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At least 775 records · Page 43Linked to original sources
PubMed1989

[A case of pneumococcal arthritis in a patient with gout].

A 62 year-old man had suffered from gout and mild renal insufficiency since he was 40 years old. He was admitted to our hospital complicated by a productive cough, high fever and a right swollen knee joint. The chest radiographs demonstrated a left upper lobe infiltration shadow. Streptococci pneumoniae were found in the sputum, arterial blood and synovial fluid of the right knee joint, suggesting a severe pneumonia followed by pneumococcal septicemia which led to purulent arthritis. He was treated with cefamandole (CMD) and penicillin G (PC-G) for one week, but the chest X-ray findings were not improved. After treatment with cefbuperazone (CBPZ) and latamoxef (LMOX), his fever and other symptoms gradually resolved. Streptococcus pneumoniae is an uncommon organism of septic arthritis. Pneumococcal arthritis in a patient without immunodeficiency such as this case is very rare, and has not been reported in Japan.

Arthritis, Infectious↗
PubMed1967

Glutathione reductase in red blood cells: variant associated with gout.

A variant of red cell gluta thione reductase, characterized by greater electrophoretic mobility, in creased enzyme activity per unit of hemoglobin, and an autosomal mode of inheritance, has been found in Negro populations. There appears to be an association of this variant with primary gout.

Black or African American↗
PubMed1978

Saturnine gout: lead-induced formation of guanine crystals.

Intravenous injection of a sublethal dose of lead acetate into a domestic pig resulted in a 4.5-fold increase of guanine in the urine, indicating an impairment in the conversion of guanine to xanthine. This impairment is probably due to the inhibition of guanine aminohydrolase (guanase), since the activity of this enzyme is inhibited by Pb2+ (the inhibition constant being 3.0 X 10(-6)M). Postmortem histological examination revealed concretions of crystalline material in the epiphyseal plate of the femoral head. Extraction of the section containing the concretions showed that they were guanine. The relation of these findings to saturnine gout is discussed.

Animals↗
PubMed1981

Familial gout and renal failure.

Clinical gout and renal failure was seen in a 9-year-old girl. The family tree showed that 9 out of 11 young females in three generations suffered from hyperuricaemia and normal (n = 1), or impaired (n = 8), renal function. One set of twins occurred in each generation and there is only one living male subject. In members with renal failure there was no improvement in renal function after treatment of hyperuricaemia, and in 2 sisters oral contraceptives appeared to precipitate hypertension. This clinical picture may be more common than is generally realised because of failure to compare blood uric acid values with suitable age- and sex-matched controls. The evidence from this family suggests that hyperuricaemia preceded the development of renal failure.

Adult↗
PubMed1976

Sparing effect of hemiplegia on tophaceous gout.

The sparing effect of hemiplegia on the development of tophaceous gout is described. The useless upper limb had no tophaceous deposits and the partially paralysed lower limb had only limited urate deposits. Disuse was presumably the major contributor to the limited deposition of urates on the paralysed side.

Gout↗
PubMed1979

Mechanism and treatment of hypertriglyceridaemia in gout.

Using the Intralipid lipid tolerance test we could not demonstrate any direct effect of serum triglyceride on uric acid or any influence of hyperuricaemia on triglyceride removal. This result supports previous studies suggesting that hyperuricaemia and hypertriglyceridaemia are linked through the association of obesity and alcohol excess rather than a direct cause and effect mechanism. It was possible to demonstrate significant reductions of serum triglyceride in patients with gout by reducing either their alcohol intake or body weight. Reduction of serum uric acid by probenecid had no effect on serum triglyceride or cholesterol. Similarly, allopurinol had no significant effect on serum triglyceride, but a significant fall of serum cholesterol was observed.

Alcohol Drinking↗
PubMed1981

Spontaneous rupture of the Achilles tendon in a patient with gout.

A 49-year-old man with long-standing gout suffered a spontaneous rupture of the Achilles tendon. Surgical repair was performed, and gouty tophi were found in the severed end of the tendon. The possible causes of this spontaneous rupture are discussed.

Achilles Tendon↗
PubMed1983

Spondylodiscal erosions due to gout: anatomico-radiological study of a case.

The necropsy of an 84-year-old woman with painful polyarticular gout showed a severe erosion of the L2 vertebral body due to sodium urate deposition. The radiological signs of this tophus had existed for many years; it had caused recurrent pain but no neurological complications. A small tophus and a Schmorl's node on 2 neighbouring thoracic vertebrae permitted the differentiation between vertebral plate erosion in the first, which was of bone origin, and vertebral plate remodelling in the second, which originated in the cartilaginous tissue of the disc.

Aged↗
PubMed1971

An unusual form of renal disease associated with gout and hypertension.

A family is described many of whose members suffered from renal insufficiency, hypertension, gout, and hyperuricaemia in conjunction. Adequate information was obtained on 72 subjects from five generations. In 17, one or more of the above mentioned abnormalities was or had been present. The hereditary distribution suggested an autosomal dominant disease entity. The renal disease was characterized by an early loss of urinary concentrating power, minimal proteinuria, and death at a relatively early age dominating the clinical picture. The histological picture in three biopsies and one necropsy showed predominant tubular atrophy and interstitial fibrosis, with striking tubular basement membrane thickening. It is suggested that these patients suffered from a hereditary degenerative renal disease. The question whether hyperuricaemia was primary or secondary in these cases is discussed.

Adolescent↗
PubMed1971

Phosphoribosyl transferase activity in normal subjects, gout patients, and children with mental retardation.

