G. Sabeh

Probabilities of Pituitary-Adrenal Responsiveness After Steroid Therapy

Excerpt Data accumulated in this laboratory provide a basis for some generalizations concerning pituitary-adrenal responsiveness in subjects who had received adrenal steroids or adrenocorticotrophi...

Serum growth hormone and insulin in females without glucose intolerance

Abstract In the absence of glucose intolerance, fasting blood sugar levels are significantly higher in nonobese women in succeeding age decades. This upward trend with age in fasting blood sugar levels is not evident in obesity but such women, compared to the nonobese group, already have higher fasting blood sugar levels when they are just in the third decade of life. With but minor exceptions, the serum growth hormone and the serum insulin responses to an oral carbohydrate load recorded in nonobese women without glucose intolerance are of the same order of magnitude irrespective of age. This is also true in obese women without glucose intolerance. Obesity in women is associated with serum growth hormone levels which during fasting are lower than those observed in nonobese women. In obesity the peak growth hormone levels and the sum of the growth hormone levels recorded during an oral glucose tolerance test are lower than those observed in females of normal weight. During the first two hours of a normal oral glucose tolerance test in obese women a true and absolute hyperinsulinemia is recorded, but this is then replaced by waning of serum insulin below levels characteristic of a nonobese control group.

Hydrocortisone and/or desiccated thyroid in physiologic dosage

Abstract The administration of desiccated thyroid in dosages increasing to 16 grains per day to 4 patients with muscular dystrophy reduced abnormally high levels of serum creatine phosphokinase (CPK) to normal. This therapy was also accompanied by a decrease in the urine creatine and creatinine. These dosages of desiccated thyroid appeared to be relatively innocuous, judging from clinical indices and laboratory observations during the 8 months of therapy. However, certain changes associated with spontaneous or induced excesses of thyroid hormones such as tachycardia and systolic hypertension were noted. In 2 of the patients an increase in hand strength may have occurred, judging from serial contractions of a rubber bulb attached to a recording ergometer. However, it is more likely that this represented increased aptitude in manipulating the bulb rather than increased strength. This conclusion is supported by the fact that muscle strength as reflected by a single contraction of an individual hand or as estimated by a physical therapist did not increase in any of the patients. The improvement in the performance on the recording ergometer occurred when the daily dosage of thyroid reached 5 or 7 to 13 grains. The subsequent loss of a part of this increment or even a deterioration of muscle strength may have resulted from thyrotoxic myopathy or progress of the disease as the daily intake of desiccated thyroid was raised to 16 grains.

Serum lipids during oral contraceptive exposure.

The serum total cholesterol did not change significantly du ring 6 to 60 months of exposure to an oral contraceptive steroid combination (mestranol and norethynodrel). Alpha lipoprotein levels increased and remained slightly elevated. Serum total triglycerides increased during the sixth to eighteenth month of exposure only.

Growth hormone in insulin-treated diabetes mellitus.

Diabetes mellitus of juvenile or adult onset under treatment with insulin is characterized by higher serum growth hormone levels prior to and during disposal of an oral glucose load. The possible role of such growth hormone excesses in diabetic microangiopathy is discussed.

Growth hormone and insulin levels in newly discovered glucose intolerance

Abstract Newly discovered glucose intolerance in nonobese and in obese adult females is associated with fasting levels of immunoassayable growth hormone in serum lower than those found in nonobese female control subjects without glucose intolerance. When glucose intolerance without or with obesity is present, the peak levels of growth hormone and the sums of the growth hormone levels recorded after an oral glucose load are lower than those recorded in control subjects. When carbohydrate is ingested by women with newly-identified glucose intolerance, the average insulin increment during the induced hyperglycemia appears to be excessive. Actually, the insulin responses prove to be deficient in relation to the concomitant increments in blood sugar during the early as well as the late hours of the tolerance test. This deficiency is evident in nonobese and obese persons with glucose intolerance. The insulin responses cited above represent average findings in a series of patients. The individual groups include some persons with glucose intolerance whose insulin responses in relation to increments in the blood sugar equal or even exceed those recorded in healthy control subjects with a normal glucose tolerance.

