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)

A marked cutaneous axonal dystrophy has been observed electronmicroscopically for the first time in the skin of three patients: (a) lesion of pityriasis lichenoides chronica in a patient with bronchogenic carcinoma, (b) non involved skin of a patient with malignant melanoma and (c) non involved skin of a patient with gout and retinal damage after prolonged use of chloroquine. The affected myelinated and non myelinated axons showed distinct alterations of mitochondria and multiple osmiophilic lamellated bodies (LK). These changes were interpreted as a (poly-)neuropathy, due to the influence of toxic systemic agents, such as malignant tumor and abuse of drugs. Chloroquine is known to induce neural damage. Moreover, some other compounds (ergotamine, ethaverine, analgetic preparations) may also be responsible for the drug-induced axonal dystrophy described in this study.
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PMID:[Tumor- and drug-induced cutaneous axonal dystrophy. An electronmicrocopy proof of multiple lamellated bodies]. 17 47

Although Charcot's disease and its association with diabetes have been described many times in the literature, it is still often misdiagnosed and incorrectly treated as osteomyelitis, arthritis, or gout. The best safeguard is a high index of suspicion. A warm, swollen foot in a diabetic patient with long-standing neuropathy without local or systemic signs of infection must be considered Charcot's disease until proven otherwise. The principal treatment is total abstinence from putting weight on the foot until warmth, swelling, and redness subside. Protective weight-bearing methods may then be slowly instituted.
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PMID:Charcot's disease in diabetic patients. Correct diagnosis can prevent progressive deformity. 200 Mar 50

Although colchicine has been used for centuries, its neuromuscular toxicity in humans is largely unrecognized. In this report we describe a characteristic syndrome of myopathy and neuropathy and present 12 new cases of the condition. Colchicine myopathy may occur in patients with gout who take customary doses of the drug but who have elevated plasma drug levels because of altered renal function. It usually presents with proximal weakness and always presents with elevation of serum creatine kinase; both features remit within three to four weeks after the drug is discontinued. The accompanying axonal polyneuropathy is mild and resolves slowly. Electromyography of proximal muscles shows a myopathy that is marked by abnormal spontaneous activity. Because of these features, colchicine myoneuropathy is usually misdiagnosed initially, either as probable polymyositis or as uremic neuropathy. The myopathy is vacuolar, marked by accumulation of lysosomes and autophagic vacuoles unrelated to necrosis or to the mild denervation in distal muscles. The morphologic changes in muscle suggest that the pathogenesis involves disruption of a microtubule-dependent cytoskeletal network that interacts with lysosomes. Correct diagnosis may save patients with this disorder from inappropriate therapy.
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PMID:Colchicine myopathy and neuropathy. 303 72

The possibility of bilateral femoral neuropathy after microsurgical tuboplasty for the reversal of sterilization is possible. There seems to be little awareness of this condition by gynecologists and fertility surgeons. This type of femoral neuropathy has an excellent prognosis and only physiotherapy is necessary to aid muscular function. Some cases have been reported where recovery has been extremely slow, normal functions had taken months, and some disability lasted years. The femoral nerve is not included in the pelvis, therefore injury through operative procedures are unlikely. The self-retaining retractors were used in all reported cases and verified through clinical experience. There are 2 types of injury to the femoral nerve: Direct pressure on the nerve itself by retractor blades, and impingement of the psoas muscle and the nerve against the lateral pelvic muscle. Factors that increase the possibility of this condition include diabetes mellitus, rheumatism, gout, alcoholism, malnutrition, syphilis, tuberculosis, typhoid fever, tetanus, liver abscesses, sepsis of distal parts of the body, polyarteritis nodosa, anticoagulants, and bleeding diseases. Femoral neuropathy has been observed after using self-retaining retractors such as O'Connor, O'Sullivan, Mann, Collin and Balfour. The preventive measures suggested are to use a retractor with appropriate blade depth.
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PMID:Bilateral femoral neuropathy after microsurgical reversal of tubal sterilization: case report and analysis of contributing factors. 362 33

One hundred and two consecutive patients receiving maintenance hemodialysis were interviewed and examined to analyze their musculoskeletal problems. Radiographic abnormalities of renal osteodystrophy were found in 23 and there were periarticular calcifications in 5. Only one patient had apatite associated knee arthritis and none had gout or calcium pyrophosphate deposition disease. Twenty patients had arthralgias, 3 polyarthritis, and 4 knee effusions all of which were incompletely explained. Correlations of arthralgias with radiographic findings was poor. Muscle cramps were seen in 24 patients, multiple fractures in one, symmetrical distal neuropathy in 18, and carpal tunnel syndrome in 9.
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PMID:Musculoskeletal manifestations in hemodialysis patients. 409 22

