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Biomedical subjects

Mark R Burge

Publications and source records attributed to Mark R Burge.

15 recordsLinked to original sources
PubMed2006

Efficacy of a pedometer-based physical activity program on parameters of diabetes control in type 2 diabetes mellitus.

The aim of the study was to determine whether a recommendation to walk 10000 steps per day would result in significant improvements in glycemic control, insulin sensitivity, and cardiovascular risk in patients with type 2 diabetes mellitus. The study was a 6-week randomized controlled trial that included 30 patients with type 2 diabetes mellitus. After 10 days of baseline activity, patients were randomized into 2 groups: control and active. The control group (n = 15) was instructed to continue with their baseline activity for 6 weeks. The active group (n = 15) was instructed to walk at least 10000 steps per day 5 or more days per week, for 6 weeks. Data relevant to glycemic control and other parameters of health were collected at study weeks 0 and 6. There were no differences in the baseline activity between groups (P = .36). Subjects in the active group significantly increased physical activity by 69% during the intervention phase of the study (P = .002), whereas there was no change in the physical activity of the control group (P > .05). High-density lipoprotein cholesterol and resting energy expenditure significantly increased in the active group (P < .05). Finally, plasminogen activator inhibitor 1 (PAI-1) activity was reduced by exercise relative to the control group (P = .03). There were no differences in any other study parameters during the 6-week study. In conclusion, short-term intervention with a pedometer increased physical activity and positively affected plasminogen activator inhibitor 1 activity in previously inactive patients with type 2 diabetes mellitus. The use of a pedometer may prove to be an effective tool for promoting healthy lifestyle changes that include daily physical activity and self-monitoring of therapeutic goals.

Adult↗
PubMed2005

Methimazole-induced hypothyroidism paradoxically decreases homocysteine.

Clinical hypothyroidism is associated with hyperhomocysteinemia, whereas the opposite is seen in hyperthyroidism. The effects of mild thyroid dysfunction on homocysteine concentrations are not known. We performed the following study to investigate this. Total homocysteine, vitamins B6 and B12, folate, fibrinogen, plasminogen activator inhibitor type 1, and lipids were measured in 11 subjects at baseline and after methionine loading. Subjects began methimazole (MMI), 40 mg daily, and were restudied during 2 stages of hypothyroidism. Liothyronine was added and subjects were restudied once thyrotropin normalized. Methimazole was stopped and studies were repeated during 2 stages of hyperthyroidism. Data were analyzed using repeated-measures analysis of variance. Post-methionine homocysteine decreased in each hypothyroid study compared with baseline (28.8+/-10.7, 27.5+/-9.9 vs 34.4+/-9.2 micromol/L, respectively). In addition, both fasting and post-methionine homocysteine decreased in the euthyroid/MMI study arm compared with baseline despite equivalent thyrotropin values (fasting, 7.5+/-3.0 vs 8.8+/-3.5 micromol/L, P<.05; and post-methionine, 27.2+/-10.6 vs 34.4+/-9.2 micromol/L, P<.05, respectively). Fasting homocysteine decreased in the first hyperthyroidism study arm compared with baseline (6.6+/-2.3 vs 8.8+/-3.5 micromol/L, P<.05) and post-methionine homocysteine decreased in both hyperthyroid arms compared with baseline (25.2+/-8.1, 24.2+/-10 vs 34.4+/-9.2 micromol/L, P<.05 respectively). In conclusion, mild thyroid dysfunction changes homocysteine metabolism. Unexpectedly, our results suggest a homocysteine-lowering effect of MMI.

Adolescent↗
PubMed2004

Insulin edema in the twenty-first century: review of the existing literature.

