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Biomedical subjects

U M Kabadi

Publications and source records attributed to U M Kabadi.

At least 19 recordsLinked to original sources
PubMed1995

Serum thyrotropin in primary hypothyroidism. A possible predictor of optimal daily levothyroxine dose in primary hypothyroidism.

BACKGROUND: Pretreatment thyrotropin levels may be a reliable predictor of the optimal daily dose of levothyroxine sodium in patients with primary hypothyroidism. However, the older method of serum thyrotropin determination, with the reference range of less than 1 to 8 mU/L, has given way to a newer, supersensitive thyrotropin assay, with a reference range of 0.5 to 5.0 mU/L. Thus, at present, the previously established relationship between the levothyroxine dose and the pretreatment serum thyrotropin concentration may not be reliable in predicting the optimal daily dose of levothyroxine. METHODS: We reassessed the relationship between the optimal daily levothyroxine dose and the pretreatment serum thyrotropin concentration as determined by the newer assay in 192 consecutive patients with primary hypothyroidism referred to an endocrinology clinic over a period of 4 years. RESULTS: The optimal daily dose of levothyroxine sodium ranged from 25 to 225 micrograms, with most patients (65%) requiring 100 to 150 micrograms/d and a median dose of 125 micrograms. Multiple regression analysis documented a significant curvilinear correlation between the mean pretreatment serum thryrotropin concentration and the optimal daily levothyroxine dose for individual groups divided according to available tablet strengths (r = .994, P < .001). A simple linear regression was also significant (r = .92, P < .001), although with an intercept much higher than the minimum levothyroxine sodium dose of 25 micrograms/d. However, the relationships markedly improved when the linear regressions were determined separately for two further subgroups at the median daily dose of 125 micrograms, providing equations to predict even the smallest optimal daily dose of levothyroxine. CONCLUSION: Pretreatment thyrotropin levels determined by new assays may also provide a useful guideline in determining the optimal daily maintenance dose of levothyroxine in patients with primary hypothyroidism.

Adult↗
PubMed1995

Pancreatic ketoacidosis: ketonemia associated with acute pancreatitis.

Ketonaemia is well documented as a consequence of prolonged starvation, acute alcoholism, and uncontrolled diabetes mellitus. However, its occurrence in acute pancreatitis has not been described. In this report, three patients who manifested ketoacidosis at the time of presentation of acute pancreatitis are described. In none of these patients could ketoacidosis be attributed to any of the well known pathogenetic factors such as ethanol, diabetes mellitus or prolonged starvation. In one patient, both the serum ketone titres and increased anion gap persisted for several days during the recovery period, despite appropriate therapy (including restriction of oral intake or nasogastric suction, intravenous fluids, and analgesic administration), before declining in parallel with a decrease in serum lipase levels, and became undetectable following near normalisation of serum lipase. Therefore, we believe that pancreatic ketosis or ketoacidosis may be a distinct syndrome with ketogenesis being promoted and maintained by extremely high circulating pancreatic lipase concentrations.

Acid-Base Equilibrium↗
PubMed1995

Renal calculi in primary hyperaldosteronism.

Increased urinary calcium (Ca++) excretion and the presence of negative Ca++ balance is well documented in primary hyperaldosteronism. However, renal calculi as a major manifestation of this disorder has not previously been described. This report describes a patient who presented with renal calculi in association with primary hyperaldosteronism. We believe that primary hyperaldosteronism was a major pathogenetic factor in the formation of renal calculi since the increased urinary excretion of Ca++ and uric acid noted at onset declined following a short-term spironolactone administration and remission from renal calculi has persisted following initial nephrolithotomy and continued spironolactone therapy, which also corrected hypertension and hypokalemia, a hallmark of this disorder.

Humans↗
PubMed1994

Acceptability of capillary blood glucose testing with Companion 2 after intensive individual patient training.

This study determined the accuracy and precision of the MediSense Companion 2 Blood Glucose Monitoring System in the hands of newly trained patients, after individual training. 101 subjects attending a diabetes clinic at a Veterans Affairs Medical Center participated in the study. Subjects were individually trained in the use of the Companion 2 system. They performed 10 practice control solution tests prior to two capillary blood glucose tests. Venous blood was collected within 15 minutes for comparative laboratory analysis. The comparisons were performed by both the linear regression and the total Grid analysis. The correlation between the first capillary blood glucose test results and the laboratory values was highly significant (r = 0.94, p = 0.0001). Total Error Analysis also revealed that the Systematic Error (SE), Random Error (RE) and Total Error (TE) were all well within the acceptable norms at two glucose levels of 5.5 mmol/(100 mg/dL) and 11.1 mmol/L (200 mg/dL); (SE < 15%, RE < 10% and TE < 15%). Therefore, this study demonstrates that Companion 2 provides precise and accurate values during capillary blood glucose testing by newly trained subjects following intensive individual training.