Entrapment neuropathy associated with gout is a rare occurrence. We report two cases of entrapment neuropathy of ulnar tunnel syndrome and carpal tunnel syndrome caused by gouty tophi. Problems related to its mechanism and treatment are discussed.
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PMID:Entrapment neuropathy caused by tophaceous gout. 651 73

The presented case concerns a 77-year old man who had been chronically taking colchicine for treatment of gout. He was admitted because of a transient ischemic cerebrovascular attack with motor aphasia and complained of preexisting paraesthesias in the lower extremities. Neurological examination revealed a global muscular weakness, absent myotatic reflexes and a diminished sensation. Serum creatine kinase (CK) levels were increased and electromyography showed spontaneous fibrillations in deltoid muscles, positive spikewaves in deltoids and anterior tibial muscles. Motor and sensory conduction velocities were mildly reduced. Nerve biopsy findings were compatible with a chronic axonal neuropathy having produced a significant loss of myelinated axons and also denervation features of unmyelinated axons. In muscle, combined neurogenic and myogenic features were found. The former result from the axonal neuropathy. The latter were mainly characterized by focal myofibrillar disorganisation and accumulation of autophagic vacuoles in muscle fibres. The presented neuromuscular symptoms and signs, the increased CK values, the electromyographic and nerve conduction velocity findings as well as nerve and muscle biopsy observations, are consistent with the diagnosis of colchicine-induced myopathy and neuropathy. Furthermore, the disappearance of paraesthesias, normalisation of CK values, and disappearance of fibrillations and positive spike waves in deltoid and anterior tibial muscles on electromyography, after stopping of the colchicine therapy, supported the diagnosis.
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PMID:Chronic colchicine-induced myopathy and neuropathy. 772 94

Colchicine has been widely used in the treatment of gout and familial mediterranean fever. Overdose is rare mostly in childhood. Colchicine overdose always causes gastrointestinal side effects, bone marrow depression and sometimes neuropathy. The mechanism of colchicine upon the microtubules, provides a better understanding of the pharmacology and also of the multiorgan involvement. We report the case of a ten year old child who ingested 0.6 mg/kg colchicine with a good outcome.
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PMID:[Colchicine poisoning apropos of a pediatric case]. 787 1

Colchicine causes both muscle and peripheral nerve toxicity of subacute onset in patients with renal insufficiency. We report three cardiac transplant recipients, treated with colchicine for cyclosporin A (CyA)-induced gout, who developed acute weakness due to colchicine myoneuropathy. The onset of disabling weakness occurred over a 1-2 week period. All three patients had concomitant renal insufficiency and an elevated serum creatine kinase and two elevated CyA levels at the time of presentation. Electromyography revealed features of myopathy and motor axonal neuropathy in all three patients. Two underwent muscle biopsy which confirmed the presence of sarcoplasmic vacuoles characteristic of colchicine-induced myopathy. All patients rapidly improved with either colchicine dose reduction or drug discontinuation. In conclusion, cardiac transplant recipients treated with CyA and colchicine may be at increased risk of developing colchicine-induced myoneuropathy especially in the setting of concurrent renal insufficiency. In patients with post-transplantation gouty arthritis, other treatment modalities are suggested; and if colchicine is administered, the dose should be reduced, CyA levels should be monitored closely and patients should be assessed for signs of neuromuscular toxicity.
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PMID:Acute onset of colchicine myoneuropathy in cardiac transplant recipients: case studies of three patients. 949 3

The main objective of the treatment of gout is to protect the major organs. Almost all gout patients require medication throughout their lives. Gout patients are asymptomatic during intercritical periods, even if they are not receiving antihyperuricemic drugs. Some patients, therefore, misinterpret that their gout is cured and may cease taking medication of their own accord. Thirty-two gout patients who had received continuous treatment with antihyperuricemic drugs for more than 3 months were selected. The sensation of heaviness was relieved by antihyperuricemic drugs in 14 (44%) of 32 patients. The heaviness did not exist or change in the other patients. Benzbromarone, probenecid, and allopurinol were found to be effective. The sensation of heaviness occurred after increased physical activity in 10 of 14 patients. Of 14 patients, 12 did not notice that the sensation of heaviness was relieved by antihyperuricemic drugs. Two hypotheses for the cause of heaviness are considered. One is mild gouty neuropathy, the other low-grade inflammation. A proper understanding that this symptom is relieved by antihyperuricemic drugs may serve as additional motivation for gout patients to take their medication regularly.
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PMID:Subjective sensation of heaviness in gout patients. 1092 May 75


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