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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The arthritis urica is defined as a relatively rare, at the same time facultative symptom of different metabolic and other disturbances (primary and secondary gout). As a rule it is observed only several years of the beginning of the hyperuric-anemia nearly exclusively in males and is only one form of manifestation of the wide-spread complex gout syndrome. It is proposed to supplement the criteria for gout or arthritis urica of Rome 1961 and New York 1966 by new knowledge on the uncharacteristic gouty arthropathy. It is particularly referred to method problems of the determination of uric acid in the serum.
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PMID:[Diagnostic problems of gout]. 99 60

Molybdenum toxicity and the interactions between copper, molybdenum and sulphate are reviewed. The main signs of molybdenum poisoning are poor growth and anaemia (rat, chick, rabbit, cattle and sheep), anorexia (rat), diarrhoea and achromotrichia (cattle and sheep), joint and bone deformities (rat, rabbit, cattle), central nervous system degeneration and loss of crimp in wool (sheep). The following topics are discussed: (1) The effect of sulphate and sulphur compounds on molybdenum toxicity. (2) The effect of molybdenum on tissue copper levels. (3) The effect of molybdenum on the distribution of copper in plasma. (4) The effect of molybdenum on uptake and excretion of copper. (5) The possible existence of copper(II) molybdate in vivo. (6) The influence of molybdenum on sulphide production by ruminal micro-organisms. (7) Competition between molybdenum and sulphate in intestinal transport. (8) Interaction of sulphur with copper in vivo. (9) The possible involvement of molybdenum in gout and multiple sclerosis in humans.
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PMID:Molybdenum toxicity: interactions between copper, molybdenum and sulphate. 100 22

From November 1970 to August 1974 small intestinal bypass was performed in 475 patients for morbid obesity with an operative mortality of 1.6%. Immediate postoperative complications were superficial wound infection (17 patients), pulmonary complications (seven patients), cardiac complications (five patients), wound dehiscence (nine patients), intestinal tract fistula (four patients), and miscellaneous complications (14 patients). Delayed complications included hypokalemia (28%), hypocalcemia (9%), anemia (11%), calcium oxalate urinary calculi (6%), gout (2%), and hepatic failure (1.4%). Fourteen patients died of late complications. Ventral incisional hernia occurred in 3% of the patients; failure to lose sufficient weight in 21%, all but one occurring in patients with end-to-side shunts. Thirteen end-to-side shunts have been converted to end-to-end shunts because of insufficient weight loss. A team concept is important in the handling of the morbidly obese. Small bowel bypass is effective in producing sustained weight reduction in these patients. Careful and continued study of these patients for the rest of their lives is of paramount importance.
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PMID:Metabolic intestinal surgery. Its complications and management. 113 Oct 9

Hypertensive patients over the age of 60 years were admitted to a double-blind placebo-controlled trial. Patients in the actively treated group received a combined potassium-losing and -sparing diuretic (triamterene 50 mg plus hydrochlorothiazide 25 mg; n = 416); this dose could be doubled and methyldopa (up to 2 g, daily) was added in 35% of patients when blood pressure remained high. The placebo group (n = 424) received matching capsules and tablets. Adverse effects were assessed in the double-blind period of the trial by calculating the incidence of abnormal biochemical results, investigator reports of diseases and prescriptions of concomitant therapy and a self-administered symptom questionnaire completed by patients. In 1000 hypertensive subjects over 60 years of age, 1 year of active treatment would prevent 11 fatal cardiac events, 6 fatal and 11 non-fatal strokes and 8 cases of severe congestive heart failure. No unexpected adverse treatment effects were observed. A significant excess incidence rate (per 1000 person years) was found in the active group compared with placebo for: (1) impaired renal function, a serum creatinine greater than 180 mumol/l (2.0 mg/dl); (2) mild hypokalaemia, a serum potassium less than 3.5 mmol/l; (3) reports of gout; and (4) an elevated serum uric acid greater than 0.52 mmol/l in men or greater than 0.46 in women. Elevated blood sugar and prescriptions for hypoglycaemic drugs tended to be more frequent in the actively treated group, but this difference was not statistically significant. In both groups, there was a low incidence (less than 7 per 1000 person years) of anaemia and depression and diseases of the liver, gall bladder or pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risks and benefits in the trial of the European Working Party on High Blood Pressure in the Elderly. 185 85

