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)

The present review concentrates on environmental factors which influence the outcome of peptic ulcer disease by acting from the outside. Endogenous risk factors, such as acid output, pepsin secretion and serum pepsinogen, gastritis and mucosal defense, blood group, and secretor status, are only dealt with when they help to explain the mechanism by which exogenous risk factors affect the upper gastrointestinal mucosa. After outlining the wax and wane of peptic ulcer, it is concluded that these changes resulted from similar temporal patterns of occupational workload in the general population. Cross sectional studies also support the contention of occupational workload being a risk factor in peptic ulcer, explaining several characteristic features of peptic ulcer, such as its sex, race, and social class distribution, increased incidence in immigrant workers, seasonal variation, healing by bed rest, and urban versus rural distribution. Susceptible subjects may react to a rise in occupational workload and acute exposure to stressful life events by increased gastric secretion which, in turn, leads to ulceration and symptoms. Cigarette smoking, intake of aspirin and related drugs, dietary salt, and alcohol abuse represent additional environmental risk factors, which form the etiologic link of the association of peptic ulcer with chronic lung disease, rheumatoid arthritis, hypertensive disease, and liver cirrhosis, respectively.
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PMID:Factors which influence the incidence and course of peptic ulcer. 307 62

A defined general population of 159,200 male and female native Swedes born in the period of 1911-1940, from an urban catchment area of the then only general hospital, was followed over a decade (1970-1979) with regard to inpatient hospitalization for all kinds of diagnoses. Psoriasis cases (n = 372) are significantly (p less than 0.001) associated with a spectrum of diseases: male as well as female psoriatics seem to show excess rates of viral infections, alcoholism, hypertension, pneumonia, liver cirrhosis, urticaria, and rheumatoid arthritis. Psoriasis in males only seem to be associated with iritis and ankylosing spondylitis, whereas psoriasis in females only is associated with lung cancer, diabetes, obesity, myocardial infarction and asthma.
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PMID:Diseases associated with psoriasis in a general population of 159,200 middle-aged, urban, native Swedes. 308 49

Hyaluronan (hyaluronic acid) is a linear polysaccharide formed from disaccharide units containing N-acetylglucosamine and glucuronic acid. It is ubiquitously distributed in the organism but is found in the highest concentrations in soft connective tissues. The molecular weight of hyaluronan is usually in the order of 10(6) to 10(7). Due to hydrogen bonding, the chain is rather stiff and the molecule behaves in solution as an extended, randomly kinked coil. Molecules of hyaluronan start to entangle already at concentrations of less than 1 g/l and form a continuous polymer network. Some of the functions of the polysaccharide have been connected with the unique physical chemical characteristics of the network such as its rheological properties, flow resistance, osmotic pressure, exclusion properties and filter effect. Hyaluronan is synthesized in the cell membrane by adding monosaccharides to the reducing end of the chain. The precursors are UDP-glucuronic acid and UDP-N-acetylglucosamine. The polysaccharide grows out from the cell surface and it can be shown that fibroblasts, for example, surround themselves with a coat of hyaluronan. The rate of biosynthesis is regulated by various factors, such as growth factors, hormones, inflammatory mediators, etc. The responsible enzyme, hyaluronan synthase, is a phosphoprotein and the regulation of the synthetic rate is apparently via phosphorylation. The hyaluronan is at least partly carried by lymph flow from the tissues. Part of the material is taken up and degraded in the lymph nodes. Another part is carried to the general circulation and taken up in the endothelial cells in the liver sinusoids. These cells have specific receptors for hyaluronan, which also recognize chondroitin sulphate. The uptake in the liver of high-molecular weight hyaluronan is very efficient and its normal half-life in serum is only in the order of 2 to 5 min. The polysaccharide is rapidly degraded in the lysosomes to low-molecular weight products, lactate and acetate. The total turnover of hyaluronan in serum is in the order of 10-100 mg/24 h. The normal concentration of hyaluronan in serum is less than 100 micrograms/l with a mean of 30-40 micrograms/l. High serum levels have been noted in liver cirrhosis (impaired uptake in the liver) and rheumatoid arthritis (increased synthesis in the tissues). Hyaluronan has been shown to interact specifically with certain proteins and cell surfaces. It binds to proteoglycans in cartilage and other tissues and fills an important structural role in the organization of the extra-cellular matrix.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemistry of hyaluronan. 312 95

Twenty-three patients with severe rheumatoid arthritis were treated with oral methotrexate (MTX) for more than 10 years. MTX was given as a bolus of 5-15 mg/week; the total cumulative dose ranged from 4,690 mg to 10,230 mg. Liver biopsies were performed on 21 of the patients to assess possible fibrosis and cirrhosis. Grade I histopathologic changes were found in 13 of the 21 biopsy samples, grade II changes were found in 3, and grade IIIA changes (mild fibrosis) were found in 5 specimens. None of the biopsy samples showed cirrhosis. Repeat biopsies were performed on the 5 patients with grade IIIA changes while they were still taking MTX. No progression of the fibrosis was noted. Two of the 5 samples, however, were graded IIIB because of portal and perilobular inflammation. Our findings support the premise that prolonged administration of oral MTX, when given as a weekly bolus at a low dose, does not cause cirrhosis or severe fibrosis in the rheumatoid arthritis patient who does not abuse alcohol.
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PMID:Histopathologic findings in the liver of rheumatoid arthritis patients treated with long-term bolus methotrexate. 319 64

Chronic constrictive pericarditis may complicate both rheumatoid arthritis and systemic lupus erythematosus. To our knowledge, however, this is the first time it has been described in a patient with dermatomyositis. This association should be kept in mind as constrictive pericarditis should be considered in the differential diagnosis of liver cirrhosis and Budd-Chiari syndrome in rheumatic diseases.
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PMID:Constrictive pericarditis complicating dermatomyositis. 320 78

