Ramesh C. Khurana
University of Pittsburgh
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Hormone Research in Paediatrics | 1972
T. S. Danowski; E. Livstone; A.R. Gonzales; Y. Jung; Ramesh C. Khurana
Increases in serum growth hormone which characterize acute starvation in non-obese individuals were usually absent in anorexia nervosa. Serum LH was decreased with serum FSH apparently normal in the m
Metabolism-clinical and Experimental | 1972
T. S. Danowski; E.R. Fisher; Ramesh C. Khurana; S. Nolan; T. Stephan
Abstract Calculations of the minimum rather than the average basement membrane thickness of muscle capillaries established that widening of this structure was only rarely encountered in juvenile-onset diabetes of 1–6 yr duration. The basement membrane was usually, but not always, thickened, however, in childhood-onset diabetes present for 7 or more yr. The presence or absence of basement membrane thickening did not appear to be related to age at onset of diabetes, the degree of hyperglycemia in an oral glucose tolerance test, any residual ability to secrete insulin, the type, dosage or schedule of insulin therapy, history of ketoacidosis and shocking, blood pressure, or the state of the kidneys. However, each of the patients with an increase in the width of the basement membrane of muscle capillaries did have microaneurysms. Our data are consonant with the hypothesis that thickening of the basement membrane generally appears toward the end of the first decade following the diagnosis. Since duration and age tend to be related, such thickening was more common in the older persons with juvenile-onset diabetes. Also, in such patients serum creatinine tended to be higher and proteinuria was more frequent, two variables known to be influenced by duration of diabetes and increased chronologic age.
Diabetes | 1973
T. S. Danowski; Ramesh C. Khurana; S. Nolan; T. Stephan; Charles G Gegick; Soo Chae; Carlos Vidalon
Hyperinsulinemic patterns are a well recognized feature of equivocal glucose tolerances of the chemical diabetes type, i.e. those that are neither definitely nondiabetic nor clearly diabetic. A more complete characterization of such insulin responses is obtained when the data are expressed in terms of increments in insulin from the zero time point. Thus, two patterns of insulin increments after oral glucose become evident when the equivocal zone of glucose tolerance is divided into lower and upper segments. Tests in the lower segment show normal increments at the halfhour point of the test; at one hour these tests show excessive increments which persist throughout the five hours of observation. On the other hand, tests in the upper zone show delays in the serum insulin rise at the half-hour point, followed by normal increments at one hour and excessive increments thereafter. The pattern is the same whether or not obesity is present. It is suggested that tests in the equivocal zone of Glucose Tolerance Sum values be taken to be indicative of chemical diabetes. Tests with the Sum in the lower half of the equivocal zone could then represent chemical diabetes with mild intolerance stemming from insulin ineffectiveness, since insulin increments in this group are at or above the mean values recorded in nondiabetic controls. On the other hand, chemical diabetes with moderate glucose intolerance and Glucose Tolerance Sums in the upper half of the equivocal zone would be understood to result from a combination of an initial delay in the serum insulin rise followed by normal and then excessive increments in serum insulin with the latter two indicative of insulin ineffectiveness. However, insulin ineffectiveness may also be present at the time of the insulin delay. High glucose:insulin ratios in tests indicative of chemical diabetes are almost always attributable to higher glucose increments with insulin increments normal or excessive compared to normal glucose tolerances. Deficient insulin increments contribute to the high ratios only at the half-hour point in tests with Glucose Tolerance Sums in the upper zone of equivocal glucose tolerances.
Journal of the American Geriatrics Society | 1973
C. Vidalon; Ramesh C. Khurana; S. Chae; C. G. Gegick; T. Stephan; S. Nolan; T. S. Danowski
ABSTRACT: In non‐obese women with unimpaired glucose tolerance (1,185 oral glucose tolerance tests) the serum level of growth hormone (GH) in the fifth and sixth age decades was below that in the third and fourth decades. Although obesity was associated with serum GH levels below those characteristic of non‐obese women, there was no evidence of a further age‐related decrease of the type observed in the non‐obese subjects. The lower serum GH level in women of the later age decades may well be related to the menopause with its decrease in the serum level of estrogen. Since there is no further age‐related decline in GH in obesity, it would appear that in obese premenopausal females, estrogen does not exert its usual GH‐enhancing effects.
The American Journal of Medicine | 1971
T. S. Danowski; Ramesh C. Khurana; Alejandro R. Gonzalez; Edwin R. Fisher
Abstract Electron microscopy of 104 biopsy specimens revealed thickening of the basement membrane of skeletal muscle capillaries of the type and degree observed in diabetes mellitus in only one third of a series of thirty-five patients with glucose intolerance and myopathy or neuromyopathy. Hence, the delayed disposal of glucose observed in various myo- or neuromyopathies including myotonia dystrophica, facio-scapulo-humeral muscular dystrophy and Cushings syndrome, without thickening of the basement membrane appears to be an entity distinct from diabetes. It may merely represent diminished muscle participation in the disposal of glucose and might be classified therefore as falling in the category of pseudodiabetes. Our series also includes ten patients with myopathy or neuromyopathy in whom glucose tolerance was entirely normal but the basement membranes were greatly thickened. Although this may represent prediabetes, it is conceivable that increased minimal basement membrane thickness can be a hitherto unrecognized manifestation of certain muscle, neurologic or endocrine disorders.