Generalized insulin edema, although rare, is a well-recognized complication of insulin therapy. It is mainly appreciated in patients with newly diagnosed or poorly controlled diabetes mellitus after starting intensive insulin therapy. Although the condition is self-limiting, progression to overt cardiac failure and development of pleural effusion have been reported. With current trends toward intensive insulin therapy, clinicians should be aware of the existence of the insulin edema syndrome, and its occurrence should be documented and differentiated from other causes of edema. In this article, we present a recent case that illustrates the clinical features of insulin edema. Specifically, a young male with newly diagnosed type 1 diabetes mellitus developed significant, reversible peripheral edema after starting insulin therapy. A detailed case description is accompanied by the only known published photographs of insulin edema. The overall purpose of this article is to review the scanty existing medical literature surrounding the topic of insulin edema and to raise awareness about its continued occurrence.

Adult↗
PubMed2004

Hypoglycaemia in elderly patients with diabetes mellitus: causes and strategies for prevention.

Achieving target glycaemic goals while avoiding hypoglycaemia is a major challenge in the management of elderly patients with diabetes mellitus. Repeated episodes of hypoglycaemia may cause extreme emotional distress in such patients, even when the episodes are relatively mild. Moreover, evidence is mounting that hypoglycaemia among elderly patients is a very real and costly health concern. The strongest predictors of severe hypoglycaemia in the elderly are advanced age, recent hospitalisation and polypharmacy. Education is the key to preventing recurrent or severe hypoglycaemia. As such, there should be close coordination of care between the patient, physician and all other healthcare providers in identifying the cause of hypoglycaemia in elderly patients, and appropriate steps should be taken to prevent further episodes. Prevention of hypoglycaemia has the potential to improve psychosocial aspects of elderly health, including enhanced quality of life, boosted confidence, improved compliance with antidiabetic regimens and avoidance of long-term complications. Since the elderly population represents a unique group, it is imperative to focus on the aetiologies that are exclusive to this group. Advanced age itself is a risk factor for hypoglycaemia, and elderly patients with comorbidities are at increased risk when they are hospitalised. Elderly patients with diabetes often have compromised renal function, which intereferes with drug elimination and thus predisposes them to prolonged life-threatening hypoglycaemia. In addition, patients on five or more prescription medications are prone to drug-associated hypoglycaemia. Although sulfonylurea-associated hypoglycaemia is common, drugs such as ACE inhibitors and nonselective beta-adrenoceptor antagonists can also predispose patients to hypoglycaemia. Greater attention should be paid to the avoidance of hypgolycaemia in nursing home residents. Recurrent hypoglycaemia in elderly patients is not only detrimental to achieving good glycaemic control, it is also a substantial economic burden. Once the causes of hypoglycaemia have been identified, it is crucial to formulate and institute a prevention plan. Firstly, global evaluation of the patient should be carried out to identify possible predisposing risk factors. Secondly, target glycaemic goals should be tailored to each patient. Thirdly, selection of antidiabetic agents should be judicious, then patients and family should be educated to recognise and treat hypoglycaemia. Finally, coordinated care should be provided to identify, treat and prevent hypoglycaemia.

Adrenergic beta-Antagonists↗
PubMed2003

The role of ethnicity in post-pancreatitis diabetes mellitus.

Hispanic ethnicity and a prior history of pancreatitis are both known risk factors for the development of diabetes, but the role of ethnicity in the pathogenesis of post-pancreatitis diabetes is not known. We hypothesized that Hispanic patients would have an increased incidence of diabetes following hospitalization for acute pancreatitis compared with non-Hispanic white patients. A query of the University of New Mexico Hospital billing database revealed 887 Hispanic and non-Hispanic white patients admitted with a diagnosis of acute pancreatitis between 1991 and 1995. A retrospective, chart review study of 98 cases of post-pancreatitis diabetes was performed. Ethnicity was designated as Hispanic or non-Hispanic white by surname using the previously validated GUESS program. The main outcome measure for the study was the frequency of occurrence of post-pancreatitis diabetes according to ethnicity. Thirty seven (8.8%) of the 421 non-Hispanic white patients had post-pancreatitis diabetes compared with 61 (13.1%) of the 466 Hispanic patients (p < 0.05 by chi(2)). Relative to previously published diabetes incidence rates from the northern Rio Grande Valley, patients with a prior history of pancreatitis were significantly more likely to develop diabetes: odds ratio = 3.65 (95% confidence interval = 2.31, 5.76; p < 0.001). Adjustment for age did not affect this relationship. The risk of developing diabetes among Hispanic patients compared with non-Hispanic white patients, however, did not differ between the patients with post-pancreatitis diabetes in the current study and those without a history of pancreatitis in previously published reports. Although patients with a history of acute pancreatitis have an increased incidence of diabetes mellitus, the inherent genetic predisposition of Hispanic individuals to diabetes does not appear to increase the rate of development of post-pancreatitis diabetes.