Adult↗
PubMed1992

Is hepatic glycogen content a regulator of glucagon secretion?

The role of plasma glucose as a major regulator of glucagon secretion is well established. However, this feedback regulation appears to break down in several states in which a closer relationship is apparently evident between plasma glucagon and hepatic glycogen content. Therefore, we assessed plasma glucagon as well as glucose response (delta glucose) to intravenous (IV) bolus administration of 1 mg glucagon after an overnight fast (a reliable and accurate estimate of the magnitude of hepatic glycogen content) in a population of normal subjects and subjects with hepatic cirrhosis and hyperthyroidism, both of which are disorders characterized by hepatic glycogen depletion. Plasma glucose concentrations were not significantly different in either group. However, plasma glucagon and insulin concentrations were significantly increased and delta glucose significantly decreased in both cirrhotic patients and hyperthyroid patients as compared with normal subjects. Furthermore, a significant relationship (r = -.55, P less than .0001) was noted between delta glucose and plasma glucagon, but not plasma insulin. Therefore, we believe that pancreatic alpha-cell function may be dependent on hepatic glycogen content. Moreover, the primary action of glucagon may be to induce gluconeogenesis in the absence of hepatic glycogen stores due to declining insulin concentrations or insulin resistance.

Adult↗
PubMed1992

Metabolic control following transfer from mixed bovine-porcine insulin to human insulin in subjects with IDDM: influence of the presence of insulin antibodies.

Although no distinct advantage of Human insulin (HI) over mixed Bovine-Porcine insulin (BPI) including antigenicity has been noted, initiation of therapy with HI in subjects with new onset IDDM as well as changeover from BPI to HI regimen even in subjects with well controlled DM with BPI has recently become a routine clinical practice. In this study, we assessed metabolic control by determination of fasting plasma glucose and HbA1C levels as well as serum cholesterol and triglyceride concentrations in 12 men and 2 women (ages 43-74 yrs) with uncontrolled DM while receiving BPI and again at the end of 6 months following changeover to HI with identical insulin regimen in terms of the type of insulin as well as the dosage. The subjects were divided into two groups according to the presence of antibodies to insulin of both bovine and porcine forms in their sera. Metabolic control improved significantly in 6 subjects, with positive antibody titers to bovine-porcine insulin as reflected by lowering of all metabolic parameters (p < 0.05 of all comparisons). However, the remaining 8 subjects with negative antibody titers failed to show a significant change in any of the parameters. Therefore, this study suggests that a changeover from BPI to HI maybe recommended in subjects with presence of BPI antibodies and not in all DM subjects treated with BPI regimen. Moreover, it may be feasible to initiate therapy with BPI regimen in new onset IDDM and change later to HI on occurrence of BPI antibodies; since if HI regimen is used at onset and antibodies to HI develop; the only option available then, may be the increased dosage of HI.

Adult↗
PubMed1992

Urine glucose testing: reliable backup for whole blood glucose monitoring.

Urine glucose testing has been deemed by some to be nonessential in the management of diabetes mellitus since the technique and equipment for self-monitoring of blood glucose has become available. However, most physicians have experienced pitfalls in the management of diabetes mellitus when insulin dosage is adjusted daily based solely on the patient's monitoring of blood glucose. There have also been recent reports suggesting the use of urine glucose testing as a reliable and a reasonable alternative to monitoring of blood glucose in the management of diabetic subjects, including those using insulin as the mode of therapy. In this report, we describe a patient in whom diabetic ketoacidosis occurred during hospitalization as a result of inadequate insulin administration due to inaccurate capillary blood glucose test results. Furthermore, urine glucose and ketone values obtained simultaneously had been disregarded. If insulin therapy had been adjusted according to urine glucose results rather than blood glucose readings, diabetic ketoacidosis could have been averted in this patient. Urine glucose testing may provide a reliable backup for suspect whole blood glucose values and may prevent catastrophic events requiring expensive hospitalization. This report also delineates several potential procedural problems that exist in the technique of whole blood glucose monitoring and provides recommendations to overcome these deficiencies.

Adult↗
PubMed1992

Management of NIDDM.

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Diabetes Mellitus, Type 2↗
PubMed1991

Glucagon-induced changes in plasma thyroid hormone concentrations in healthy dogs resemble "euthyroid sick syndrome".

