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)

Splenectomy for massive splenomegaly and hypersplenism carries a significant morbidity and mortality. We have used partial splenic embolization (PSE) as an effective alternative to splenectomy. Ten PSE procedures were performed on nine patients without mortality and with minimal morbidity. The age of the patients ranged from 8 months to 32 years (mean 14 years). The causes of splenomegaly and hypersplenism included cystic fibrosis with cirrhosis (2), tyrosinemia and cirrhosis (1); thalassemia (1), hemophilia with Human Immune Deficiency Virus infection (2), chronic hepatitis with portal hypertension (1), malignant histiocytosis (1), and Wiskott-Aldrich Syndrome (1). All procedures were performed under local anesthesia with sedation. A percutaneous femoral artery approach to the splenic artery was used to deliver Ivalon sponge particles (280-800 microns) into the spleen. Splenic infarction was assessed by postembolization angiograms. All of the patients except one demonstrated improvement of hematologic parameters. In one patient, however, cytopenia improved only after a second embolization. In the total series, there was an early mean rise of 8,600/mm3 in the leukocyte count (range 2,900-14,900) and 212,000/mm3 in the platelet count (range 30,000-718,000). Follow-up ranged from 4 months to 7 years. Improvement of the blood picture has been persistent in seven of the eight patients who showed initial improvement. Transient procedural complications included fever (5), pleural effusion (2), pneumonia (1), and splenic abscess (1). One patient had paralytic ileus lasting for 10 days and one patient developed a streptococcal peritonitis 3 weeks after embolization. No patient developed pancreatitis or vascular compromise of other abdominal viscera.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. 226 5

We compared the jobs, estimates of exposures, and mortality experience of short-term (less than or equal to 1 year) and long-term (greater than 1 year) workers from nine plants producing formaldehyde or formaldehyde products. There were few jobs that were filled solely or primarily by newly hired workers. The estimated median level of formaldehyde exposure experienced by short-term workers on their first job was nearly identical to that for long-term workers, although short-term workers were more likely to be in jobs exposed to particulates than were long-term workers. As duration of employment increased, there was little change in the average estimated exposure level of formaldehyde, but the likelihood of being exposed to particulates decreased. Short-term workers had greater risks than long-term workers of dying from diseases of the circulatory system, arteriosclerotic heart disease, emphysema, diseases of the digestive system, cirrhosis of the liver, motor vehicle accidents, suicide and malignant neoplasms, particularly cancers of the stomach, colon, lung, prostate, and brain.
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PMID:Comparison of jobs, exposures, and mortality risks for short-term and long-term workers. 240 25

An oral water load of 20 ml kg-1 body weight was given to 11 patients with early hepatic cirrhosis and to 16 healthy control subjects. Urinary output (V), free water clearance (CH2O), urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), and plasma concentration of arginine vasopressin (AVP) were determined before and during the first 4 h after loading. During basal conditions, PGE2 excretion was the same in patients (75 pg min-1, median, range 15-569) and controls (78 pg min-1, range 22-262), but during the first hour after water loading, PGE2 increased to a significantly higher level in cirrhotic patients (423 pg min-1, median) than in control subjects (162 pg min-1) (P less than 0.05). No difference in PGF2 alpha excretion was found between the two groups. Urinary output and CH2O were significantly lower after water loading in patients than in controls. Arginine vasopressin before water loading did not differ between patients and control subjects, but after loading it was unchanged in the patients, whereas a significant reduction (1.9 to 1.4 pmol l-1, P less than 0.01) was found in the control subjects. In controls, but not in patients, PGE2 was significantly positively correlated to V and CH2O, and negatively correlated to AVP after water loading. Thus, renal PGE2 excretion is increased and CH2O is decreased after water loading in patients with early hepatic cirrhosis, and a disturbed relationship seems to exist between PGE2 on the one hand, and AVP and renal water excretion, on the other, in these patients after water loading.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbed relationship between urinary prostaglandin E2 excretion, plasma arginine vasopressin and renal water excretion after oral water loading in early hepatic cirrhosis. 313 26

In 5 patients with cirrhosis and ascites the glomerular filtration rate (GFR), free water clearance (CH2O) and urinary excretion of prostaglandin E2(PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured before and after a 3-day treatment with sulindac (400 mg/day). The administration of sulindac induced a marked fall of urinary excretion of PGE2 (from 24.2 +/- 5.5 to 3.8 +/- 1.1 ng/h; p less than 0.05), 6-keto-PGF1 alpha (from 19.9 +/- 2.9 to 5.6 +/- 1.1 ng/h; p less than 0.02) GFR (from 111 +/- 15 to 67 +/- 10 ml/min; p less than 0.01) and CH2O (from 7 +/- 1.5 to 3.7 +/- 1.3 ml/min; p less than 0.02) in all patients studied. The plasma concentration of the active metabolite sulindac sulfide in cirrhotics was 400% of that found in 6 healthy volunteers (9.6 +/- 1.7 vs. 2.4 +/- 0.6 ng/ml). Our results indicate that sulindac, at a dose of 400 mg/day, inhibits the renal synthesis of prostaglandins and impairs renal function in cirrhotics with ascites. These effects are probably related to the marked alteration of sulindac kinetics that occurs in these patients.
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PMID:Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in cirrhosis with ascites. 351 19

