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)

A retrospective cohort study was conducted to examine mortality among 18,811 male farm owners and operators in New York State from 1973-1984. Farm Bureau membership lists were used to identify the study population, and vital status was determined through record linkage with death certificate and motor vehicle files. The comparison group consisted of the 1980 United States Census population of men who resided in the same towns as did the farmers. The results indicated that the study cohort experienced fewer than the expected numbers of deaths overall and for each major cause category except accidents. Specific causes with significant mortality deficits included cancer of the lung (standardized mortality ratio [SMR] = 47.0); diabetes mellitus (SMR = 57.5); ischemic heart disease (SMR = 65.3); bronchitis, emphysema, and asthma (SMR = 26.7); and cirrhosis of the liver (SMR = 29.7). The only specific cause with a significantly elevated mortality was accidents other than motor vehicle (SMR = 146.5). The investigation differs from previous research in method, setting, and population, but the pattern of findings is generally consistent with that of other studies.
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PMID:A retrospective cohort study of mortality among New York State Farm Bureau members. 366 7

A proportionate mortality ratio (PMR) study was undertaken of 7,121 members and retirees of the United Association of Plumbers and Pipefitters in California who died in 1960-79. The PMR for all malignant neoplasms was 1.24, with a major contribution from lung cancers (PMR = 1.41). Lung cancer PMRs were consistently elevated, through the 20-year study period, across the pipe trades and within different birth cohorts. Sixteen mesothelioma deaths occurred, suggesting asbestos as a risk factor. PMRs for malignancies of the stomach, kidney, brain, and lymphopoietic system were also elevated, especially among plumbers. Chronic rheumatic heart disease, emphysema, liver cirrhosis, and all external causes of death were the major non-cancer causes with significantly elevated PMRs. There were significant deficits in diabetes mellitus, all pneumonia, chronic nephritis, and vascular lesions of the central nervous system (CNS). PMRs for successive birth cohorts among all study subjects revealed decreasing emphysema risk, suggesting previous reduction of a risk factor for this disease. Among plumbers, PMRs for death due to several non-respiratory malignancies showed an increasing trend with recency of birth cohort.
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PMID:Patterns of mortality among plumbers and pipefitters. 374 68

Severe lung disease and liver disease are not recognised features of the PiMZ phenotype, which is associated with alpha 1 antitrypsin deficiency. A 31 year old woman with this phenotype was found to have emphysema and complete heart block and showed evidence of hepatic cirrhosis, although her three sisters, all of whom had the same phenotype, were clinically normal. This case supports the possibility of a causal relation between the PiMZ phenotype and chronic lung and liver disease, but an association between alpha 1 antitrypsin deficiency and complete heart block could not be proved in this patient.
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PMID:Emphysema, cirrhosis, and heart block in a young patient with partial alpha 1 antitrypsin deficiency (PiMZ phenotype). 393 36

The characteristics of emphysema and cirrhosis in Pi ZZ (alpha-1-antitrypsin deficiency) and SZ patients are reviewed. The clinical and laboratory data have been incorporated into a simple hypothesis on the development of these diseases. The PiZ protein can not be secreted normally from the liver cells. The accumulation of alpha-1-antitrypsin in the liver may result in cirrhosis, and the deficiency in serum to emphysema.
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PMID:Alpha-1-antitrypsin deficiency in pulmonary and liver degeneration. 454 76

The basal lamina is an extracellular scaffold positioned between parenchymal cells and connective tissue. Parenchymal cells attach to one of its surfaces and the other is anchored to connective tissue. By its presence it defines the spatial relationships among similar and dissimilar types of cells and between these cells and the space occupied by connective and supportive tissues. Replenishment of cells which have died during normal functioning or have become damaged in course of injury occurs with new cells in an orderly way along the framework of the basal lamina scaffold. This process appears to be aided by the polarity of the basal lamina and by an apparent specificity for cell types, and it enables multicellular organisms to reconstitute histologic structures of most tissues and organs to what they were prior to loss of cells. If the basal lamina is destroyed, the healing in most tissues results in formation of scar and loss of function. The properties of the basal lamina concerned with maintenance of histologic order in organs and tissues offer new ways to interpret the pathogenesis of several common disorders, including emphysema, scars, adhesions, cirrhosis of liver and excessive accumulation of basal lamina material as, for example, it occurs in patients with diabetes mellitus.
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PMID:Basal lamina scaffold-anatomy and significance for maintenance of orderly tissue structure. 461 71