Upon hospital admission a patient was found to have severe anemia and a strongly positive direct antiglobulin test (DAT). The patient was taking probenecid periodically for gout. An antibody was detected in the patient's serum that only reacted with red blood cells (RBCs) when probenecid was added. Eluates from the patient's RBCs, with and without the presence of drug, were nonreactive. Upon the discontinuation of probenecid, the patient's hemoglobin level improved steadily. We believe this to be the first reported case of immune hemolytic anemia associated with probenecid.
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PMID:Immune hemolytic anemia associated with probenecid. 403 70

Pain patterns vary greatly in the different types of arthritis, from the localized agony without mental overtones in acute gout to the diffuse disorder we call rheumatoid arthritis, where inflammation of many joints, systemic illness, anaemia, anxiety, and depression are usually all present in some degree. Each pain pattern calls for a different therapeutic approach, physical, psychological, and pharmacological. Few patients suffer as much pain and suffering over many years as do chronic arthritics. It is all the more important to instruct them in the essentials of their own treatment. A patient with an occupied and instructed mind usually suffers less than an ignorant and depressed one, fearful of her disease and its complications and of the dark uncertain future that lies ahead.
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PMID:Pain patterns in the rheumatic disorders. 411 70

There has been an explosion of knowledge in disorders of purine and pyrimidine metabolism during the last 20 years. During this time, more than 10 diseases have been discovered and their metabolic bases studied. Hyperuricemia and gout remain the most common clinical disorder. Rarely these disorders are explainable by an inherited enzyme abnormally, such as hypoxanthine-guanine phosphoribosyltransferase deficiency, phosphoribosyl-pyrophosphate synthetase deficiency, or glucose-6-phosphatase deficiency. The description of immunodeficiency syndromes in association with purine enzyme deficiency has led to a novel area of investigation encompassing the biochemical basis for immune function. Although less information is available concerning the other diseases associated with renal calculi, myopathy, anemia, and central nervous system dysfunction, further research will elucidate important metabolic relationships. These will no doubt expand our understanding of the pathogenesis of these disorders and provide innovative therapeutic approaches.
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PMID:Disorders associated with purine and pyrimidine metabolism. 609 39

Purine nucleotide degradation refers to a regulated series of reactions by which human purine ribonucleotides and deoxyribonucleotides are degraded to uric acid in humans. Two major types of disorders occur in this pathway. A block of degradation occurs with syndromes involving immune deficiency, myopathy or renal calculi. Increased degradation of nucleotides occurs with syndromes characterized by hyperuricemia and gout, renal calculi, anemia or acute hypoxia. Management of disorders of purine nucleotide degradation is dependent upon modifying the specific molecular pathology underlying each disease state.
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PMID:Metabolic basis for disorders of purine nucleotide degradation. 626 3

A 69-year-old man was given 8 mg of colchicine intravenously to treat an acute attack of gout. A maintenance dose of 2 mg/day of oral colchicine was then used to prevent recurrence. Three months later, the patient developed thrombocytopenia, followed by leukopenia and then by anemia at three and four months distance, respectively. The patient had shown no signs of acute toxicity with intravenous colchicine, but liver enzymes were raised after two months of oral treatment. The sequential involvement of the three blood precursor lines, in the order to their physiological half-lives, suggests direct toxicity, rather than idiosyncrasy, due to slow accumulation of the drug within target cells. The prophylactic use of colchicine, especially in the elderly, is questioned.
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PMID:Marrow aplasia following colchicine treatment for gouty arthritis. 653 22

A 43-year-old man with lifelong anaemia showed features which indicate him to have a previously undescribed variant of congenital dyserythropoietic anaemia (CDA), type II. The main clinical features--of which the first two are unique or very unusual in CDA--have been severe tophaceous gout, massive splenomegaly, gall stones mecessitating cholecystectomy and haemosiderosis affecting the liver and probably the heart. At age 41 he sustained a spontaneous retinal detachment. In the peripheral blood there were large numbers of nucleated red blood cells and marked macrocytosis; otherwise the picture was typical of CDA type II. The bone marrow contained many bi- and multi-nucleated erythrocyte precursors. There were increased levels of a number of red cell enzymes and a slightly raised level of HbF. Uncharacteristically, the red cells failed to lyse with acidified normal serum. The cells were strongly agglutinated by anti-i and were of the rare Kpb-negative phenotype. Plasma lipid analysis showed very low levels of cholesterol and vitamin E. Lipid peroxidation was markedly increased. Ultrastructural studies showed reduplication of the erythrocyte, granulocyte, and platelet cell membranes.
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PMID:Congenital dyserythropoietic anaemia (CDA) with severe gout, rare Kell phenotype and erythrocyte, granulocyte and platelet membrane reduplication: a new variant of CDA type II. 737 99


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