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T J Wilkin

Publications and source records attributed to T J Wilkin.

At least 19 recordsLinked to original sources
PubMed1992

Poor growth in school entrants as an index of organic disease: the Wessex growth study.

OBJECTIVE: To establish whether poor height or height velocity, assessed during the year of school entry, might identify children with previously undiagnosed organic disease. DESIGN: Observation of a total population and their case controls. SETTING: Community base. SUBJECTS: All 14,346 children in two health districts entering school during two consecutive years were screened for height by school nurses, and those whose height lay below the 3rd centile according to Tanner and Whitehouse standards (n = 180) were identified. After excluding 32 with known organic disease, five from ethnic minorities, and three who refused to take part, the remaining 140 short normal children were matched with 140 age and sex matched controls of average height (10th-90th centile) and their height velocities over 12 months measured. MAIN OUTCOME MEASURES: Height, height velocity, previously diagnosed organic disease, and organic disease diagnosed as a result of blood tests and specialist examination. RESULTS: Twenty five of the 180 short children (14%) were already known to have chronic organic disease which could explain their poor growth. Blood tests and specialist examination revealed a further seven with organic disease, which was acquired rather than congenital in three, and a second cause of short stature in one with known organic disease. These eight conditions had been missed at the school entry medical examination. The shorter the child, the more likely an underlying organic disorder, with seven of the 12 children whose heights were more than 3 standard deviations below the mean having some organic disease. Height velocity measured over 12 months, however, did not distinguish short normal children from those with disease or from their matched controls. CONCLUSIONS: Height, but not height velocity, is a useful index for identifying unrecognised organic disease at school entry. The shorter the stature the greater the prevalence of organic disease. The frequency of newly diagnosed remediable disease in this study (1 in 3-4000) is similar to that of neonatal hypothyroidism, which is routinely screened for. Routine investigation of all very short school entrants is recommended.

Body Height↗
PubMed1992

Expression of an islet regenerating (reg) gene in isolated rat islets: effects of nutrient and non-nutrient growth factors.

The expression of a novel regenerating (reg) gene has been reported previously in the regenerating islets of a surgical model of diabetes in rats. We exposed collagenase-isolated rat islets for three days to nutrient and non-nutrient growth factors in minimally supplemented RPMI medium (2.7 mmol/l glucose, 2% fetal calf serum), and investigated the relationship between reg gene expression and islet cell replication. RNA was prepared from half of the islets by homogenisation in guanidinium isothiocyanate followed by phenol/chloroform extraction. Northern/dot blot analyses were used to semi-quantify reg mRNA. Islet cell replication was estimated by culturing the remaining islets in radiolabelled thymidine to determine de novo DNA synthesis. Thymidine uptake was stimulated by the following factors: 11 mmol/l glucose (50% increase); 10% amino acids (126% increase); 10% fetal calf serum (39% increase); 100 ng/ml insulin (45% increase); 250 ng/ml growth hormone (65% increase); 1.5 nmol/l aldosterone (29% increase); 2 U/ml platelet derived growth factor (116% increase). The results are expressed as a percentage of the thymidine incorporated into control islets cultured in minimal RPMI (1118 +/- 100 (SD) cpm/microgram protein, n = 15). Increased islet cell replication was paralleled in each case by a clear rise in reg mRNA expression compared to controls. Furthermore, the rank order for reg gene expression was the same as that for thymidine uptake (r = 0.90). The present findings suggest a clear association between reg gene expression and islet cell replication in vitro, and are the first to demonstrate reg gene expression in response to individual growth factors.

Aldosterone↗
PubMed1992

Autoantibodies to endogenous growth hormone in short children (the Wessex Growth Study).

Small stature is associated with low growth hormone secretion, but in most cases the reason is unknown. The commonest cause of hormone insufficiency is autoimmunity, and autoantibodies to hormones are often found where there is autoimmune disease of the corresponding gland. Displaceable growth hormone binding by the sera of 125 short (< 3rd centile) but otherwise normal school entrants was significantly higher (P < 0.05) than by the sera of 100 age-matched children of normal height (10th-90th centile), and binding in 21 (17%) of the small children exceeded the upper limit of 95% of the normal population. Furthermore, urinary growth hormone excretion was significantly lower in the small children (total overnight output 0.6-1.7 ng) compared with controls (1.5-3.7 ng) (P < 0.05) even when corrected for body surface area. Thus, growth hormone binding and growth hormone excretion discriminated between two groups of children selected only on the basis of height. The assay used for growth hormone binding was specific for IgG, suggesting that the binding factor was antibody. Autoimmunity merits further investigation as a basis for poor growth.

Autoantibodies↗
PubMed1979

Short-term triiodothyronine in prevention of temporary hypothyroidism after subtotal thyroidectomy for Graves' disease.

To determine whether short-term thyroid hormone replacement prevents or merely delays temporary hypothyroidism after surgery for Graves' disease, serum T3, thyroid-stimulating hormone, and T4 were measured every 2 months for 18 months in two groups of Graves' disease patients who had had subtotal thyroidectomy. Group I (18 patients) were given T3 20 microgram four times daily from surgery through the twelfth postoperative month. Group II (18 patients) received no treatment. Hypothyroidism occurred at some time during the 18-month period in 10 group-II patients, but was temporary in 7. Temporary hypothyroidism did not occur in group-I patients, whose mean T4 level rose to that in group II within 2 months of T3 withdrawal. Short-term T3 replacement after surgery for Graves' disease thus prevents (and does not simply delay) temporary postoperative hypothyroidism without increasing the frequency of permanent hypothyroidism.