Ceftizoxime (CZX), a parenteral cephalosporin derivative belonging to the so-called third generation cephalosporin is reported to have a broad antibacterial activity, particularly against Gram-negative aerobic bacilli and some anaerobes, such as Bacteroides fragilis and a good stability to beta-lactamases. Clinical study was performed on a total of 20 cases, 9 females (1 case had urinary tract infection 3 times) and 11 males, aged from 27 to 82 years. All patients had the underlying diseases. They were bronchial asthma in 3 cases, influenza in 1, chronic pulmonary emphysema in 1, pulmonary fibrosis in 1, chronic bronchitis with strongyloidiasis in 1, lung cancer in 3, esophagus cancer in 2, stomach cancer in 1, hepatoma with urolithiasis in 1, liver cirrhosis with diabetes mellitus in 1, alcoholism with strongyloidiasis in 1, cholelithiasis in 1 and congestive heart failure in 1, respectively. Clinical diagnoses for infections were 2-acute bronchitis, 2-exacerbation of chronic bronchitis, 2-broncho-pneumonia, 2-pneumonia including one suspected case, 1-obstructive pneumonia, 2-secondary pulmonary infection, 1-pulmonary infection, 3-urinary tract infection (UTI), 1-UTI with sepsis, 1-sepsis, 1-sepsis with purulent meningitis, 1-biliary tract infection and 1-infected bronchoesophageal fistula. CZX was given by intravenous drip infusion, at a dose of 1 to 2 g, twice daily for 3 to 15 days. Because of severity in infections and underlying diseases, some cases were treated either steroid, gamma-globulin preparations or other antibiotics in combination with CZX. Twelve out of 15 cases assessed clinically responded satisfactorily to the treatment and efficacy rate was 80.0%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effectiveness of ceftizoxime on various infections in patients with underlying diseases]. 609 Jul 23

alpha 1-Antitrypsin is the most abundant of several serum protease inhibitors. Its deficiency is associated with an increased incidence of emphysema in adults, jaundice in newborns, and childhood cirrhosis. We describe an automated functional assay for the Instrumentation Laboratory's Multistat III Microcentrifugal Analyzer with N-alpha-benzoyl-DL-arginine-p-nitroanilide as trypsin substrate. The assay is standardized in terms of moles of trypsin active sites inhibited per liter of serum, by use of a chromogenic titrant for trypsin active sites, p-nitrophenyl-p'-guanidinobenzoate. The method is rapid, precise, and independent of trypsin supplier, and results correlate well with those by a manual chromogenic and a nephelometric assay.
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PMID:Automated assay for alpha 1-antitrypsin with N-alpha-benzoyl-DL-arginine-p-nitroanilide as trypsin substrate and standardized with p-nitrophenyl-p'-guanidinobenzoate as titrant for trypsin active sites. 628 Aug 95

A deficiency in the plasma protease inhibitor alpha 1-antitrypsin can cause chronic obstructive emphysema or infantile liver cirrhosis. This deficiency results from a single amino acid substitution created by a G to A transition in the gene for alpha 1-antitrypsin. Chemically synthesized specific oligonucleotide probes (19-mer) have been used to develop a sensitive and direct test for the presence or absence of the mutant gene in any individual, which can be used for prenatal diagnosis of the deficiency syndrome.
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PMID:alpha 1-antitrypsin deficiency detection by direct analysis of the mutation in the gene. 630 78

alpha 1-Antitrypsin, the major serum protease inhibitor, is a glycoprotein synthesized in the liver. Severe deficiency results in protease-antiprotease imbalance, which predisposes to severe emphysema at a young age. Reduced serum levels reflect inadequate release of alpha 1-antitrypsin by the liver, which may be caused by specific defects in biosynthesis. The deficiency is inherited, with multiple codominant alleles at a single autosomal locus. Homozygous individuals, with severely reduced alpha 1-antitrypsin levels, have dyspnea, pulmonary function abnormalities, and respiratory disability from emphysema, usually in the fifth decade of life, with smokers being affected one decade earlier. Heterozygous individuals have intermediate alpha 1-antitrypsin levels and a more benign clinical course. Heterozygous smokers may have mild pulmonary function abnormalities, but these are of uncertain clinical significance. Hepatic involvement with transient neonatal hepatitis and cirrhosis with subsequent liver failure in adulthood represent the major extrapulmonary manifestations, occurring in 10% of homozygous individuals.
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PMID:alpha 1-Antitrypsin deficiency. 632 84

We studied, over a four-year period, two adolescents with alpha 1-antitrypsin (AAT) deficiency who subsequently died from complications of hepatic cirrhosis. Serial pulmonary function studies indicated mild obstructive lung disease involving peripheral airways in both patients. Postmortem histologic and pulmonary morphometric studies indicated mild diffuse airspace and bronchial gland enlargement, and slight dilation of small airways. This airspace enlargement may represent the early stage of lung disease in AAT-deficient subjects and suggests that pulmonary anatomic changes may occur long before the onset of clinically and pathologically significant emphysema.
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PMID:Unusual abnormalities in adolescent siblings with alpha 1-antitrypsin deficiency. 660 Jun 73


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