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)

We report a case of colchicine-induced myopathy related to short-term, customary administration of colchicine. A 49-year-old male was admitted because of muscle weakness and myalgia that had developed 10 days previously. He had received renal transplantation 5 years previously and took cyclosporine as an immunosuppressant. Two weeks before admission, gout was developed and he took colchicine (1.2 mg b.i.d) by himself for three days. Colchicine-induced myopathy was clinically suspected, and colchicine intake was stopped immediately. After that, clinical symptoms gradually improved and serum muscle enzyme returned to normal. In this case, mild renal dysfunction and drug interaction between cyclosporine and colchicine wee suggested to be the precipitating factors of colchicine-induced myopathy.
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PMID:Acute myopathy induced by colchicine in a cyclosporine-treated renal transplant recipient--a case report and review of the literature. 917 24

When to suspect and thus investigate for inborn errors of purine and pyrimidine metabolism is a dilemma for even the most observant investigator. Often parents of affected children, or a history involving siblings, can provide valuable clues. The recognition of new purine and pyrimidine disorders requires skill and serendipity. But even identifying known disorders can prove difficult, since they cover a broad spectrum of illnesses, can have more than one symptom, or lead to early death. This problem is compounded by the fact that they are relatively recently described and therefore often little known, either in the clinic or laboratory. The considerable heterogeneity in clinical expression within families as well as between families means that asymptomatic homozygotes may not be recognized or can present at any time from early childhood through adolescence up to their eighth decade. Consequently, all siblings should be screened. These disorders should be suspected in any case of unexplained anaemia, failure to thrive, susceptibility to recurrent infection, or neurological deficits with no current diagnosis, including autism, cerebral palsy, delayed development, deafness, epilepsy, self-mutilation, muscle weakness, the inability to walk or talk, and-unusual in children and adolescents-gout, sometimes with renal disease. Some disorders present with radiolucent kidney stones, in acute or chronic renal failure, alone or with any of the above, or as an intolerance/sensitivity to therapy (e.g. 5-fluorouracil in malignancies or azathioprine immunosuppression in organ transplantation), often with life-threatening consequences. Several parameters need to be evaluated to ensure correct diagnosis. Pitfalls which can mask diagnosis using only a single test are renal failure, blood transfusion, diet or drugs.
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PMID:When to investigate for purine and pyrimidine disorders. Introduction and review of clinical and laboratory indications. 921 Nov 94

A 59-year-old man with chronic obstructive pulmonary disease (COPD), atrial fibrillation, and gout developed acute dyspnea, cough, and diffuse muscle aches and pains. He had commenced colchicine (0.6 mg b.i.d. p.o.), for the first time, one month earlier for recurrent gout attacks. Clinical examination revealed atrial fibrillation, an exacerbation of his pulmonary disease, tender muscles, especially calves, and diffuse muscle weakness. Laboratory results included creatinine phosphokinase 6961 U/l (1% MB), microscopic hematuria, myoglobinuria, elevated creatinine 1.6 mg/dl, and blood urea nitrogen 17 mg/dl. COPD and atrial fibrillation were treated and colchicine was discontinued. The patient made a full recovery. This 2nd reported case of colchicine induced rhabdomyolysis is the first reported in the treatment of gout.
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PMID:Colchicine induced rhabdomyolysis. 933 Sep 53

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 authors present a patient with a history of chronic lateral ankle instability and pain. Physical and diagnostic evaluation revealed anterior ankle instability and peroneus brevis weakness. An MRI showed an attenuated anterior-talofibular ligament and a longitudinal tear of the peroneus brevis tendon. Surgical exploration exhibited tophaceous gout within the tear of the peroneus brevis as well as within the attenuated anterior-talofibular ligament. Presented is an unusual case of a longitudinal tear of the peroneus brevis tendon with tophaceous gout infiltration.
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PMID:Peroneus brevis tendon rupture with tophaceous gout infiltration. 1055 50

