Timothy M.E. DavisWichai SupanaranondSasithon PukrittayakameeSanjeev KrishnaR. Hart GillianJacky M. BurrinSomchai LooareesuwanNitatt VilaiwannaNicholas J. whiteMahidol UniversityJohn Radcliffe HospitalHammersmith HospitalPaholpolpayuhasena Hospital2018-06-142018-06-141990-01-01Transactions of the Royal Society of Tropical Medicine and Hygiene. Vol.84, No.3 (1990), 330-33518783503003592032-s2.0-0025324559https://repository.li.mahidol.ac.th/handle/20.500.14594/15975Abnormal thyroid function is strongly associated with mortality in severe non-thyroidal illness. We have assessed the pituitary-thyroid axis serially in 18 Thai adults with severe falciparum malaria and in 18 matched controls. The admission total serum thyroxine (T4) concentrations of the patients (median [range]: 64 nmol/litre [ < 30-91]) were significantly lower than those of controls (81 nmol/litre [61-133] ; 2P < 0·01), and remained depressed until alter fever and parasite clearance. Two patients who died in hospital had admission serum T4 concentrations < 35 nmol/litre. The admission basal serum thyrotropin (TSH) levels of the patients (0·9 mU/litre [ < 0·2-3·1]) were similar to those of controls (1·3 mU/litre [ < 0·2-3·7], 2P > 0·1) and remained normal throughout fever and parasitaemia. Thirty-minute TSH increments during a thyrotropin-releasing hormone test on admission were reduced in 13 patients with severe malaria (4·1 mU/litre [0·7-8·1]) relative to those in convalescence (7·1 mU/litre [1·7-14·4] , n = 10, 2P < 0·01) and controls (5·6 mU/litre [3·3-12·9], n = 9, 2P < 0·05). These findings suggest that thyrotroph and thyroid gland function are depressed during acute, severe malaria. As these changes may be an adaptation to accelerated catabolism, the role of thyroid replacement in such patients is uncertain. © 1990, Royal Society of Tropical Medicine and Hygiene. All rights reserved.Mahidol UniversityImmunology and MicrobiologyMedicineArticleSCOPUS10.1016/0035-9203(90)90305-X