Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report the second case of a female with typical Lesch-Nyhan syndrome. She exhibited athetoid movement, self-multilation, mental retardation and spasticity. Laboratory investigations revealed hyperuricaemia, hyperuricosuria and decreased erythrocyte hypoxanthine guanine phosphoribosyl transferase activity. She has normal female external genitalia and karyotype. Her parents are non-consanguineous and there is no family member with gout, nephropathy or any psychoneurological disorder. To prevent self-stimulation, it was necessary to fix the patient's upper extremities to the backrest of her wheelchair. The authors also describe an apparatus that limits elbow flexion.
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PMID:A female patient with Lesch-Nyhan syndrome. 161 15

We performed renal transplantation on 67 patients (living 37, cadaver 30) between November 1975 and December 1987. Twenty-seven of the 67 patients had hyperuricemia (serum uric acid: male greater than or equal to 8.0 mg/dl, female greater than or equal to 7.0 mg/dl) and 2 of them had episodes of gout. However, there was no correlation between serum creatinine and uric acid in 27 hyperuricemic patients. Twelve of 27 hyperuricemic patients were treated with either allopurinol or benzbromarone. These therapies were effective for 9 of them and serum uric acid level controlled well. One of 2 gouty patients developed gout 4 years after cadaveric renal transplantation. She was treated with anodyne and benzbromarone for gout. These treatments were effective and she has been in good condition. We consider it necessary to treat hyperuricemia after renal transplantation and to control serum uric acid well.
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PMID:[Clinical studies on hyperuricemia and gout after transplantation]. 223 90

We report a case of calcium oxalate arthropathy in a woman undergoing intermittent peritoneal dialysis who was not receiving pharmacologic doses of ascorbic acid. She developed acute arthritis, with calcium oxalate crystals in Heberden's and Bouchard's nodes, a phenomenon previously described in gout. Intermittent peritoneal dialysis may be less efficient than hemodialysis in clearing oxalate, and physicians should now consider calcium oxalate-associated arthritis in patients undergoing peritoneal dialysis who are not receiving large doses of ascorbic acid.
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PMID:Arthritis associated with calcium oxalate crystals in an anephric patient treated with peritoneal dialysis. 340 40

An elderly female presented with a systemic febrile illness and acute polyarthritis as the first manifestation of gout. She improved dramatically with anti-inflammatory therapy.
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PMID:An unusual systemic presentation of gout. 1122 28

Colchicine, a microtubule polymerization inhibitor, can very occasionally induce myopathy. We report two cases of colchicine myopathy. Both patients presented with myalgia and proximal muscle weakness. The first patient, an 80-year-old woman, had chronic renal failure related to renal amyloidosis. She had been treated by colchicine for 4 months. The second, a 75-year-old man with normal renal function, suffering from gout, was treated by colchicine for 3 weeks. Muscle biopsies displayed the same alterations, but the degree of severity was different. Conventional histology revealed vacuolar changes characterized by acid phosphatase-positive vacuoles and myofibrillar disarray foci. The lesions were selective for type I fibers. Ultrastructural study demonstrated autophagic vacuoles. Most of the vacuoles expressed dystrophin but not merosin. Several fibers reacted with anti-MHC class I antibody and granular deposits of membrane attack complex were observed on the surface of numerous myofibers. Anti-alphaB-crystallin antibody strongly reacted with vacuolar content. Physiopathologically, microtubules are primordial for vesicle movements and colchicine induces autophagic vacuole accumulation by preventing their fusion with lysosomes. The selective type I involvement is probably due to the higher tubulin amount in type I fibers. AlphaB-crystallin overexpression is related to its microtubule protection properties. Moreover, we suggest that vacuoles randomly floating in sarcoplasm might occasionally meet the plasma membrane and open in the extracellular space, leading to complement activation. Accurate diagnosis of colchicine myopathy is relevant because the treatment is based on colchicine interruption.
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PMID:Colchicine myopathy: a vacuolar myopathy with selective type I muscle fiber involvement. An immunohistochemical and electron microscopic study of two cases. 1181 Jan 74

Pustular drug eruptions are uncommon and usually present with an acute illness. A 75-year-old-woman presented with a widespread pruritic pustular erythematous skin rash. She was otherwise well and had been commenced on allopurinol for gout 3 weeks before developing the rash. A skin biopsy was consistent with a pustular drug eruption, with features of acute generalized exanthematous pustulosis (AGEP). Allopurinol was the probable causative agent and withdrawal resulted in resolution of her eruption within 6 weeks. A diagnosis of AGEP was considered; however, this patient did not fulfil the diagnostic criteria.
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PMID:Allopurinol-induced pustular eruption: an unusually mild case. 1198 73

