Hyperinsulinism in infants of diabetic mothers: suppression by somatostatin infusion.
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Biomedical subjects
Publications and source records attributed to P Brunelle.
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The usual values of serum IgE were determined by age group (at birth, 3--8 days, 9--45 days, 46--75 days and 76--105 days) in 80 infants under 4 months using the paper-radioimmuno-sorbent test (PRIST). There was a highly significant correlation between these values and the infants' age. Systematic search for specific anti-cow's milk IgE by a related technique (RAST) consistently gave negative results. The same techniques were used in 38 infants with clinical symptoms of intolerance to cow's milk. It would appear that these patients can be divided into two groups according to the presence of absence of extra-digestive symptoms. In the first group, there was a significant increase in total serum IgE, and the RAST was positive in 14 out of 17 patients. In the second group (21 infants), IgE levels were not increased and the RAST was always negative, which suggests that this type of intolerance is not reagin-mediated.
The low serum concentration of ADH requires extraction prior to assay. Various methods are compared (direct extraction by acetone, adsorption on talcum powder. Florisil, silicilic acid, Fuller's earth, QUSO, carbon-dextran, adsormone, then elution with hydrochloric acetone). The technic finally used was extraction with Florisil. The antibody used was commercially accessible. The separation of bound from free hormone required a second antibody fixed on Sephadex (DASP). The usual values found in 31 normal subjects from 22 to 89 years were: 7,4 . 4,1 pmol/l (M 2 sigma) 1 pmol/l = 1,08 pg/ml. These assays were carried out on tissue extracts prepared by mashing tumour fragments or lymph nodes removed from a patient with the Schwartz Bartter syndrome. They showed the existence in these tissues of high concentrations of ADH immunologically identical with that present in the serum of normal subjects.
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Changes in plasma adenosine 3'5' (cAMP) and guanosine (cGMP) monophosphate, measured by specific radioimmunoassay, after 150 USP/M2 of bovine parathyroid hormone (bPTH) iv administered were studied in children with pseudohypoparathyroidism, and idiopathic hypoparathyroidism, and in normal controls. Basal concentrations of plasma cAMP (17 nmole/1 +/- 1, 6 SEM) and cGMP (8,7 nmole/1 +/- 1, 3 SEM) were the same in all studied children. Plasma cAMP in normal and idiopathic hypoparathyroid children significantly (30-fold, P less than 0.001) and constantly rose with a peak value (537 nmole/1 +/- 210 SEM) observed 5--10 min after bPTH injection. By contrast, no significant change in plasma cAMP occurred in children with pseudohypoparathyroidism. The data confirmed further the unability of pseudohypoparathyroid children to increase cAMP after exogenous PTH, while the cGMP response did not appear to be significantly modified. It is suggested that an injection of 150 USP/m2 bPTH with plasma samples for cAMP assay taken before and 10 min after hormone administration represents a simplified assessment of Ellsworth-Howard's test.
16 premature infants with normal trophicity were studied during the 1st week of life using serum parathormone (IPTH) dosage and evaluation of renal tubule maturation by the effect of exogenous parathormone (PTE) on urinary elimination of 3':5'-cyclic adenosine monophosphate (cAMP). As of the 1st day, IPTH levels reached or surpassed those in the adult. Prematurity thus does not appear to influence parathormone response. Given the specificity of the dosage antiserum, it appears reasonable that the PTH detected is biologically active. After PTE, urinary elimination of cAMP does not appreciably increase until the 6th day, while still remaining much lower than adult levels. The lower the weight of the premature infant, the less intense the response of the kidney. It thus seems possible that the later development of renal parathormone receptor in the premature infant may be a factor responsible for neonatal hypocalcemia with hyperphosphatemia.
Eleven patients with primary hyperparathyroidism confirmed by histologic examination were subjected to a comparative study of the results of quantitative determination of parathormone and of quantitative bone biopsy. Quantitative radioimmunologic determination of parathormone was carried out with the aid of an N-terminal specific anti serum, while the histologic features studied were the periosteocytic and osteoclastic absorption surfaces. On the basis of a combination of the results of these two techniques, the diagnosis could be made in all the cases studied. A statistically significant correlation was observed between the results of quantitative determination of parathormone and those of histologic examination of the surfaces of periosteocytic lacunae (r = 0.63; p = 0.05).
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Biological abnormalities, in particular increased T3 and sometimes TSH, are frequently found in thyrotoxic patients treated with radioactive iodine and subsequently enthyroid. A high T3, associated with an increase in FT4 and a low TSH precedes a relapse. An increase in TSH may indicate progression towards hypothyroidism; even if FT4 and T3 levels are within normal limits. Caution must be exercised before affirming that an increased TSH with a high T3 and normal FT4 is indicative of thyroid equilibrium. At all events, the risk of hypothyroidism despite the use of small doses of radioactive iodine is such that the classical limit for the treatment of patients with thyrotoxicosis should be increased beyond the age of 40. In patients with a high TSH despite being clinically euthyroid, the use of thyroid extract in low dosage (50 mg/day) would appear to be desirable in avoiding the subsequent development of hypothyroidism.
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We propose a simplified assessment of response to parathyroid hormone which could replace the traditional Ellsworth Howard test for the differential diagnosis of pseudohypoparathyroidism in man. We have demonstrated that bovine parathyroid hormone in normal and hypoparathyroid subject increases plasma cAMP except in pseudohypoparathyroid subjects. It is an efficient, reliable method without any collection of urine samples.
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A radio-immunoassay method of parathyroid hormone in peripheral circulation is described utilizing both commercially available antibody and bovine PTH preparation for iodination. As a standard, the bovine PTH delivered from the Medical Research Council (MRC) is used. Antibody-bound hormone is separated from free hormone by solid phase immunoprecipitation. Good cross reactivity of this antiserum to human PTH is shown, but because of the lack of human standard, it is demonstrated, that results may be expressed in reference to the MRC bovine hormone. The coefficient of interassay variation is 12% and the detection limit is 300 pg/ml. In every healthy subject, immunoreactive PTH is detected: the normal distribution range (n equals 31) was 400 to 1800 pg/ml. Two hypoparathyroid patients have undetectable levels. There is a slight overlap between normal and those from hyperparathyroid patients. The present method gives results expressed in international units (MRC standard). The reliability of the PTH radio-immunoassay is dependent on the characteristics of the antiserum. This method provides a basis for the establishment of PTH values with the possibility of comparing results in health and disease.
The cross-reaction for hPTH radioimmunoassay and the multiple forms of hPTH circulating, pose several problems in interpreting results. This communication reports a sensitive radioimmunoassay for hPTH utilising a guineapig antiserum which is reactive with the amino-terminal region retaining biological activity, and which cross-reacts completely with hPTH, indicating levels of hPTH expressed as bovine PTH equivalent that would be correct.
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