Acute Disease↗
PubMed2003

Diabetes mellitus associated with atypical anti-psychotic medications.

Diabetes or hyperglycemia associated with the use of atypical anti-psychotic agents is a subject of growing concern among health care providers and the patients who use the drugs. Although much attention has been relegated to this topic in the mental health literature, there has been little attention devoted to it in the diabetes literature. The purpose of this report is to review the problem of diabetes mellitus associated with atypical anti-psychotic use from an endocrinology perspective. This paper will specifically present (a) a review of the increased prevalence of diabetes in the setting of schizophrenia, (b) a compilation and critical assessment of the existing publications that have documented the association of hyperglycemia and atypical anti-psychotic use, (c) a discussion of the potential mechanisms through which antipsychotics may lead to disturbances in glucose homeostasis, and (d) recommendations for the effective monitoring and treatment of affected patients.

Adult↗
PubMed2002

The mechanism of glucose-induced catecholamine stimulation.

Catecholamines are important hormones for maintaining homeostasis and may be secreted in response to several different stimuli. A report by Robertson and Porte in 1974 made the unexpected observation that acute administration of hypertonic glucose stimulates catecholamine secretion. Our study reassessed this observation by measuring individual catecholamines, explored its potential mechanism, and quantitated it relative to exercise and hypoglycemia-stimulated catecholamine secretion. We hypothesized that the mechanism of glucose-induced catecholamine secretion was related to an acute increase in plasma osmolality, which we tested with the nonmetabolizable hexose mannitol. In 56 studies, 14 normal adults underwent 4 partially randomized studies. The 4 study conditions consisted of the following: (1) rapid intravenous injection of 20 g of glucose; (2) rapid intravenous injection of 20 g of mannitol; (3) acute exercise (80 J/kg); and (4) insulin-induced hypoglycemia. Our results demonstrate that a significant increase in plasma catecholamine concentration occurs following each of the above stimuli, but its composition differs relative to the magnitude of epinephrine versus norepinephrine secretion. We conclude that the mechanism of glucose-induced catecholamine stimulation is the acute elevation in plasma osmolality induced by glucose, and that its stimulation is less than that which occurs following exercise for norepinephrine and less than that which occurs following hypoglycemia for epinephrine.

Adult↗
PubMed2002

Frequency of the dawn phenomenon in type 2 diabetes: implications for diabetes therapy.

This study was designed to assess the frequency of the dawn phenomenon in patients with type 2 diabetes. A secondary aim was to examine the influence of varying treatment regimens on the frequency of the dawn phenomenon. The dawn phenomenon was defined as a rise in plasma glucose levels of > or = 0.5 mmol/L (10 mg/dL) between 0500 and 0900 h occurring after a growth hormone surge of > or = 5 microg/L. Sixteen subjects (six men, 10 women) with type 2 diabetes were studied overnight on their current mode of therapy in the General Clinical Research Center. Additionally, six of these subjects were restudied in random order after each of the following three therapeutic regimens: (1) 6 weeks of glipizide, (2) 6 weeks of bedtime NPH insulin, and (3) 3 days of intensive insulin therapy with multiple injections of regular insulin followed by assessment during overnight intravenous infusion of insulin. Thus, a total of 34 overnight studies were performed under various treatment conditions to provide an approximate frequency of the dawn phenomenon in type 2 diabetes. Blood was drawn every 30 min between midnight and 0800 h for measurement of glucose, insulin, C-peptide, and growth hormone levels. Additional counterregulatory hormone levels were determined during 24 of the studies, and the integrity of growth hormone secretion in response to insulin-induced hypoglycemia was assessed in 12 of the 16 patients. The subjects were aged 51 +/- 15 years with a body mass index of 31 +/- 5 kg/m(2) and a mean glycosylated hemoglobin of 8.1 +/- 1.2%. The dawn phenomenon occurred in only one of 34 (3%) studies. Moreover, the four different treatment regimens did not affect the frequency of occurrence of the dawn phenomenon. Ten of the 12 patients tested failed to secrete growth hormone in response to insulin-induced hypoglycemia. These data suggest that the dawn phenomenon is unusual in type 2 diabetes. Previously reported high prevalence rates in studies using similar sample size may be attributable to a Biostator-induced artifact. Decisions regarding therapies for type 2 diabetes should not be based on the assumption that the dawn phenomenon routinely causes early morning hyperglycemia.

