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Plasma levels of nitric oxide products and endothelin in pulmonary hypertension with congenital heart disease

bral degeneration, severe seizures, psychomotor retardation and lens dislocation, and biochemically by increased quantities of sulphite, S-sulphocysteine, taurine and thiosulphate in urine, with cysteine being low, in the presence of normal serum urate. Xanthine dehydrogenase functions in the degradation of purines, isolated deficiency of which results in calculi in kidney and xanthine deposits in muscle, xanthinuria and hypouricaemia with no clinical symptoms (2, 3). In our patient, who exhibited the combination of some clinical and laboratory features of both enzymes, we showed deficient sulphite oxidase activity in cultured skin fibroblasts. A very low serum uric acid level indicated xanthine dehydrogenase deficiency, albeit indirectly (4). In MCD, no therapeutic attempts have been successful in reversing the clinical symptoms. Although the prognosis of MCD is unfavourable, correct diagnosis is still essential, when the availability of the prenatal diagnosis, by demonstrating sulphite oxidase deficiency in the chorionic villus samples or increased S-sulphocysteine in amniotic fluid, is considered (5, 6). Therefore, blood uric acid measurement should be included in the battery of tests to be performed in all refractory neonatal seizures.