Enhanced postglucose hypophosphatemia during starvation therapy of obesity

Abstract In obese persons without and with glucose intolerance, the hyperglycemic response to an oral glucose load was increased and prolonged by 10 to 14 days of total fasting. The insulin and growth hormone responses of these individuals to oral glucose were not altered by the fast, but the associated hypophosphatemia was markedly accentuated. The accentuated hypophosphatemic response to glucose observed during starvation raises the possibility that fasting is associated with shunting of the disposal of the carbohydrate load from liver to muscle. Fasting did not modify the blood sugar, serum inorganic phosphate, insulin or growth hormone responses to tolbutamide, arginine, or glucagon infusion.

Insulin patterns prior to and after onset of diabetes

Abstract In two of three adults in whom responses to an oral glucose load were studied before and after diabetes had appeared, the increases in serum insulin in response to an oral glucose load taken during the diabetic phase were definitely greater than those recorded before the diabetes appeared. Thus, in two patients the ratio of the increment in blood sugar to the increment in insulin recorded after glucose intolerance had appeared was lower than that documented one year earlier during the pre-diabetic phase, indicating an enhanced insulin response. In other words, a true hyperinsulinemia relative to the rise in blood sugar was present in these two persons with newly-discovered diabetes. The enhanced glucose-induced hyperinsulinemia in these newly-discovered diabetic persons indicates that in them the diabetes stemmed from inadequacy of hypoglycemic action of the insulin either because the insulin molecule was defective, pro-insulin was present, insulin action was vitiated by plasma or tissue antagonism, or absorption of glucose was enhanced. The finding of diminished insulin increments in relation to increases in blood sugar following an oral glucose load in one other adult with diabetes of one years duration or less suggests that this may be another pattern in some diabetic persons. Alternatively, it is possible that the true hyperinsulinemia noted in our other two patients is a transient phase which may disappear within a year. In the one child in this series, fasting and postglucose hyperinsulinemia was present during the prediabetic phase relative to the insulin responses recorded in control studies in nondiabetic children. After diabetes had developed and prior to any therapy, an oral glucose load did not evoke a rise in serum insulin.

Glucose tolerance prior to and during therapy with contraceptive steroids

Oral glucose tolerance remained within the pretherapy range during cyclic administration of norethynodrel and ethinyl estradiol 3‐methyl ether (mestranol) in a single tablet to 17 women for 5 to 48 months. Our data and those in the literature indicate that in evaluations of oral contraceptive agents the pretherapy glltcose tolerance, the particular steroids prescribed, the schedule of dosage, and the dmation of therapy and other variables may be critical in establishing effects on glucose tolerance.

Hydrocortisone and/or Desiccated Thyroid in Physiologic Dosage XV. Thyroid Therapy, Serum CPK, and Other Indices in Muscular Dystrophy

Abstract The administration of desiccated thyroid in dosages increasing to 16 grains per day to 4 patients with muscular dystrophy reduced abnormally high levels of serum creatine phosphokinase (CPK) to normal. This therapy was also accompanied by a decrease in the urine creatine and creatinine. These dosages of desiccated thyroid appeared to be relatively innocuous, judging from clinical indices and laboratory observations during the 8 months of therapy. However, certain changes associated with spontaneous or induced excesses of thyroid hormones such as tachycardia and systolic hypertension were noted. In 2 of the patients an increase in hand strength may have occurred, judging from serial contractions of a rubber bulb attached to a recording ergometer. However, it is more likely that this represented increased aptitude in manipulating the bulb rather than increased strength. This conclusion is supported by the fact that muscle strength as reflected by a single contraction of an individual hand or as estimated by a physical therapist did not increase in any of the patients. The improvement in the performance on the recording ergometer occurred when the daily dosage of thyroid reached 5 or 7 to 13 grains. The subsequent loss of a part of this increment or even a deterioration of muscle strength may have resulted from thyrotoxic myopathy or progress of the disease as the daily intake of desiccated thyroid was raised to 16 grains.