Blood Glucose↗
PubMed2002

Control of postprandial hyperglycemia: optimal use of short-acting insulin secretagogues.

OBJECTIVE: This study was designed to compare the efficacy of acute premeal administration of glipizide versus nateglinide in controlling postprandial hyperglycemia in subjects with non-insulin-requiring type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 20 subjects (10 female, 10 male) with non-insulin-requiring type 2 diabetes were admitted overnight to the General Clinical Research Center on four occasions. In random order, 10 mg glipizide (30 min premeal), 120 mg nateglinide (15 min premeal), 10 mg glipizide plus nateglinide (30 and 15 min premeal, respectively), or placebo pills (30 and 15 min premeal) were administered in a double-blind fashion before a standardized breakfast. Blood was drawn for analysis of glucose, insulin, and C-peptide at -0.05, 0, 0.5, 1, 2, 3, and 4 h relative to the meal. RESULTS: The subjects were aged 56 +/- 2 years and were moderately obese (BMI 31 +/- 1 kg/m(2)), with a mean HbA(1c) of 7.4 +/- 0.4%. The peak postprandial glucose excursion above baseline was higher with placebo (6.1 +/- 0.5 mmol/l) than glipizide (4.3 +/- 0.6 mmol/l, P = 0.002), nateglinide (4.2 +/- 0.4 mmol/l, P = 0.001), or glipizide plus nateglinide (4.1 +/- 0.5 mmol/l, P = 0.001). The area under the curve for the glucose excursion above baseline was also higher with placebo (14.1 +/- 1.8 mmol/h. l) compared with glipizide (6.9 +/- 2.4 mmol/h. l, P = 0.002), nateglinide (9.7 +/- 2 mmol/h. l, P = 0.004), or glipizide plus nateglinide (5.6 +/- 2.2 mmol/h. l, P < 0.001). Peak and integrated glucose excursions did not differ significantly between glipizide and nateglinide. However, by 4 h postmeal, plasma glucose levels were significantly higher with nateglinide (9 +/- 0.9 mmol/l) compared with the premeal baseline (7.8 +/- 0.6 mmol/l, P = 0.04) and compared with the 4-h postprandial glucose level after administration of glipizide (7.6 +/- 0.6 mmol/l, P = 0.02). Integrated postprandial insulin levels were higher with glipizide (1,556 +/- 349 pmol/h. l) than nateglinide (1,364 +/- 231 pmol/h. l; P = 0.03). Early insulin secretion, as measured by insulin levels at 30 min postmeal, did not differ between glipizide and nateglinide. CONCLUSIONS: Acute premeal administration of nateglinide or glipizide has equal efficacy in controlling postbreakfast hyperglycemia in type 2 diabetes when each drug is administered at the optimum time before the meal. Glipizide causes a more pronounced and sustained postmeal insulin secretory response compared with nateglinide. Glipizide facilitates the return to near-fasting glucose levels at 4 h postmeal, but with the possible risk of increased frequency of postmeal hypoglycemia in drug-naive patients. The clinical decision to use glipizide versus nateglinide should be based on factors other than the control of postprandial hyperglycemia in type 2 diabetes.