Two of our patients experienced myotoxicity associated with colchicine administration. The first was a 54-year-old woman who was receiving dialysis and came to the emergency department with progressive generalized weakness and vomiting. She recently had taken colchicine for the treatment of gout. Physical examination revealed proximal muscle weakness and tenderness on palpation. Her creatine kinase (CK), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were elevated at 7185, 563, and 541 U/L, respectively. Drug-induced myopathy was suspected and colchicine was discontinued. The patient was discharged after symptom resolution 1 week later. The second patient was an 83-year-old woman with chronic renal insufficiency who came to the hospital with anorexia, diarrhea, and inability to get out of bed due to progressive weakness. Her colchicine dosage recently had been increased for gout management. Physical examination revealed generalized muscle weakness and tenderness on palpation. Her CK, ALT, and AST levels were elevated at 1797, 147, and 172 U/L, respectively. Electromyographic results were consistent with colchicine myopathy. The patient was discharged with minimal residual muscle weakness 1 week after discontinuation of colchicine. A literature search identified 82 documented cases of colchicine-induced myotoxicity. Most patients had a history of proximal weakness and pain with elevated CK, ALT, and AST levels. Onset of symptoms generally occurred days to weeks after initial administration of colchicine at the usual dosage in patients with renal impairment or a change in underlying disease state in those receiving long-term therapy. Muscle toxicity was not necessarily accompanied by gastrointestinal symptoms. Concomitantly administered drugs often were cyclosporine or corticosteroids. Diagnosis may be confirmed by electromyography or muscle biopsy. Colchicine-induced myotoxicity is a rare adverse effect but is well described in the literature. Clinicians should recognize that renal impairment is the primary risk factor for development of colchicine-induced myotoxicity, and that dosage adjustment or alternative therapy may be required.
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PMID:Colchicine myotoxicity: case reports and literature review. 1558 44

An 89-year-old woman was admitted for high fever and debilitating pelvic pain, notably in the pubic area. Physical examination revealed multiple gouty tophi in her hands and feet. Laboratory investigation revealed severe leukocytosis and a sharply increased C-reactive protein level. The patient was treated with broad-spectrum antibiotics in view of the possibility of a serious bacterial infection, but there was no clinical effect. CT of the pelvis revealed an osteolytic process and a mass anterior to the pubic symphysis. Histological investigation of a biopsy revealed an inflammatory infiltrate with signs of gout. Culture of the biopsy specimen was negative. The diagnosis was confirmed by the finding ofneedle-like urate crystals under the polarizing microscope. After treatment with colchicine and later with prednisone, the symptoms disappeared. She was given uric acid-lowering therapy with allopurinol as a preventive measure.
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PMID:[Gout as an unusual cause of pelvic pain]. 1646 19

Poisoning by colchicine may occur following ingestion of this alkaloid used for the treatment of acute gouty arthritis. The authors report two fatalities and describe a liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS-MS) triple-quadrupole method for the determination of colchicine in autopsy samples. One milliliter of heart blood, femoral blood, urine, bile, gastric, and vitreous each were extracted with saturated NH4Cl at pH 9.6 and dichloromethane/5% isopropanol. Separation was achieved on a C18-Xterra column with a mobile phase consisting of 2 mM ammonium formate buffer (pH 3)/acetonitrile in a gradient mode. Four product ions of the protonated molecule were monitored. The method was fully validated in whole blood (1 mL) and was linear in the range of 0.5-50 ng/mL (r2>0.99). The limit of detection was 0.1 ng/mL (50 times S/N), and the limit of quantitation was 0.5 ng/mL with RSDs<11.8% intraday (n=6), <18.7% interday (n=18), and accuracy<3% (n=18). Case #1: a 33-year-old nurse committed suicide by the ingestion of 80 colchicine 1-mg tablets. She died 61 h later after resuscitation procedures. Colchicine was found in heart blood at 5.2 ng/mL, femoral blood at 17.4 ng/mL, urine at 19.4 ng/mL, bile at 42.8 ng/mL, gastric at 348 ng/mL, and vitreous at 3 ng/mL. Case #2: a 57-year-old man with gout was found dead at home. Colchicine was found in heart blood at 22.8 ng/mL, femoral blood at 21.9 ng/mL, lung blood at 45.2 ng/mL, urine at 148.5 ng/mL, bile at 1818.5 ng/mL, gastric at 219.8 ng/mL, and vitreous at 0.5 ng/mL. These results were consistent with death. Because of its good sensitivity, this LC-ESI-MS-MS triple-quadrupole method is suitable for the determination of colchicine not only in fatalities but also for pharmacokinetic studies.
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PMID:Liquid chromatography-tandem mass spectrometry for the determination of colchicine in postmortem body fluids. Case report of two fatalities and review of the literature. 1713 57

We report a case of tophaceous gout in a 32-year-old woman who had suffered from anorexia nervosa since the age of 15. She had been taking a diuretic, mainly furosemide, to lose weight since she was 18. She was referred for orthopedic surgery because of a tophus at her right metatarsophalangeal joint. Because of a discharging sinus associated with the tophaceous deposits, surgery was performed. Use of the diuretic was stopped after surgery and the serum uric acid concentration returned to normal. It was thought that long-term abuse of a diuretic induced the tophaceous gout in this premenopausal woman.
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PMID:A case of female premenopausal tophaceous gout requiring surgical management. 1714 97


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