Twenty-six patients with severe rheumatoid arthritis who had completed a randomized crossover trial of methotrexate elected to continue to receive the drug in a long-term prospective study. At 36 months, 16 patients remained in the study. Over this period of time, significant improvement was noted in the number of painful and swollen joints, physician and patient global assessments, erythrocyte sedimentation rate, and prednisone dose. Adverse reactions occurred in 16 patients (62%), including nausea, alopecia, headache, stomatitis, herpes zoster, and diarrhea. Mild leukopenia (3 patients), thrombocytopenia (3 patients), and elevated transaminase levels (8 patients) resolved with temporary drug discontinuation. No patient withdrew due to drug toxicity. Liver biopsy specimens in 17 patients after 24 months of treatment showed no evidence of fibrosis or cirrhosis. A significant increase in the percentage of T3 and T4 blood cells and increases in lymphocyte proliferation to concanavalin A and purified protein derivative of tuberculin were found after 2 years of therapy. Our findings indicate that methotrexate has remained effective over 36 months of therapy, with acceptable toxicity levels and no evidence of systemic immunosuppression.
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PMID:Long-term prospective trial of low-dose methotrexate in rheumatoid arthritis. 291 60

Epidemiologic evidence shows a strong relationship between gastric cancer and cerebrovascular disease. It was speculated that salt intake might be the linking factor causing hypertension and vascular damage as well as damage to the gastric mucosa. This study tested whether hypertensive diseases, such as ischemic heart disease and cerebrovascular disease, occurred more frequently in patients with gastric cancer and gastric ulcer than expected by chance alone. In addition, it was studied whether gastric and duodenal ulcer coincided more frequently with other diseases that in the past have been associated with peptic ulcer, such as liver cirrhosis, chronic lung disease, and rheumatoid arthritis. The German statistics of rehabilitation were used to assess the frequency of coincidences. The statistics include a description of the primary, secondary, and tertiary diagnoses leading to rehabilitation. This study confirms the presence of a high coincidence of both ulcer types with liver cirrhosis. In patients with rheumatoid arthritis, both ulcer types also occurred more frequently than expected from their general distribution. Gastric but not duodenal ulcer coincided more frequently with ischemic heart disease than expected. Gastric cancer occurred more frequently in patients who had concomitant ischemic heart disease or cerebrovascular disease. Duodenal ulcer was not associated with an increased risk for any disease related to hypertension. The results of the study support the contention that gastric diseases and diseases related to hypertension share a common etiologic factor.
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PMID:Concordant occurrence of gastric and hypertensive diseases. 337 23

The Tc-99m sulfur colloid liver-spleen scintigrams of nine patients with Felty's syndrome (a triad of rheumatoid arthritis, splenomegaly, and neutropenia) were reviewed. The characteristic scintigraphic findings include (1) moderate or severe splenomegaly, (2) the reversal of liver-to-spleen uptake ratio despite normal liver function tests, and (3) virtually no visualization of the bone marrow uptake and no pulmonary radiocolloid sequestration. In a late stage of cirrhosis of the liver, moderate-to-severe splenomegaly with the reversal of liver-to-spleen uptake ratio almost always accompanies abnormal liver function, and sometimes there may be associated pulmonary radiocolloid uptake. It was therefore concluded that in a proper clinical setting, a radiocolloid scintigraph may differentiate between Felty's syndrome and cirrhosis of the liver in a late stage.
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PMID:Radiocolloid scintigraphy in Felty's syndrome. 348 13

Hyaluronan (HA) was discovered over 50 years ago but its metabolism and cellular interactions have only recently received detailed attention. HA is synthesized in the plasma membrane by addition of monosaccharides to the reducing terminal. In tissues, it occurs bound to plasma membranes, aggregated with other macromolecules, or as free polysaccharide. Tissue HA enters the bloodstream in significant amounts through the lymph and is rapidly absorbed via a receptor into liver endothelial cells, where degradation follows. HA levels in serum are normally 10-100 micrograms/l, but can be elevated in cirrhosis, rheumatoid arthritis and scleroderma, due either to impaired hepatic uptake or to increased production. Studies on aqueous humour, middle ear secretion, amniotic fluid, lung lavage fluid, urine, skin diseases and cancer have identified other causes of deranged HA metabolism. HA can be visualized on some cell surfaces as a coating impermeable to particulate material. Specific HA binding occurs on lymphoma cell lines, lung macrophages and SV-3T3 cells but, except in synthesis or uptake, the significance of membrane-associated HA is incompletely understood. It has been reported to activate macrophages and granulocytes, protect cells, control cell migration, and cooperate with intercellular matrix in cell detachment; it also plays a central role in growth control, cellular differentiation and tissue morphogenesis.
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PMID:The properties and turnover of hyaluronan. 381 25

The findings of liver studies in 29 patients who were treated with low dose pulse methotrexate for rheumatoid arthritis (RA) are described. The biopsy specimens of 22 patients (76%) showed liver abnormalities, but cirrhosis did not develop in any patient. There were no statistically significant differences in age, duration of treatment, or cumulative dose between patients in whom abnormal liver histology developed and those in whom it did not. Our findings showed that isolated elevations of the aminotransferase enzymes or alkaline phosphatase levels did not predict liver disease, nor did the absence of elevation of these enzymes assure the absence of liver disease. Serial elevations of the aminotransferase and/or alkaline phosphatase enzyme levels and the development of hypoalbuminemia during treatment were specific indicators of the development of liver disease. In the patients studied, significant liver disease did not develop before 2 years of therapy or with a cumulative dose of methotrexate of less than 1500 mg.
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PMID:Methotrexate and the liver. 383 62


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