C-Peptide↗
PubMedDate not supplied

Potential association of thyrotoxicosis with vitamin B and folate deficiencies, resulting in risk for hyperhomocysteinemia and subsequent thromboembolic events.

OBJECTIVE: To describe a patient with severe thyrotoxicosis attributable to Graves' disease who had a thrombotic cerebrovascular accident and hyperhomocysteinuria, which resolved on correction of the thyrotoxicosis, and to present findings in a pilot study undertaken to investigate the relationship among thyrotoxicosis, homocysteine, folate, and vitamin B(12). METHODS: We present a case report of the index case, with clinical and laboratory details. For the investigative analysis, 21 patients who were 18 to 50 years old and had newly diagnosed, untreated Graves' disease and 10 age-and sex-matched euthyroid control subjects were studied. Of the patients with Graves' disease, 11 underwent studies both at diagnosis and after treatment. Fasting blood tests were performed for thyrotropin, free thyroxine, homocys-teine, vitamin B(12), folate, and methylmalonic acid, a marker of vitamin B(12) deficiency. RESULTS: Vitamin B(12), folate, homocysteine, and methylmalonic acid levels were not significantly different between the thyrotoxic and control or posttreatment groups. In patients with thyrotoxicosis, however, free thyroxine was positively correlated with both homocysteine (r = 0.67; P = 0.03) and methylmalonic acid (r = 0.89; P = 0.003). CONCLUSION: The positive correlation between free thyroxine levels and both homocysteine and methylmalonic acid suggests that thyrotoxicosis may be associated with functional vitamin B(12) deficiency. Such a deficiency may result in clinically important hyperhomocysteine-mia.

Adolescent↗
PubMedDate not supplied

Effects of kelp supplementation on thyroid function in euthyroid subjects.

OBJECTIVE: To study the effects of ingestion of two different doses of supplemental kelp on the thyroid function of healthy euthyroid subjects. METHODS: We conducted a double-blind prospective clinical trial involving 36 healthy euthyroid subjects, who were randomly assigned to receive placebo (4 alfalfa capsules per day), low-dose kelp (2 kelp capsules and 2 alfalfa capsules per day), or high-dose kelp (4 kelp capsules per day) for 4 weeks. Thyrotropin (thyroid-stimulating hormone or TSH), free thyroxine, and total triiodothyronine were assessed at weeks 0, 4, and 6. Response to thyrotropin-releasing hormone stimulation, urinary iodine excretion, and basal metabolic rate were determined at weeks 0 and 4. RESULTS: TSH concentrations did not differ significantly between week 0 and week 4 in the placebo group (P = 0.16) but increased significantly in both the low-dose kelp (P = 0.04) and high-dose kelp (P = 0.002) groups. Free thyroxine concentrations decreased slightly but significantly after 4 weeks of placebo but were unchanged in the low-dose and the high-dose kelp groups. In contrast, total triiodothyronine levels did not differ significantly after 4 weeks of placebo or low-dose kelp therapy but were significantly decreased after high-dose kelp therapy (P = 0.04). Similarly, the thyrotropin-releasing hormone stimulation test showed no significant change in poststimulation TSH after 4 weeks in the placebo or low-dose kelp groups but revealed a significantly increased response after high-dose kelp therapy (P = 0.0002). The 24-hour urinary iodine excretion showed dose-dependent increases in the two kelp study groups. Basal metabolic rate did not change significantly in any study group during the 4-week study period. All thyroid laboratory values returned to baseline 2 weeks after cessation of kelp supplementation, except for TSH in the high-dose kelp group, which was significantly decreased. CONCLUSION: Short-term dietary supplementation with kelp significantly increases both basal and poststimulation TSH. These findings corroborate previous studies on the effects of supplemental iodide given to euthyroid subjects for a similar period. Further studies are needed to determine whether long-term kelp supplementation would cause clinically significant thyroid disease.

Adult↗