (2). The overall case-fatality rate was 57%. Three strains were resistant to cotrimoxazole. Aeromonas species should be taken into account as a cause of peritonitis in patients with cirrhosis or who are undergoing CAPD.
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PMID:Aeromonas peritonitis. 805 35

We report a case of meningitis due to Listeria monocytogenes that occurred following colonoscopy. The patient had cirrhosis, a portosystemic shunt, and diarrhea for which she was being evaluated. Only one previous report has linked colonoscopy to listeriosis. We review the pathogenesis of listeriosis and, in particular, the evidence that prior fecal colonization is followed by bacteremia in a susceptible host. The findings in this case are consistent with this pathogenetic sequence.
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PMID:Colonoscopy-associated listeriosis: report of a case. 811 Sep 32


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