Activity of hypoxanthine-guanine and adenine phosphoribosyl transferase enzymes has been assayed in erythrocytes from 10 normal adults, 37 subjects with gout, and 21 mentally retarded children with high and normal urinary uric acid:creatinine ratios. These were compared with one case of known HGPRTase deficiency. Apart from the last subject, no cases of HGPRTase deficiency were found.

Adenine↗
PubMed2003

Co-existent gout and septic arthritis at the wrist: a case report.

This article presents an exceptional clinical manifestation of gout in the wrist. The patient suffered from an association of septic and urate-crystal-induced arthritis. At the time, the serum uric acid concentration was still normal. The association of septic and urate-crystal-induced arthritis has been reported in other locations. The pathophysiology of the precipitation of urate crystals in the presence of an infectious process is discussed.

Anti-Bacterial Agents↗
PubMed1992

Decreased renal phosphate threshold in patients with gout.

Serum and 24-hour urinary phosphate levels in primary gout patients and control subjects were measured. About 45% of gouty patients showed mild hypophosphatemia. However, mean 24-hour urinary excretion of phosphate was significantly elevated as compared with that of controls. Gouty patients showed a significantly decreased tubular reabsorption of phosphate and renal phosphate threshold. It seems that tubular phosphate transport in gouty patients is impaired, and this is the major cause of hypophosphatemia.

Adult↗
PubMed1978

Overproduction disease in man due to enzyme feedback resistance mutation. Purine overproduction in gout due to excessive activity of mutant feedback-resistant phosphoribosylpyrophosphate synthetase.

Physiologically superactive phosphoribosylpyrophosphate (PRPP) synthetase, due to feedback resistance mutation, was found in a family with excessive purine production, gout and uric acid lithiasis. The superactivity of the mutant enzyme was manifest in the propositus' erythrocytes and cultured fibroblasts, in increased generation, content and metabolic availability of PRPP, leading in the fibroblasts to acceleration of the rate of purine synthesis de novo. One of the propositus' two siblings was similarly affected, but the propositus' father, his second brother and four sons, were all clinically and biochemically normal. The mother was clinically normal and normouricemic, but hyperuricosuric. Cultured fibroblasts from her skin exhibited variability in PRPP content and availability and in the rate of purine synthesis de novo. The mother's cultures were found to contain a mosaicism of two cell populations, one with normal and the other with mutant PRPP synthetase, indicating an X-linked pattern of inheritance of the PRPP synthetase abnormality in this gouty family.

Adolescent↗
PubMed1968

Variations in purine metabolism of cultured skin fibroblasts from patients with gout.

Purine metabolism was studied in fibroblasts cultured from three patients with gout in an attempt to determine the biochemical bases of their disease. The rate of purine biosynthesis de novo was normal in one line of cells, but the rate of catabolism of adenine nucleotides to hypoxanthine and inosine was greatly increased. The rate of purine biosynthesis de novo was increased in two lines of cells, and this was associated with increased concentrations of 5-phosphoribosyl 1-pyrophosphate. Purine synthesis was also less sensitive than normal to feedback inhibition. The catabolism of inosinate synthesized de novo was increased.

Adenine Nucleotides↗
PubMed1975

Mutant feedback-resistant phosphoribosylpyrophosphate synthetase associated with purine overproduction and gout. Phosphoribosylpyrophosphate and purine metabolism in cultured fibroblasts.

We have reported previously two siblings with gout and uric acid lithiasis associated with excessive purine production. In the erythrocytes of these patients, phosphoribosylpyrophosphate (PRPP) synthetase exhibited resistance to feedback-inhibition by normal cell constituents such as guanosine-5'-diphosphate (GDP) and adenosine-5'-diphosphate (ADP), resulting in superactivity of the mutant enzyme and consequently in increased PRPP content and availability for nucleotide synthesis. Erythrocyte PRPP content and availability were normal in the propositus' parents, his healthy brother and three sons, and they all had normal serum level and urinary excretion of uric acid, except for the mother who was hyperuricosuric. To further characterize this mutation we studied PRPP and purine metabolism in cultured fibroblasts of the affected family. PRPP synthetase in dialyzed lysates of fibroblasts from the propositus and his mother exhibited increased specific activity, more markedly at low inorganic phosphate concentration, and decreased sensitivity to inhibition by ADP and GDP, PRPP content and availability and the rate of de novo purine nucleotide synthesis were markedly increased in the fibroblasts of the propositus and to a lesser extent in the fibroblasts of his mother but were normal in the fibroblasts of the other family members investigated. The fibroblast studies demonstrate the following sequence of abnormalities: feedback-resistance of PRPP synthetase; superactivity of this enzyme in normal physiological milieu; increased availability of PRPP; and increased de novo synthesis of purine nucleotides. The pattern of inheritance of this disorder is compatible with both an X-linked recessive and autosomal dominant traits.

Adolescent↗
PubMed2006

Gout: new insights into an old disease.

Gout is an autoinflammatory disorder associated with deposition of monosodium urate (MSU) crystals in joints and periarticular tissues. Recent advances suggest that the innate immune system may drive the gouty inflammatory response to MSU. These findings prompt questions concerning how the innate immune system recognizes MSU and the identities of the receptors involved. In this issue of the JCI, Chen et al. show that the IL-1 receptor and its signaling protein myeloid differentiation primary response protein 88 (MyD88) but not the "classical" innate immune receptors, TLRs, are central for MSU-induced inflammation (see the related article beginning on page 2262).

Adaptor Proteins, Signal Transducing↗