Iodothyronine autoantibodies in two sisters.
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Biomedical subjects
Publications and source records attributed to J F Speed.
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We describe the clinical features of members of a family with an atypical form of thyroid hormone resistance syndrome, affecting thyroxine predominantly. Relevant diagnostic clinical and biochemical investigations are outlined and discussed.
We describe two siblings with artefactually increased results for free thyroxin in serum as measured with the Amerlex analog method, despite normal thyroxin transport. The cause of the artefact is identified as a variant albumin with enhanced affinity for the Amerlex thyroxin-analog.
The urine albumin/creatinine ratio was measured in random urine samples in a range of diabetic subjects as a guide to urinary albumin excretion rate in diabetic patients. In 74 control subjects the 95th percentile for the albumin/creatinine ratio was 1.3. In 39 diabetic patients the random urine albumin/creatinine ratio correlated highly with the 24 hour urine albumin excretion (r = 0.9371, p less than 0.001). In 337 insulin treated diabetic subjects 55% of the female and 39% of the male values exceeded 1.3. In 98 noninsulin treated diabetic subjects 67% of female and 62% of male values exceeded 1.3. Selecting albumin/creatinine ratios between 2.5 to 26.8 corresponding to albumin excretion rates between 20 mg and 250 mg/day, 26.1% of the insulin treated group were in this microalbuminuric range, and 8.7% had overt albuminuria. Higher figures were seen in the noninsulin treated group. Within these two large diabetic groups significant associations (p less than 0.005) were seen with glycaemia, blood pressure, body mass index, retinopathy and duration of diabetes. We believe that measurement of albumin/creatinine ratios on random urine samples offers a simple and convenient way of monitoring albumin excretion in large numbers of diabetic patients.
Adrenocortical function was assessed by the intravenous short synacthen test in 22 control subjects and 68 patients admitted to hospital with acute severe asthma. The cortisol increment was subnormal in 19 of the 68 asthmatics. This included 11 of the 14 patients on continuous oral steroids, seven of the 29 patients who had had occasional courses of oral steroids, one of the seven on inhaled steroids only, and none of the 18 who had had no steroids. Adrenal suppression was greatest in those patients taking oral steroids in divided daily doses. Nineteen of 43 patients were on or had taken oral steroids in this fashion. Of those 19 patients with low cortisol increments only one half had received supplementary steroids in the 24 hours preceding admission. Based on the synacthen test, serum DHEA-SO4 values were not a good discriminant of adrenocortical function. Adrenal insufficiency may be an important cause of death in acute severe asthma in New Zealand.
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Dehydroepiandrosterone sulphate (DHEA-SO4) values were measured as a guide to adrenal function in 72 asthmatic patients admitted to the Waikato Hospital with severe bronchospasm. In a reference sample 700 micrograms/l was taken as the lower limit of the reference range for DHEA-SO4 concentrations. All DHEA-SO4 values in 20 patients with known primary or secondary adrenal insufficiency were less than this value. In the asthmatic group, 10 of 14 DHEA-SO4 values were low in patients taking oral steroid therapy, eight of 23 values in patients taking inhaled steroids, and six of 29 values in patients on no known steroid therapy. Five of six patients who had been on oral steroids within a month of admission also had low values. In total 40% of all values were less than 700 micrograms/l. These data provide inferential evidence of possible adrenal suppression in a substantial number of patients requiring hospital admission for treatment of severe bronchospasm.
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