Adult↗
PubMed1979

The behaviour of the thyroidal iodide trap after subtotal thyroidectomy for thyrotoxicosis and its implication for the T3-suppression test.

It is important to distinguish between symptomatic response and immunological cure in thyrotoxicosis because it has been suggested that surgery, in addition to providing a rapid symptomatic response, may also cause the disappearance of thyroid-stimulating antibodies. The evidence, however, is based largely on suppression tests which we argue may not be valid in the post-operative period. Seventy thyrotoxicosis patients were treated for 6 months with a standard course of carbimazole and T3, at the end of which each patient was classified as suppressor (S) or non-suppressor (NS) according to the fall in radioiodine uptake. Group I (18 patients) and group II (18 patients) were then randomly selected for immediate surgery while group III (34 patients) continued on antithyroid drugs. All groups were reviewed every two months from the 6th month for 12 months, during which time group I was drug-free and groups II and III received T3. Twenty-min iodide uptakes were performed in all patients at each visit to compare the serial changes in mean iodide trapping capacity between treatment groups. Despite 10-fold differences in TSH levels between groups I and II, and irrespective of suppressibility before surgery, the mean uptakes in both these groups remained basal (less than 4%) throughout the period of study, while the serial mean uptakes in group III S (no TSH, by implication no TSAB, but intact iodide trap) were consistently higher than those of group I NS (high TSH, by implication TSAB as well, but reduced iodide trap size). The data points to an absence of dose-responsiveness between TSH and the surgical-remnant's iodide trap, implying that post-thyroidectomy suppression tests (at least during the first year) cannot measure changes in iodide trapping, and therefore do not measure the same phenomenon after subtotal thyroidectomy as they do before operation when the thyroid is intact. We therefore question the validity of comparing suppressibility before and after surgery and basing the frequency of surgical cure on the result.

Adult↗
PubMed1979

The TRG Test. Which is the best index of TSH release?.

Prolonged (two hours) TRH tests were performed on 29 controls and 182 thyrotoxicosis patients of varying thyroid status after treatment with radioiodine. The object was to find which of the simple measurements of TSH from the TRH test most faithfully reflected the total amount of TSH (TTSH) released in response to the TRH. The simple indices compared were the absolute levels of TSH (ATSH) achieved at intervals during the test, and the increments in TSH (delta TSH) recorded at the same points in time. TTSH was measured by planimetry of the area beneath the response curve. Patients were classified as normo-responders, hyper-responders or hypo-responders according to normal limits for TTSH deduced from the controls. When each simple index of TSH response was substituted in turn for TTSH, the overall frequency of misclassification was considerably greater for ATSH than for delta TSH. This was largely due to the wide variability of passive or basal TSH secretion, which seriously confused the distinction between normally-responsive and hypo-responsive patients when ATSH was used. The delta TSH measured at 30 minutes gave the best overall results in terms of least classification error and closest correlation with TTSH.

Adult↗
PubMed1977

High TSH concentrations in "euthyroidism": explanation based on control-loop theory.

High concentrations of thyroid-stimulating hormone (TSH) in the serum have often been reported in apparently euthyroid patients with damaged thyroids. We have confirmed this finding in 14 patients 18 months after subtotal thyroidectomy for Graves's disease (group 1) and in 14 patients with manic-depressive psychosis (group 2) receiving lithium carbonate, which reduces thyroid reserve. One factor common to groups 1 and 2 but not to the controls was reduced thyroid reserve or functioning capacity, and, using established physical principles of servo-control, we have tried to define the mechanism. A series of curves were projected to indicate how TSH might be expected to vary with functioning thyroid capacity.

Adult↗
PubMed1977

Post-thyroidectomy hypocalcaemia: A feature of the operation or the thyroid disorder?

It has been suggested that post-thyroidectomy hypocalcaemia is related to the presence of a thyrotoxic osteodystrophy for which a high serum concentration of bone alkaline phosphatase is a marker. Changes in serum-calcium (corrected to a standard albumin concentration of 40 g/l), alkaline phosphatase (A.P.), inorganic phosphate, and albumin were studied prospectively in 54 euthyroid patients with drug-treated Graves' disease, and in 17 controls with simple non-toxic goitre, before and serially after partial thyroidectomy. All data were paired and results indicate that the pattern of biochemical change was the same in both types of patient and that the degree of change was not related to the serum-A.P. concentration in the Graves'-disease patients. Of the patients studied within the first 24 h of operation, 5 out of 12 with Graves' disease and raised serum-A.P. (group I), 9 of 20 with Graves' disease and normal serum-A.P. (group II), and 7 of 15 controls (group III) showed a fall in serum-calcium below the lower limit of the reference range. In all three groups there was a highly significant fall in serum-calcium 24 h after operation but there was no significant difference in serum-calcium between the groups either immediately before or 24 h after operation. Serum-calcium returned to pre-surgical concentrations within 7 days of thyroidectomy and serum-A.P. concentrations by 4 to 6 weeks in all groups. There was no evidence that post-thyroidectomy hypocalcaemia is related to thyrotoxic osteodystrophy and the pattern of the biochemical changes was thought to be consistent with release of thyrocalcitonin at operation.

Adult↗