Cases reported "Arthritis"

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1/112. Refractory arthropathy after intravesical bacillus Calmette-Guerin therapy. Usefulness of isoniazide.

    BACKGROUND: Arthritis associated with bacillus Calmette-Guerin immunotherapy usually responds dramatically to nonsteroidal antiinflammatory drug therapy. isoniazid is generally reserved for other complications such as granulomatous hepatitis. CASE-REPORT: A 73-year-old man was admitted for fever, arthritis of the knees and right temporomandibular joint, an inflammatory swelling over the left achilles tendon and bilateral conjunctivitis. The symptoms started in the wake of a course of intravesical bacillus Calmette-Guerin immunotherapy. Laboratory tests showed evidence of severe inflammation. Cultures of blood, urine and joint fluid specimens were negative, as were tests for autoantibodies and serologic tests for organisms known to cause reactive arthritis. Nonsteroidal antiinflammatory therapy was ineffective and glucocorticoid therapy produced only a partial response. All the symptoms resolved under isoniazid therapy in a dosage of 300 mg/day for three months. CONCLUSION: Use of antituberculous agents may be required in some cases of arthritis associated with bacillus Calmette-Guerin immunotherapy, most notably those with severe pyrexia.
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2/112. Systemic adverse effect of antithyroid drugs.

    Antithyroid drugs adverse effects are varied and rare. Autoimmune disorders (vasculitis, lupus erythematosus, polyarthritis...) are unusual and serious complications of antithyroid drugs. Since 1945, fewer than 100 cases of systemic manifestations related to antithyroid drugs have been reported in the literature, most frequently with propylthiouracil. The outcome is usually good after drug discontinuation, but some fatal cases have been reported. Because possible cross-sensitivity with other antithyroid drugs, the appropriate treatment for hyperthyroidism relapse if a patient has had an antithyroid drug adverse reaction, should be 131I-iodine or surgery. We report four new cases of systemic manifestations during propylthiouracil therapy.
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3/112. Polyarthritis as a complication of intravesical bacillus Calmette-Guerin immunotherapy for bladder cancer.

    bacillus Calmette-Guerin (BCG) is the most effective agent currently available for the treatment of superficial bladder cancer. However, this form of treatment is associated with some complications, including arthritis. In this report, we present a 69-year-old woman who developed inflammatory polyarthritis following BCG treatment for superficial bladder cancer. The arthritis resolved following treatment with a non-steroidal anti-inflammatory drug and chloroquinine.
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4/112. Pseudoporphyria associated with Relafen therapy.

    Various oral medications including nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with pseudoporphyria, although the pathogenetic basis has not been elucidated. A novel NSAID nabumetone (Relafen) has become popular because of its minimal gastrointestinal side effects. Its association with pseudoporphyria is not reported save for its listing in the Physician's Desk Reference (PDR) as a possible side effect. Biopsies of lesional skin from 4 patients manifesting blisters and erosions on the hands and face within 4 months of starting nabumetone were submitted for light microscopic and immunofluorescent (IF) studies. Histories and serology were obtained. Two patients had rheumatoid arthritis (RA), 1 had mixed connective tissue disease (MCTD), and 1 received diltiazem. All 4 had antinuclear antibodies. Characteristic clinical, light microscopic and IF features in the absence of elevated urine porphyrin levels confirmed a diagnosis of pseudoporphyria in all 4 patients. Biopsies in three patients showed features attributed to underlying connective tissue disease (CTD), including ectasia of the superficial vascular plexus, mild leukocytoclastic vasculitis, superficial and deep perivascular lymphocytic infiltrates with dermal mucinosis, granular deposition of IgM along the dermoepidermal junction indicative of a positive lupus band test, and of IgG and C5b-9 within keratinocytes. Nabumetone (Relafen) can provoke pseudoporphyria; an underlying CTD diathesis may be a predisposing factor.
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5/112. Drug-induced lung disease.

    Since there are no diagnostic studies to confirm the presence of a drug-induced lung reaction the physician will make a correct diagnosis only if he is aware of the drugs which have been identified to cause pulmonary reactions and their specific manifestations. Failure to recognize a drug-induced lung disease can lead to significant morbidity and in some cases mortality. The major drug-induced lung diseases are reviewed, the drugs being presented in the context of their clinical use and the reactions on the basis of common pathogenetic mechanisms.
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6/112. Remitting seronegative symmetrical synovitis with pitting edema (RS3PE syndrome).

    A 63-year-old man presented with acute symmetrical polysynovitis associated with pitting edema of both the hands and feet. He was seronegative for rheumatoid factor and no radiologically evident erosion was noted in the joints of his hands and feet. Evaluation excluded congestive heart failure, nephrotic syndrome, and hypothyroidism as the cause of edema. Treatment with nonsteroidal anti-inflammatory drugs and low-dose steroids induced complete remission. The clinical manifestations of this patients were consistent with those of a distinctive, although rare, form of arthritis called remitting seronegative symmetrical synovitis with pitting edema (RS3PE) syndrome. This syndrome has a good prognosis in elderly patients.
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7/112. Fatal fulminant hepatitis associated with bromfenac use.