A retrospective mortality analysis was conducted in a cohort of 9,365 individuals employed as of 1940 in two chrome leather tanneries in the United States and followed to the end of 1982. Vital status as of the closing date was determined for over 95% of the cohort. Potential hazardous workplace exposures varied with department and included nitrosamines, chromate pigments, benzidine-based direct dyestuffs, formaldehyde, leather dust, and aromatic organic solvents. Mortality from all causes combined was lower than expected for each tannery, the standardized mortality ratio being 81 for one and 93 for the other. Deaths from cancer of each site, including the lung, were also lower than expected compared to those of either the population of the United States or of local state rates. A significant excess of deaths was observed, however, due to accidental causes in one tannery and cirrhosis of the liver, suicide, and alcoholism in the other. These excesses did not appear to be causally associated with occupational exposures. The findings of this study are consistent with those of the only other mortality investigation of leather tannery employees.
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PMID:Mortality of chrome leather tannery workers and chemical exposures in tanneries. 360 64

The production of fish meal from fresh and from formaldehyde- and sodium benzoate-preserved catches results in the formation of considerable dimethylnitrosamine (DMNA). This is in contrast to the prevailing opinion that only nitrite preservatives can be incriminated in producing this toxin. With capelin fish preserved in a mixture of 920 g of sodium benzoate and 920 ml of formaldehyde/hectoliter for 11 days, 7.5 mgs of DMNA/kg fish meal were produced. Pigs exposed to different daily levels of DMNA, of commercial source, proved to be rather resistant to intoxication compared with other domestic animals. Doses of 100, 200 and 500 ppm of DMNA added to a commercial pig diet, with a cumulative ingestion of 8.1 to 13.9 g pig or from 282 to 583 mg DMNA/kg body weight, resulted in extensive vasoobstructive disease over a period of 64 to 105 days. These lesions are most severe in the liver where they produce a diffuse form of cirrhosis. Additional findings include anaplastic changes in the tubules of the kidneys. A DMNA level of 15 ppm in the feed, in this experiment from fish meal, did not result in pathologic lesions over an observation period of up to 525 days.
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PMID:Dimethylnitrosamine--formation in fish meal and toxic effects in pigs. 480 17

Fifty patients who died of hepatocellular carcinoma (HCC) were autopsied at the Ciudad Sanitaria "1 degree de Octubre" and the Hospital de la Cruz Roja (Madrid) from 1974 to 1980. Formalin fixed paraffin-embedded autopsy tissue of liver and tumor from the 50 HCC and liver tissue from 50 liver cirrhosis (LC) and from 50 autopsy of non cirrhotic control cases were examined for the presence of cytoplasmic hepatitis B surface antigen (HBsAg). The study was carried out using orcein staining, immunoperoxidase technique (IP) and indirect immunofluorescence (IF). In livers with HCC the HBsAg was detected in the cytoplasm of the hepatocytes in 10 cases (20%) with the orcein staining and in 11 (22%) with the IP and IF techniques. In one case (2%) HBsAg was found in the cytoplasm of tumor cells with the three methods--In four cases (8%) of LC and 2 (4%) control cases cytoplasmic positive cells were found. In 41 patients with HCC HBsAg was studied in the serum by radio-immunoassay (RIA) (13 cases) and immunodiffussion (28 cases). 5 patients (12,1%) were positive and 36 (72%) were negative. In the 5 serum positive HBsAg HCC the staining methods for cytoplasmic HBsAg were positive (100%). In 36 serum negative HBsAg HCC the staining method were positive in 2 cases. The results let us to conclude that HBV is a probable important etiologic factor of HCC in our milieu. 54% of the patients with HCC had a previous history of alcohol abuse; however, histologic features compatible with an alcoholic etiology were found in only 5 cases. Nevertheless we consider that the described histopathologic findings do not exclude excess alcohol consumption as a possible etiologic factor for HCC in our series.
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PMID:Hepatocellular carcinoma. A study of 50 autopsy cases with detection of hepatitis B surface antigen in fixed tissues. 619 Jan 53

