Physicians and cost control.
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Beneficence↗
Biomedical subjects
R C Osburne
Publications and source records attributed to R C Osburne.
Concurrent renal hypomagnesemia and hypoparathyroidism with normal parathormone responsiveness.
A 24-year-old woman presented with clinical features suggesting hypoparathyroidism: tetany, basal ganglia calcification, and a history of a seizure disorder. Hypocalcemia was present on admission despite therapy with calcium and vitamin D. Hormonal evaluation revealed undetectable parathormone levels and a normal cyclic AMP and phosphaturic response to parathormone infusion, suggesting the diagnosis of idiopathic hypoparathyroidism. Additional testing, however, revealed hypomagnesemia and elevated urinary magnesium levels. Normomagnesemia could not be consistently achieved despite oral magnesium administration. When the serum magnesium level was temporarily normalized via intravenous magnesium supplementation, parathormone levels rose into the normal range. These data indicate that the patient's hypomagnesemia was most likely due to renal magnesium loss. The normalization of her parathormone level during magnesium replenishment, along with the parathormone infusion data, suggests that this patient's hypomagnesemia was responsible for decreased parathormone synthesis and/or secretion, while target tissue responsiveness to parathormone was maintained.
Adult↗
Adaptation to hypocaloric feeding: physiologic significance of the fall in serum T3 as measured by the pulse wave arrival time (QKd).
We have investigated the physiologic significance of the decline in serum triiodothyronine (T3) occurring during hypocaloric feeding by measurement of changes in cardiovascular function. The QKd interval, the interval between the Q wave of the electrocardiogram and the onset of Korotkoff sounds at diastolic pressure at the brachial artery, is the sum of the preejection period and pulsetransmission time, and has proven to be a sensitive and effective measure of the effect of thyroid hormones on the cardiovascular system. Fifteen euthyroid obese volunteers underwent successive 2 wk periods of hypocaloric feeding (200-400 calories per day) interspersed with periods of at least 2 wk of re-feeding on a weight-maintaining diet (1500 calories). In a later phase subjects received oral supplementation of triiodothyronine (T3) in addition to the diet to prevent the fall in serum T3. In the last study phase, subjects on the diet received supplementation with oral thyroxine (T4), which prevented the fall in serum T3 and resulted in a slight increase in serum T4. During the first 2 wk period of hypocaloric feeding, there was a statistically significant increase in QKd, and a decrease in pulse rate, compatible with a hypothyroid state relative to initial measurements. When oral T3 supplementation was given, the rise in QKd and fall in pulse rate were prevented. Likewise, with oral T4 supplementation, the changes in QKd and pulse were prevented. Thus, the fall in serum T3 occurring during hypocaloric feeding is associated with changes in the cardiovascular system which are qualitatively similar to those observed during hypothyroidism. The present data, taken with other data in the literature, suggest that the decline in serum T3 during hypocaloric feeding may be an adaptive mechanism to conserve energy during caloric deprivation.
Adaptation, Physiological↗
Fasting decreases thyrotropin responsiveness to thyrotropin-releasing hormone: a potential cause of misinterpretation of thyroid function tests in the critically ill.
We have previously reported that caloric deprivation inhibits peripheral T4 metabolism and blunts the TSH response to TRH in euthyroid obese subjects. To determine whether these phenomena also occur in hypothyroid subjects, T4, T3, rT3, and the TSH response to TRH were measured initially and after a 60-h fast in seven hypothyroid patients. Short term fasting caused a 29% decrement in the maximum serum TSH increment and a 32% decrement in the integrated TSH response to TRH (P less than 0.01). In two subjects with mild hypothyroidism, basal TSH as well as the TSH response to TRH were reduced to levels within the normal range. Specifically, basal TSH values decreased from 7.6 to 3.5 microU/ml and from 11 to 4.1 microU/ml. In the seven subjects, mean serum T3 decreased significantly from 88 to 60 ng/dl, (P less than 0.05) and rT3, initially undetectable in six of seven subjects, rose to detectable or low normal values in four of seven subjects, serum T4 remained at 2.7 micrograms/dl during both study periods. We conclude that 1) fasting induces changes in both peripheral thyroid hormone metabolism and the hypothalamic-pituitary axis in hypothyroid individuals which are qualitatively similar to those that occur in euthyroid subjects; and 2) in certain hypothyroid subjects, fasting alone can decrease basal TSH values to within the normal range. If these data can be extrapolated to critically ill subjects whose caloric intake may be diminished, they suggest that basal TSH concentrations in moderately and severely hypothyroid critically ill subjects will accurately reflect the biochemically hypothyroid state. However, mild degrees of hypothyroidism in critically ill subjects might be overlooked due to the lowering effect of fasting or poor caloric intake alone on basal TSH concentrations.