We recently demonstrated that glucagon infusion induced a decline in T3 and a rise in rT3 in anesthetized dogs. These changes in T3 and rT3 may be attributed, at least in part, to anesthesia itself, since general anesthesia is known to cause lowering of T3 and an elevation in rT3 during the perioperative period. Therefore, to eliminate the contribution, if any, of anesthesia to these changes in T3 and rT3, we assessed plasma glucose, T3 resin uptake (T3RU), T4, free T4, T3 and rT3 concentrations following intravenous glucagon (0.5 mg) or normal saline (0.5 ml) administration at frequent intervals for 3 h in 6 conscious dogs fasted for 16 h. No significant alterations were noted in T4, free T4, and T3RU levels during either study. However, glucagon infusion alone induced a significant fall in T3 (0.33 +/- 0.06 in nmol/l vs -0.03 +/- 0.03 nmol/l with normal saline; p less than 0.01) and marked elevations in glucose (3.66 +/- 0.22 mmol/l vs 0.61 +/- 0.11 nmol/l with normal saline, p less than 0.001) and rT3 concentrations (0.11 +/- 0.02 nmol/l vs 0.005 nmol/l; p less than 0.001). Furthermore, the integrated responses of T3 and rT3 as assessed by cumulative changes and areas under the curves were markedly greater during glucagon infusion when compared with saline administration (p less than 0.01 for all comparisons). Since the elevations in levels of stress hormones known to ensue during anesthesia do not occur during a conscious resting state, we believe that hyperglucagonemia may be a major contributor of thyroid hormone alterations observed in several euthyroid sick states, not associated with stress, and may enhance these changes during euthyroid sick syndrome associated with stressful crises. Finally, these changes may be attributed to altered metabolism of iodothyronines in peripheral tissues as reflected by lowered T3/T4 and increased rT3/T4 ratios.

Animals↗
PubMed1991

Dose-kinetics of pancreatic alpha- and beta-cell responses to a protein meal in normal subjects.

A protein meal is well known to induce a prompt secretion of insulin and glucagon. However, the data regarding the dose-response relationship between the protein meal and the insulin and glucagon responses are sparse. This study assessed the effects of ingestion of protein meals of varying amounts on plasma glucose [S], insulin [I], and glucagon [G] concentrations in eight normal subjects. Protein meals were administered after an overnight fast in a randomized sequence at intervals of 10 days in four different quantities: 250 mg/kg body weight (BW) (A), 500 mg/kg BW (B), 1 g/kg BW (C), and 2 g/kg BW (D). Mean S levels were not significantly altered following A, B, or C, although significant decreases in S responses were noted after C and D as reflected by absolute changes (delta) and/or the cumulative responses (CR) and the areas under the curve (sigma). Mean I increased promptly to peak concentration by 30 minutes, although in individual subjects the peak was achieved either at 30 or 60 minutes following all protein meals. The increase was progressively greater and the return was delayed with increasing quantities resulting in progressive elevations in delta I and percent increase from basal concentration (%), as well as CRI and sigma I. G increased following all protein meals as well. The mean peak G concentrations were achieved by 90 minutes, although in individual subjects the peak G was reached at 90 or 120 minutes, a significant delay in comparison to the peak I levels. G returned to base line only following ingestion of A during the study period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Altered regulation of atrial natriuretic peptide in essential hypernatremia.

Hypothalamic osmoreceptor dysfunction resulting in hypodipsia and altered regulation of vasopressin secretion is well established as the pathogenetic mechanism in the syndrome of 'essential hypernatremia'. However, little is known about the secretory pattern of atrial natriuretic peptide (ANP) in this syndrome. Therefore, we assessed ANP regulation by determining ANP concentrations in a patient manifesting this syndrome of essential hypernatremia during several well-established experimental protocols. The serum ANP level was within normal limits despite severe euvolemic hypernatremia (serum Na+ 163 mEq/l) during one of the many admissions and remained unchanged following normalization of serum Na+. Furthermore, a decline in serum ANP instead of an appropriate rise was noted when hypernatremia (serum Na+ 152 mEq/l) was induced by either hypertonic (3%) saline infusion or following a high-Na+ (300 mEq/day) diet for several days (serum Na+ 161 mEq/l). Similarly, exogenous pitressin administration failed to cause a rise in ANP, although an appropriate fall in ANP concentration occurred following fluid deprivation. Therefore, it is apparent that ANP regulation may be significantly altered in essential hypernatremia. However, further studies are required to define whether it plays a role in the pathogenesis of hypernatremia in this syndrome.

Adult↗
PubMed1991

Type II diabetic subjects with secondary failure: treatment with prebreakfast mixed ultralente and regular insulin with a sulfonylurea.

