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)

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

This article reviews, through illustrative cases, five rheumatic diseases associated with drug treatments: statins and myopathy, quinolones and tendinopathy, viscosupplementation and pseudoseptic arthritis, diuretics and gout, barbiturates and adhesive capsulitis. Due to the rarity of such cases, we lack validated therapeutic recommendations. Announcement to the adverse drug reaction reporting system is the best way to enhance our knowledge and to improve the public health.
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PMID:[Iatrogenic rheumatic diseases]. 1555 49

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

We report a fatal case of toxic myopathy in a patient with a transplanted heart for severe ischemic coronary artery disease. He was on long-term cyclosporine, prednisone, and mycofenolate. Four months before the development of proximal muscle weakness, his simvastatin dose was doubled, and he was also started on colchicine for acute exacerbation of gout. He developed progressive muscle weakness leading to shortness of breath and hospitalization for respiratory failure. Colchicine and simvastatin were stopped on admission. He received high-dose methylprednisolone for continued muscle weakness while he was sedated with propofol. These changes led to a marked elevation of creatine kinase, peaking at 33,580 U/ml. The muscle biopsy revealed toxic vacuolization, mitochondrial damage, and no evidence of inflammation. Based on the timing of events, the combination of propofol, high-dose methylprednisolone, and cyclosporine have triggered rhabdomyolysis, which may have been facilitated by prior administration of colchicine and simvastatin.
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PMID:Fatal toxic myopathy attributed to propofol, methylprednisolone, and cyclosporine after prior exposure to colchicine and simvastatin. 1762 39

Colchicine myopathy can complicate standard treatment of gout, especially in those patients with underlying renal insufficiency. The symptoms of this disorder are frequently insidious, and the diagnostic tests used in its evaluation are mostly nonspecific. It is important to be aware of this entity, as the discontinuation of colchicine will allow a prompt remission. Definitive diagnosis usually requires histologic examination where a characteristic vacuolar myopathy is typically present. Magnetic resonance imaging can be useful in the localization of optimal biopsy sites, although its use as a diagnostic modality in these patients is speculative.
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PMID:Colchicine neuromyopathy. 1907 54

(1) Renal failure, either pre-existing or induced by a nephrotoxic drug, increases the risk of adverse effects in patients taking colchicine; (2) Combining colchicines with a macrolide (except for spiramycin) carries a risk of life-threatening pancytopenia; (3) Ciclosporin co-administration can aggravate the neuromuscular adverse effects of colchicine; (4) Combining colchicine with lipid-lowering drugs (statins and fibrates) can cause myopathy; (5) Several mechanisms have been implicated: competition for cytochrome P450 or P-glycoprotein, additive adverse effects (especially on muscle), and colchicine accumulation due to a reduction in its renal excretion; (6) Patients with gout should use colchicine only after failure of symptomatic treatment: ice application, paracetamol, and possibly ibuprofen, a nonsteroidal antiinflammatory drug with well-documented adverse effects; (7) If colchicine is nevertheless used, it should be at the minimum effective dose. Close clinical monitoring is required in order to detect early signs of adverse effects, especially diarrhoea, the earliest sign in patients with renal failure and in the elderly.
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PMID:Colchicine: serious interactions. 1949 85

A 67-year old man was hospitalized due to an aorto-coronary bypass and cecal perforation. After administration of atorvastatin, amiodarone, and fluconazole, rhabdomyolysis developed with electrolyte disturbances (hyperphosphatemia, hyopcalcemia) and a massive increase in creatine kinase and myoglobin. In the clinical course, other complications manifested such as acute renal failure, critical illness myopathy, acute gout on the knee, and sternal infection with coagulase-negative staphylococci. After stopping the assumed causal agents and treating the complications, the patient could be transferred for rehabilitation after a more than two months hospital stay. We discuss the causes and symptoms of muscle diseases as well as the epidemiology, mechanisms, treatment, and prevention of drug-induced myopathies with a focus on statins.
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PMID:[Rhabdomyolysis associated with atorvastatin combined with amiodarone and fluconazole]. 2136 57

Parathyroid dysfunction, leading to severe clinical symptoms and radiographic changes, has decreased over the last years due to routine laboratory checks including serum calcium levels. Thus, abnormal calcium levels are detected early in the course of the disease and the underlying cause treated accordingly. Hyperparathyroidism often leads to osteoporosis and low-trauma fractures. When evaluating secondary osteoporosis analysis of calcium, phosphate and intact parathyroid hormone levels are mandatory. Osteitis fibrosa cystica and brown tumors are less frequent findings of hyperparathyroidism. However, in patients with arthritis or bone symptoms, hyperparathyroidism has to be evaluated as a possible reason. Other manifestations of hyperparathyroidism include myopathy, tendon ruptures and unspecific symptoms of the muscles and skeleton. Gout as well as pseudogout may be associated with hyperparathyroidism. Hypoparathyroidism may cause musculoskeletal diseases mimicking ankylosing spondylitis or diffuse idiopathic skeletal hyperostosis. Myopathies are sometimes induced by hypoparathyroidism. An association between systemic lupus erythematosus and hypoparathyroidism seems to exist.
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PMID:[Parathyroid dysfunction and rheumatic manifestations]. 2198 74


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