Metabolism-clinical and Experimental | 1973
Ramesh C. Khurana; Allan L. Drash; Judith Howland; T. S. Danowski
Criteria employed for the diabetic or nondiabetic designation of oral glucose tolerance test results obtained in children are not uniform. The use of the venous blood glucose tolerance sum calculation, which is the sum of the blood glucose levels at 0, 12, 1, and 2 hr (GTS0–2 hr) or at 0, 1, 2, and 3 hr (GTS0–3 hr) of an oral glucose tolerance test (1.75 g/kg), simplifies the evaluation of test results. When the venous blood GTS0–2 hr value is 500 or less in children, the probability is 98% or better that the test does not meet the criteria of the World Health Organization, the United States Public Health Service, the British Diabetic Association, or those of Fajans and Conn for diabetes mellitus. On the other hand, venous blood GTS0–2 hr values of 701 or higher indicate that the test results meet each of these four sets of standards for the diagnosis of diabetes mellitus. Venous blood GTS0–2 hr values between 501 and 700 indicate an equivocal glucose tolerance; the test results would be deemed to be nondiabetic by some of the criteria but not by others. The equivocal range of venous blood GTS0–3 hr values lies between 451 and 650. Three-hour glucose tolerance sums below 451 indicate that the results are nondiabetic by the four sets of criteria and those above 650 signify that the test would be classified as diabetic by these same four sets of standards. In children with unimpaired oral glucose tolerance with GTS0–2 hr value of 500 or less, the glucose: insulin ratios yield values of 1.0 or less. This is within the range established in healthy young adult nonoverweight females.
Hormone Research in Paediatrics | 1973
T. S. Danowski; H.R. Wilson; Ramesh C. Khurana; Y. Jung; Alejandro R. Gonzalez; J. H. Sunder
Quingestanol acetate (17-α-ethynyl-19-nortestosterone acetate, 3-cyclopentylenol ether), a synthetic progestational steroid, was well tolerated at a dosage of 300 µg/day per os by 17 diabetic women wh
Clinical Pharmacology & Therapeutics | 1971
T. S. Danowski; J. H. Sunder; D.G. Corredor; Y. Jung; John W. Vester; Ramesh C. Khurana; J. P. Wingert
Sodium dextrotriiodothyronine (Na‐DT3) at a dosage of 1 mg. per day for 24 weeks produced an approximately 75 mg. per cent decrease in serum total cholesterol in hyper‐and normolipidemic subjects. Na‐DT3 usually lowered the level of serum leva‐thyroxine (LT4) to the myxedema range, but the subjects remained euthyroid, suggesting that Na‐DT3 was exerting a thyroid hormone‐replacement effect. The failure to observe the changes to be expected in the in vitro levo‐triiodothyronine (LT3) uptake by blood cells when the serum protein‐bound iodine (PBI) had increased indicates that perhaps Na‐DT3 occupies binding sites other than those used by LT3 that Na‐DT3 is loosely bound to plasma proteins and is readily displaced by LT3, or both. An unexplained rise in urine total protein was observed during the first 6 weeks of Na‐DT3 therapy but not at 12 weeks. Serum total globulins were increased in the twenty‐fourth week. Minor changes within the normal range were recorded in plasma 11(OH)‐corticosteroids and in urine Porter‐Silber chromogens. All other indices remained within the pretherapy range.
Hormone Research in Paediatrics | 1973
T. S. Danowski; Edwin R. Fisher; T. Stephan; S. Nolan; D.W. Clare; Ramesh C. Khurana
In an adult with a virilizing adrenocortical adenoma and in six similar published instances, the high levels of urinary 17-ketosteroids usually present were associated with normal excretion of 17(OH)c
Clinical Pharmacology & Therapeutics | 1973
T. S. Danowski; H. Randolph Wilson; John W. Vester; Edwin R. Fisher; Ramesh C. Khurana; S. Nolan; T. Stephan; J. H. Sunder
The monthly ingestion of quingestanol acetate (2.5 mg) and quinestrol (2 mg) for 1 year by menopausal women was associated with increased numbers of superficial cells in Daginal smears and decreases in intermediate and parabasal cells. High serum FSH and LH levels were promptly returned to normal and remained normal. Serum triglyceride and T4 levels and plasma 11(OH) corticosteroids were consistently increased. Serum inorganic phosphorus and calcium levels decreased during the first month of treatment and remained decreased throughout the year. The calcium and phosphorus changes could reflect a protein‐anabolic effect with deposition of these ions in bone salts, but alternative explanations can be suggested. Serum solutes other than those already cited, serum enzymes, hematologic findings, electrocardiographic tracings, urinary steroids and creatinine, glucose tolerance and the associated serum insulin and growth hormone patterns, and a number of other routine laboratory procedures were not consistently affected by therapy with these dosages of quinestrol and quingestanol acetate. After 1 year of treatment urinary steroids and their responses to oral metyrapone were unchanged. Possible side etfects occurred in 3 of 18 patients: malaise, generalized pruritus, nausea, vomiting, and dizziness.