    OBJECTIVE: To report a case of fulminant hepatic failure associated with the use of bromfenac, a new analog of the phenyl acetate class of nonsteroidal antiinflammatory drugs. CASE SUMMARY: A 60-year-old white woman with liver failure who had no known history of chronic liver disease was transferred to the liver transplant unit for evaluation. For three months preceding her illness, the patient was treated with bromfenac 25 mg po qid for arthritic pain. Prior to the initiation of bromfenac, her liver function test results were normal. Etiologic evaluation at presentation was unremarkable. The patient's condition continued to deteriorate, with the development of hepatic encephalopathy and worsening liver function test results while awaiting liver transplantation. Progressive hepatic and renal dysfunction along with respiratory decompensation ensued, and the patient died 48 days after initial presentation. CONCLUSIONS: Fulminant hepatic failure associated with the prolonged use of bromfenac appears to be an idiosyncratic response consistent with experience with other agents of its class. This case along with other cases of serious hepatotoxicity associated with the use of this agent ultimately resulted in bromfenac's removal from the market.
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8/112. Nimesulide-induced hepatitis and acute liver failure.

    BACKGROUND: Nimesulide is a relatively new non-steroidal anti-inflammatory drug that is gaining popularity in many countries because it is a selective cyclooxygenase 2 inhibitor. Occasionally, treatment is associated with mild elevation of liver enzymes, which return to normal upon discontinuation of the drug. Several cases of nimesulide-induced symptomatic hepatitis were also recently reported, but these patients all recovered. OBJECTIVES: To report the characteristics of liver injury induced by nimesulide. patients AND methods: We report retrospectively six patients, five of them females with a median age of 59 years, whose aminotransferase levels rose after they took nimesulide for joint pains. In all patients nimesulide was discontinued, laboratory tests for viral and autoimmune causes of hepatitis were performed, and sufficient follow-up was available. RESULTS: One patient remained asymptomatic. Four patients presented with symptoms, including fatigue, nausea and vomiting, which had developed several weeks after they began taking nimesulide (median 10 weeks, range 2-13). Hepatocellular injury was observed with median peak serum alanine aminotransferase 15 times the upper limit of normal (range 4-35), reversing to normal 2-4 months after discontinuation of the drug. The remaining patient developed symptoms, but continued taking the drug for another 2 weeks. She subsequently developed acute hepatic failure with encephalopathy and hepatorenal syndrome and died 6 weeks after hospitalization. In none of the cases did serological tests for hepatitis a, B and C, Epstein-Barr virus and cytomegalovirus, as well as autoimmune hepatitis reveal findings. CONCLUSIONS: Nimesulide may cause liver damage. The clinical presentation may vary from abnormal liver enzyme levels with no symptoms, to fatal hepatic failure. Therefore, monitoring liver enzymes after initiating therapy with nimesulide seems prudent.
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9/112. Cyclooxygenase-2 inhibitor celecoxib: a possible cause of gastropathy and hypoprothrombinemia.

    Gastrointestinal side effects from nonsteroidal anti-inflammatory drugs (NSAIDs) result mainly from inhibition of the enzyme cyclooxygenase (COX)-1; it is responsible for the synthesis of prostaglandin E2, which leads to increased mucosal blood flow, increased bicarbonate secretion, and mucus production, thus protecting the gastrointestinal mucosa. In inflammation, COX-2 is induced, causing synthesis of the prostaglandins in conditions such as osteoarthritis and rheumatoid arthritis. Two NSAIDs (celecoxib and rofecoxib) with very high specificity for COX-2 and virtually no activity against COX-1 at therapeutic doses have been approved for clinical use. In trials of celecoxib and rofecoxib, only 0.02% of patients had clinically significant gastrointestinal bleeding, compared to a 1% to 2% yearly incidence of severe gastrointestinal side effects with NSAIDs. Our patient had arthritis of the hips and chronic atrial fibrillation and was on warfarin therapy for stroke prevention; less than a week after starting celecoxib therapy, gastrointestinal bleeding and hypoprothrombinemia occurred.
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10/112. Nonsteroidal antiinflammatory drugs: benefits, risks, and COX-2 selectivity.

    Nonsteroidal antiinflammatory drugs (NSAIDs) are the most frequently prescribed class of medication for arthritis and other musculoskeletal disorders. NSAIDs block prostaglandin production, thereby reducing pain and inflammation, but may also cause significant side effects, particularly ulcers in stomach and duodenum. Some risk factors include age, previous history of ulcer, and high dose of NSAID. Synthetic prostaglandins, H2 blockers, and proton pump inhibitors have been employed to reduce risks with varying degrees of success. New NSAIDs that block only prostaglandins at sites of inflammation (COX-2 selective NSAIDs) may be significantly safer than traditional NSAIDs.
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