BACKGROUND: Combination therapy with sulfonylurea and insulin is reported to be effective in several recent reports on the management of non-insulin-dependent diabetes mellitus (NIDDM) and secondary failure to sulfonylurea. Most of these studies used insulin twice daily, however, and hence failed to offer a significant practical advantage over insulin therapy alone. Since a subcutaneous injection of Ultralente insulin exerts its peak effect between 16 and 18 hours after injection, its prebreakfast administration is likely to inhibit overnight hepatic glucose production, which is a primary modulator of fasting plasma glucose, a major determinant of diurnal glycemia in NIDDM: Moreover, the simultaneous administration of regular insulin tends to improve glycemia during the premeal and immediate postmeal period before the onset of sulfonylurea-induced insulin secretion. METHODS: We assessed the efficacy of a prebreakfast subcutaneous injection of mixed Ultralente and regular insulin in conjunction with prior sulfonylurea therapy in 20 NIDDM subjects after precise documentation of secondary failure to these agents initially for the period of 3 months, followed by a long-term evaluation for up to 2 years. RESULTS: Metabolic control improved significantly as reflected by a decline in fasting plasma glucose (FPG) and HbA1c concentrations (FPG, 14.4 mmol/L +/- 0.4 vs 79 mmol/L +/- 0.3 mM/L; HbA1c, 11.7% +/- 0.3% vs 8.8% +/- 0.1%; P less than .001 for both comparisons). Serum cholesterol and triglycerides decreased as well, although the change was significant for triglycerides alone. Body weights and blood pressure remained unaltered. Furthermore, metabolic control appeared to remain in the same range during the long-term follow-up period. CONCLUSIONS: Adjuvant therapy with sulfonylurea and a single prebreakfast subcutaneous injection of mixed Ultralente and regular insulin may be an effective and practical therapeutic option in the management of NIDDM with secondary failure to sulfonylurea.

Adult↗
PubMed1991

Low serum T3 and raised reverse T3 levels in hepatic cirrhosis: role of glucagon.

Hepatic parenchymal tissue is known to be one of the major sites of thyroid hormone metabolism as well as glucagon action. Alterations in circulating thyroid hormone concentrations, as well as hyperglucagonemia, are well documented in subjects with hepatic cirrhosis and advanced liver dysfunction. Also, we have documented recently that hyperglucagonemia induced in normal subjects alters thyroid hormone metabolism, with lowering of serum T3 and a rise in serum reverse T3 (rT3) levels. Thus, it is conceivable that rising glucagon concentrations are responsible for altered thyroid hormone levels in hepatic cirrhosis. To examine this hypothesis, this study determined relationships between plasma glucose, glucagon, insulin, and insulin:glucagon ratio on one hand, and thyroid hormone concentrations on the other, in 51 subjects with hepatic cirrhosis. Significant negative correlations were noted between plasma glucagon and serum T3 (r = -0.418, p less than 0.001) as well as T3:T4 ratio (r = -0.627, p less than 0.0001), whereas significant positive correlations were observed between plasma glucagon and serum rT3 (r = 0.504, p less than 0.001) as well as rT3:T4 ratio (r = 0.644, p less than 0.0001). No such significant relationships were noted between either insulin, glucose and insulin:glucagon ratio on one hand and any of thyroid hormone indices on the other. Therefore, this study indicates that, in hepatic cirrhosis, circulating glucagon concentrations may play a major contributing role in induction of altered serum thyroid hormone concentration by influencing thyroid hormone metabolism.

Adult↗
PubMed1990

Pericardial effusion in primary hypothyroidism.

Pericardial effusion is reported to occur in 30% to 80% of subjects with hypothyroidism. However, these earlier studies were conducted when the diagnosis of hypothyroidism was only suspected and was confirmed only in the presence of classic clinical features. In contrast, the diagnosis has recently been established in the early mild stage or more often in an asymptomatic stage because of more frequent or routine determinations of thyroid function tests, especially in the elderly. Thus the subjects in the older studies were severely hypothyroid at the time of diagnosis and may not be representative of the present hypothyroid population. For this reason, 30 subjects with hypothyroidism were evaluated with echocardiography to reassess the evidence of pericardial effusion in this disorder. Only two subjects demonstrated pericardial effusion, and in only one of them with severe disease could the pericardial effusion be attributed to hypothyroidism, since it resolved on the patient's attaining the euthyroid state. Thus the incidence of pericardial effusion was only 3% to 6%, depending on the inclusion of one or both subjects, an extremely infrequent occurrence when compared with that of previous studies. Moreover, the occurrence of pericardial effusion in hypothyroidism appears to be dependent on the severity of the disease. Thus pericardial effusion may be a frequent manifestation in myxedema, an advanced severe stage, as previously found, but a rare association of hypothyroidism, an early mild stage, because of the timeliness with which the latter condition is nowadays detected.

Adult↗