Nerve biopsies were performed in four patients with suspected chloroquine induced neuromyopathy. Three of the patients were treated with high doses of chloroquine for connective tissue disease, while one patient was taking this drug as malaria prophylaxis. Morphological studies demonstrated the presence of segmental demyelination and remyelination in all cases. Cytoplasmic inclusions were observed in Schwann cells, in perineurial and endothelial cells, and in some interstitial cells. They were never observed within axons. Occasional curvilinear profiles were seen in perineurial and Schwann cells. Perineurial calcifications were observed in two cases. The results of this morphological study suggest that chloroquine neuropathy is essentially due primary involvement of Schwann cells.

Morphological study of peripheral nerve changes induced by chloroquine treatment.

Carbimazole is a common treatment for hyperthyroidism in the UK. Its main side effects include a rash, agranulocytosis and rarely a lupus-like syndrome. Although vasculitis associated with antineutrophil anticytoplasmic antibodies (ANCA) has been reported on several occasions following treatment with propylthiouracil, vasculitis with carbimazole appears to be less common. We report a case of leukocytoclastic vasculitis with carbimazole therapy accompanied by acute renal failure secondary to interstitial nephritis. Interstitial nephritis has previously been reported with propylthiouracil but not carbimazole.

Leukocytoclastic vasculitis and interstitial nephritis with carbimazole treatment

When symptoms of peripheral neuropathy appear, the possibility that they have been induced by drugs should be considered. A large number of drugs of all kinds, several of which are considered indispensable, have been implicated in peripheral neuropathy. A list of some of these drugs is provided. Neuropathy is a universal and dose-limiting factor during treatment with vinca alkaloids, but is otherwise a rare complication of drug therapy. Drug-induced peripheral neuropathy is almost always due to a dose-dependent primary axonal degeneration caused either by toxic reactions or by metabolic changes in neurons or their surroundings. The use of drugs should be restricted, especially in patients with a risk for development of neuropathy or with already existing neuropathy, e.g. patients with hepatic or renal failure, diabetes mellitus, or malnutrition. Patients should be given vitamins, prophylactically or therapeutically, which will sometimes allow a treatment to be continued. In other cases of drug-induced neuropathy the drug should be stopped. Reversal depends on the severity of the neuropathy, intensity and duration of the treatment and existence of causative cofactors, but generally the prognosis is good. While waiting for recovery physiotherapy is of importance, and when paraesthesia and pain are troublesome the patient should be treated with carbamazepine, imipramine or lidocaine (lignocaine).

Prevention and management of drug-induced peripheral neuropathy.

Increased CSF protein in chloroquine-induced axonal polyneuropathy and myopathy

Adverse reactions associated to anti-thyroid drugs include fever, rash, arthralgia, agranulocytosis and hepatitis that are thought to be hypersensitivity reactions. Five cases of pleural effusion associated to thionamides have also been reported, two with propylthiouracil and three with carbimazole. We report here a case of a 75-year-old man admitted because of unilateral pleural effusion. The patient had a recent diagnosis of hyperthyroidism and 6 days after starting methimazole complained of pleuritic chest pain. He had elevated C-reactive protein and erythrocyte sedimentation rate and normal white blood cell count and liver enzymes. Chest radiography showed a moderate right pleural effusion and the ultrasound revealed a loculated effusion that was shown to be an eosinophilic exudate. The temporal relationship between methimazole intake and the development of pleural effusion combined with the extensive exclusion of alternative causes, namely infectious, neoplastic and primary auto-immune diseases, led to the diagnosis of hypersensitivity reaction to methimazole. The thionamide was stopped and corticosteroid was started with complete resolution of the pleural effusion in 3 months. Awareness of this rare adverse reaction of anti-thyroid drugs is important and methimazole can be added to the list of possible etiologies of drug-induced eosinophilic pleural effusion.

/pdf/methimazole-associated-eosinophilic-pleural-effusion-a-case-2zlzwqbd7w.pdf

Methimazole associated eosinophilic pleural effusion: a case report

Polyneuropathy during treatment with carbimazole

Neuromyopathies à la chloroquine: 4 cas au cours d'une prophylaxie anti-paludéenne.

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Polyneuropathy during treatment with carbimazole

Neuromyopathies à la chloroquine: 4 cas au cours d'une prophylaxie anti-paludéenne.