An 82-year-old man developed progressive weakness of both legs 1 month prior to admission. He reported no previous history of trauma. Spine radiography revealed marked thoracic and lumbar spondylosis. Magnetic resonance imaging of the spine disclosed segmental stenosis with cord compression at T10-11 due to an extradural soft tissue lesion. Based on a diagnosis of thoracic spondylosis with cord compression, decompression laminectomy was performed. During the operation, fragile chalky-white material was noted over the epidural space, compressing the thoracic cord. The granular lesion was meticulously removed until the dura was identified and the cord was decompressed. Histologic examination of the surgical specimen revealed deposits of needle-like crystals that were consistent with monosodium urate, demonstrating that a gouty lesion of the thoracic spine had caused the cord compression. The patient had previously experienced several attacks of gouty arthritis of his feet. The postoperative serum uric acid concentration was 8.5 mg/dL. After surgery, he was treated with benzbromarone 100 mg per day. He was able to walk 3 months after the operation. A high index of suspicion of gouty involvement of the spine is necessary in patients with gout. Surgical decompression followed by regular administration of antigout drugs can provide satisfactory results.
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PMID:Thoracic cord compression due to gout: a case report and literature review. 1092 70

A 28-year-old man with a 5-year history of gouty arthritis suffered from an acute episode of lower back pain. He visited a rehabilitative clinic and received physical therapy following his examination. Weakness and numbness of both lower legs developed rapidly after physical therapy. He was sent to our hospital with complete paralysis of both lower limbs and complete sensory loss below the umbilicus 3 hours after the physical therapy. No peripheral tophi were found. Myelography showed an extrinsic compression of the dura sac at T10. Emergency decompressive laminectomy of T9 to T11 was performed. During the surgery, caseous material was found deposited in the ligamentum flavum and the left T9 to T10 facet joint, with indentation of the dura sac. The pathologic diagnosis was spinal tophi. After surgery, the patient's neurologic function recovered rapidly. It was suspected that inappropriate physical therapy might have aggravated acute inflammation of spinal gout and resulted in a rapid deterioration of neurologic function. Though gout is a chronic medical disease, an acute attack of spinal gout may be disastrous and requires emergency neurosurgical intervention.
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PMID:Acute paraplegia in a patient with spinal tophi: a case report. 1139 17

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

Colchicine is widely employed for the treatment of gout in renal transplant patients where NSAIDs are contra-indicated and allopurinol prophylaxis is often avoided due to concomitant azathioprine immunosuppression. We report here a case of colchicine-induced myoneuropathy in a renal transplant recipient. Our patient had myalgia, muscle weakness, elevated creatine kinase levels, myopathic changes on electromyography and peripheral neuropathy. Withdrawal of colchicine resulted in recovery within 4 weeks. Renal transplant recipients are likely to be at greater risk of colchicine-induced myoneuropathy due to the unique concurrence of risk factors predisposing to toxicity in such patients. These risk factors include the high incidence of gout in this population, widespread use of colchicine as first-line therapy, impaired renal function and concomitant cyclosporin treatment. The diagnosis should be considered in any renal transplant recipient receiving the drug who develops myopathy. Prompt withdrawal of colchicine therapy should result in rapid clinical and biochemical improvement.
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PMID:Colchicine myoneuropathy in a renal transplant patient. 1212 15

Colchicine and 3-hydroxy-3-methy-glutaryl coenzyme A (HMG-CoA) reductase inhibitors are well known to cause myopathy. Myotoxicity is dose-dependent in both drugs; therefore, the onset of symptoms usually takes months or years. We report the case of a patient with chronic renal failure who had been taking simvastatin for 2 years and developed acute weakness 2 weeks after the start of treatment with colchicines for recurrent gout. The electromyography and elevated muscle enzymes indicated that his symptoms were caused by myopathy. When this patient stopped taking both drugs, his weakness resolved rapidly. Acute myopathy induced by combination therapy with colchicines and simvastatin is rare. In patients with chronic renal failure, co-administration of colchicine with simvastatin may accelerate the onset of myopathy because CYP3A4 (part of cytochrome P450) is crucial in the breakdown of both drugs. When adding colchicine to a medication regimen that includes a HMG-CoA reductase inhibitor for patients with renal insufficiency, drugs that are metabolized outside the CYP3A4 system (e.g., fluvastatin and pravastatin) should be selected instead.
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PMID:Colchicine-induced acute myopathy in a patient with concomitant use of simvastatin. 1241 59


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