Adult↗
Malignant pheochromocytoma. Severe clinical exacerbation and release of stored catecholamines during lymphoma chemotherapy.
The association of malignant pheochromocytoma and poorly differentiated lymphocytic lymphoma has not previously been reported. A case is presented of a 58-year old man with a 20-year history of malignant pheochromocytoma well controlled on Dibenzyline who was found to have poorly differentiated lymphocytic lymphoma. During lymphoma chemotherapy with cyclophosphamide, vincristine and prednisone (VCP) he developed tachycardia and syncope accompanied by severe hypertension. During the next course of chemotherapy one month later, 24-hour urinary VMA, metanephrine and catecholamine values were determined before, during and after the chemotherapy and were found to have increased two- to ten-fold. This suggests that VCP caused tumor lysis with release of catecholamines into the circulation.
Adrenal Gland Neoplasms↗
Euthyroid familial hyperthyroxinemia due to abnormal thyroid hormone-binding protein.
A family is described in which three members had an elevated total serum thyroxine level and free thyroxine index. Each affected subject was clinically euthyroid and had a normal pulse wave arrival time (QKd), serum triiodothyronine and free thyroxine levels, and a normal serum thyroxine-binding globulin (TBG) concentration. Electrophoresis of their serum with 125I-labeled thyroxine revealed increased thyroxine binding in the albumin region. In addition, this abnormal protein, like thyroxine-binding globulin, bound 125I-labeled triiodothyronine and 125I-labeled reverse triiodothyronine. However, electrophoresis of serum treated by sialidase (neuraminidase) digestion suggested that this abnormal protein is not an anomalous form of thyroxine-binding globulin "buried" in the albumin area. These cases of euthyroid familial hyperthyroxinemia due to an abnormal thyroid hormone-binding protein show that an elevated serum thyroxine level or free thyroxine index is not always sufficient to confirm the presence of thyrotoxicosis.
Child↗
Autonomous thyroid nodules in adolescents: clinical characteristics and results of TRH testing.
Seven adolescents with autonomous thyroid nodules were evaluated over a three-year period. They had hyperfunctioning nodules on radionuclide scan which failed to suppress with exogenous administration of thyroid hormone. They were clinically euthyroid and had normal T4, free T4, and basal TSH values. However, as a group they had elevated total serum T3 concentrations, blunted TSH response to TRH, and accelerated closure of cranial sutures, all of which suggested subtle hyperthyroidism. These patients have been followed for one to five years. Four have undergone partial thyroidectomy because of persistent elevation in the serum T3 concentration or enlargement of the nodule. The clinical presentation and laboratory findings in this group are similar to those found in adults with autonomous nodules.
Adolescent↗
Thyroid hormone homeostasis in states of relative caloric deprivation.
Starvation is accomplished by significant changes in the hypothalamic-pituitary-thyroid axis and in peripheral thyroid hormone metabolism. Less well studied, however, are the effects on thyroid hormone economy produced by hypocaloric feeding. We explored these changes in obese patients fed 200, 400, or 600 cal/day of either carbohydrate of protein for 28 days. T4' T3' reverse T3 and the TSH response to TRH were measured at frequent intervals. Each patient demonstrated a transient rise in reverse T3 and a fall in T2 that returned to near basal levels by the end of the study period. The TSH response to TRH on the other hand, declined to approximately 50% of control values and remained at that level throughout the course of study, regardless of the type of substrate or calorie level chosen. The results indicated that hypocaloric feeding is associated with changes in thyroid hormone economy similar to those in starvation and that peripheral (changes in T3 and rT3) and central (TRH response) events are controlled by separate mechanisms.
Diet↗
Cerebral blood flow. A predictor of recovery from ischemia in the gerbil.
Cerebral ischemia was induced in gerbils by bilateral carotid ligation for periods of 10 to 40 minutes. Cerebral blood flow (CBF) was measured by hydrogen clearance. Following ischemia, ultimate clinical and electroencephalogram recovery could be predicted in every case within the first five minutes by recovery could be predicted in every case within the first five minutes by recovery of CBF to at least 100% of the control level. In animals without EEC recovery, the postischemic CBF was always less than 80% of control and progressively declined to zero. Residual flow during ischemia appeared to minimize the likelihood of brain death. The determination of ultimate brain death appeared to coincide with a major circulatory abnormality that is probably microvascular.
Animals↗