Indications
Syprine is indicated in the treatment of patients with Wilson’s disease who are intolerant of penicillamine. Clinical experience with Syprine is limited and alternate dosing regimens have not been well-characterized; all endpoints in determining an individual patient’s dose have not been well defined. Syprine and penicillamine cannot be considered interchangeable. Syprine should be used when continued treatment with penicillamine is no longer possible because of intolerable or life endangering side effects.
Unlike penicillamine, Syprine is not recommended in cystinuria or rheumatoid arthritis. The absence of a sulfhydryl moiety renders it incapable of binding cystine and, therefore, it is of no use in cystinuria. In 15 patients with rheumatoid arthritis, Syprine was reported not to be effective in improving any clinical or biochemical parameter after 12 weeks of treatment. Syprine is not indicated for treatment of biliary cirrhosis.
Contraindications
Hypersensitivity to this product.
Warnings and precautions
Patient experience with trientine hydrochloride is limited (see CLINICAL PHARMACOLOGY ). Patients receiving Syprine should remain under regular medical supervision throughout the period of drug administration. Patients (especially women) should be closely monitored for evidence of iron deficiency anemia.
Interactions
Drug Interactions In general, mineral supplements should not be given since they may block the absorption of Syprine. However, iron deficiency may develop, especially in children and menstruating or pregnant women, or as a result of the low copper diet recommended for Wilson’s disease. If necessary, iron may be given in short courses, but since iron and Syprine each inhibit absorption of the other, two hours should elapse between administration of Syprine and iron.
It is important that Syprine be taken on an empty stomach, at least one hour before meals or two hours after meals and at least one hour apart from any other drug, food, or milk. This permits maximum absorption and reduces the likelihood of inactivation of the drug by metal binding in the gastrointestinal tract.



