Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stress and allopurinol (ALL) were investigated in rats with regard to their influence on serum uric acid and glucose concentration, gastric secretion, microcirculation (MBF) and stress ulcer index. There is a non-competitive type of interaction between severe stress and ALL-mediated xanthine oxydase inhibition (= per cent fall in serum uric acid) as compared with control conditions (= mild stress). Vmax is different (84.6 +/- 1.9 and 92.3+/-2.26; P less than 0.05), but not Km (0.39 +/- 0.09 and 0.68 +/- 0.08 mg/kg/h ALL). Serum uric acid is higher in rats with draining gastric fistula than those with closed fistula suggesting that already mild stress is associated with an increase in uricemia in this species. ALL does not significantly alter gastric acid and uric acid secretion but improves markedly gastric ulcer index during mild and severe stress. Since MBF is significantly elevated by ALL during the latter circumstances, a dissociation between MBF and acid secretion is one feature of ALL actions and might become a primary aim in treatment of this disorder.
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PMID:Urate metabolism and gastric ulcerations in rats as influenced by stress and allopurinol. 56 51

Muscle phosphofructokinase (PFK) deficiency includes both clinically and genetically heterogeneous conditions. A 22-year-old man with muscle PFK deficiency due to previously unrecognized mutation was admitted because of gastric ulcer. He had noticed mild fatigability on vigorous exercise, but had never experienced painful cramps and myoglobinuria. His history included five time relapses of gastric ulcer and gouty arthritis at ages 19 and 21 years. His laboratory data showing impaired muscle glycolysis, increased hemolysis, and myogenic hyperuricemia had aspects in common with those reported for the classic form of this disease, except that lactate concentrations in his blood increased considerably after exercise. The mutant PFK enzyme of this patient, who was demonstrated to have a missense mutation, could exert some catalytic activity that permitted glycolytic flux in vivo, thus leading to the absence of typical myopathic symptoms. The association of relapsing gastric ulcer with muscle PFK deficiency was detected for the first time. There is a possibility that oxygen radical-induced tissue damage resulting from increased hypoxanthine on exertion plays a role in the pathogenesis of ulceration, since the patient is more tolerant to exercise than reported cases with the classic form of muscle PFK deficiency.
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PMID:A new variant case of muscle phosphofructokinase deficiency, coexisting with gastric ulcer, gouty arthritis, and increased hemolysis. 760 26

A 12-year-old girl, who had been diagnosed as having Cockayne syndrome (CS), was admitted for emaciation and dehydration. On admission the patient had mild chronic renal failure (glomerular filtration rate: GFR 50 mL/min) and hyperuricemia. After rehydration, allopurinol was commenced for her hyperuricemia. Then, her renal function rapidly deteriorated (GFR 20 mL/min) with enhancement of proximal tubular dysfunction and hypertension. A renal biopsy showed that the patient had acute tubulointerstitial nephritis (ATIN). Based on this diagnosis, allopurinol was stopped and prednisolone was started (2 mg/kg per day), following which the renal tubular function improved. However, the proteinuria intensified to become nephrotic syndrome. After 1 month the patient developed a gastric ulcer. Famotidine was commenced but GFR deteriorated and renal proximal tubular dysfunction re-occurred. The renal pathology was evaluated by referring to the previous reports of renal pathology in CS. It is suggested that rapid deterioration of the renal function in CS patients might be the result of ATIN. In addition, the present nephrotic syndrome seemed to be accompanied by ATIN, as in other reports.
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PMID:Cockayne syndrome with recurrent acute tubulointerstitial nephritis. 1704 Feb 91