Tumor cell marker antibodies were used to analyze ten cases of hepatocellular carcinoma associated with cirrhosis. Clinically, eight of these cases gave a history of chronic alcoholism and the other two of hepatitis B virus infection. Formalin-fixed, paraffin-embedded sections from these cases were screened with antibodies against alpha fetoprotein (AFP), hepatitis B surface antigen (HBsAg) and carcinoembryonic antigen (CEA) using the peroxidase antiperoxidase and avidin-biotin immunoperoxidase procedures. Three cases were positive for AFP, four for HBsAg, and three for CEA; two cases had both HBsAg and CEA. Alpha fetoprotein was present only in the cytoplasm of tumor cells in three cases. Hepatitis B surface antigen, on the other hand, was present in the cytoplasm of hepatocytes in cirrhotic areas and, in one out of the four cases, was also present in hepatocellular carcinoma cells. Carcinoembryonic antigen was seen in three cases; it was present on the surface and in the cytoplasm of proliferating ducts within the cirrhotic areas and between cell surfaces of individual tumor cells in two cases. The presence of different markers was not related to the microscopic appearance of the tumors. In one case, positivity for AFP was of diagnostic help in a tissue sample obtained by needle biopsy. The avidin-biotin immunoperoxidase procedure was more sensitive than the peroxidase antiperoxidase (PAP technique in the pathological assessment of autopsy specimens. Our findings are in agreement with those of other reports and indicate that AFP and HBsAg are the most commonly found markers in hepatoma associated with cirrhosis, and that CEA staining is variable and hepatoma associated with cirrhosis, and that CEA staining is variable and probably non-contributory.
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PMID:Immunohistochemistry of hepatocellular carcinoma associated with cirrhosis. 621 34

Formalin-fixed, paraffin-embedded sections of liver and tumour tissue obtained at necropsy from 44 southern African Blacks with hepatocellular carcinoma were stained for hepatitis-B virus surface antigen by immunofluorescence, immunoperoxidase and orcein techniques. The antigen was present in the serum of 68% of the patients. Staining for tissue antigen was positive in 45% of the patients. Non-tumorous hepatocytes alone stained positively in 22.5% of patients, tumour cells alone in 12.5% and both in 10%. Antigen was present in relatively few tumour cells and the amounts detected were small; it was more readily detectable in moderately differentiated than in poorly differentiated malignant cells. Identical results were obtained with immunofluorescence and immunoperoxidase staining, but the orcein stain failed to demonstrate the antigen in tumour cells. Cirrhosis was present in the non-tumorous liver in 70% of the patients. Antigen was detected in cirrhotic tissue in 43% of the patients with cirrhosis, and in non-tumorous liver tissue in 8% of those without cirrhosis, but this difference was not significant. The antigen frequency in tumour tissue was the same in patients with and without cirrhosis. No correlation was found between the presence of liver-cell dysplasia and the presence or absence of either the antigen or cirrhosis in the non-tumorous liver tissue. Ground-glass hepatocytes were seen in non-tumorous liver tissue of 5 patients, but not in tumour tissue. While 54% of the patients with antigenaemia had demonstrable tissue antigen, 10% of patients with tissue antigen had no detectable antigenaemia.
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PMID:Hepatitis-B surface antigen in tumour tissue and non-tumorous liver in black patients with hepatocellular carcinoma. 624 94

Although an impairment in renal water excretion is a commonly encountered clinical problem in cirrhotic patients, the mechanisms responsible for this abnormality are uncertain. ADH levels are elevated in some patients with decompensated cirrhosis, but a causal relationship between these levels and impaired water excretion has not been established. Since in normal man, water immersion to the neck (NI) results in a preferential central hypervolemia (CV), without plasma compositional change, and a resultant suppression of AVP, we designed the present study to determine if the diuretic response of cirrhotic patients to NI is mediated by a decrease in AVP. 17 cirrhotic patients with ascites were studied following 14 h of dehydration on two occasions: during a seated control study (C) and during 4 h of NI. AVP, determined by RIA, was measured every 30 min. 12 of the 17 patients manifested a diuresis that equalled or exceeded that documented in normal hydropenic subjects during immersion. NI did not alter mean AVP as compared with either the pre-study hour or those of the corresponding control study. Furthermore, peak V and CH2O varied independently of prestudy AVP (r = -0.116), mean change in AVP (r = -0.060), as well as nadir AVP levels (r = -0.122). The demonstration of a diuresis in some of the subjects, occurring without concomitant suppression of plasma AVP, suggests that ADH may constitute a permissive rather than pivotal factor in the impaired water excretion of many patients with advanced liver disease.
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PMID:Relationship between plasma arginine vasopressin and renal water handling in decompensated cirrhosis. 637 13


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