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Biomedical subjects

M R Burge

Publications and source records attributed to M R Burge.

31 records · Page 2Linked to original sources
PubMed1997

Small cell carcinoma of the vagina causing Cushing's syndrome by ectopic production and secretion of ACTH: a case report.

BACKGROUND: Small cell carcinomas of pulmonary or extrapulmonary origin are neuroendocrine tumors classically associated with ectopic hormone production, particularly ACTH secretion resulting in Cushing's syndrome. However, ectopic Cushing's syndrome has not previously been reported in the setting of small cell carcinoma of the vagina. METHODS: A primary vaginal tumor with hepatic metastases was evaluated with light microscopy. Serum cortisol and plasma ACTH levels were evaluated by radioimmunoassay and immunoradiometric assay, respectively, during a standard high-dose (8 mg) overnight dexamethasone suppression test. RESULTS: Vaginal small cell carcinoma with hepatic metastases was demonstrated. Electrolyte abnormalities, elevated cortisol and ACTH levels, and failure to suppress ACTH secretion during high-dose dexamethasone administration confirmed the diagnosis of ectopic ACTH syndrome. CONCLUSIONS: This case report establishes a clinical association between vaginal small cell carcinoma and ectopic Cushing's syndrome, confirming the neuroendocrine potential of this malignancy and features common to small cell neoplasms originating in other sites.

ACTH Syndrome, Ectopic↗
PubMed1997

Idiopathic hypogonadotropic hypogonadism in a male runner is reversed by clomiphene citrate.

OBJECTIVE: To assess the efficacy of estrogen antagonist therapy on the function of the hypothalamic-pituitary-testicular axis in a young male runner with significant morbidity attributable to idiopathic hypogonadotropic hypogonadism. DESIGN: An uncontrolled case study. SETTING: The outpatient endocrinology clinic of a university tertiary referral center. PATIENT(S): A 29-year-old male who has run 50 to 90 miles per week since 15 years of age and who presented with a pelvic stress fracture, markedly decreased bone mineral density, and symptomatic hypogonadotropic hypogonadism. INTERVENTION(S): Clomiphene citrate (CC) at doses up to 50 mg two times per day over a 5-month period. MAIN OUTCOME MEASURE(S): Serum concentrations of LH, FSH, and T before and after CC therapy, as well as clinical indicators of gonadal function. RESULT(S): Barely detectable levels of LH and FSH associated with hypogonadal levels of T were restored to the normal range with CC therapy. The patient experienced improved erectile function, increased testicular size and sexual hair growth, and an improved sense of well being. CONCLUSION(S): Exercise-induced hypogonadotropic hypogonadism exists as a clinical entity among male endurance athletes, and CC may provide a safe and effective treatment option for males with debilitating hypogonadism related to endurance exercise.

Adult↗
PubMed1997

Insulins.

More than ever before in the history of diabetes therapy, patients and health care providers have the necessary pharmacologic tools available to achieve near-normal blood glucose control. Achievement of this goal, however, requires an in-depth knowledge of the pharmacology and limitations of the currently available insulins. A willingness to try new strategies combined with a creative approach to each patient will result in optimal diabetes management. Continued advances in the development of insulin analogues and investigation into alternative routes of insulin delivery are likely to expand therapeutic options in the near future. Such developments will continue to improve the quality of life and health of patients with diabetes.

Animals↗
PubMed1997

Prolonged efficacy of short acting insulin Lispro in combination with human ultralente in insulin-dependent diabetes mellitus.

Insulin Lispro is a newly FDA approved analog of human insulin that exhibits rapid absorption and a short duration of action after sc injection. Although Lispro insulin improves immediate postprandial glycemia compared to Regular insulin, long term trials of Lispro insulin have not shown improvement in overall glycemic control, as determined by glycosylated hemoglobin. We hypothesize that this lack of improvement is attributable to the development of late postprandial hyperglycemia secondary to a waning of Lispro insulin's effect in conjunction with continued meal absorption. This study was designed to evaluate the duration of Lispro-induced reductions in plasma glucose after a standardized meal when Lispro insulin is incorporated into a regimen typically employed in insulin-dependent diabetes mellitus. After establishment of euglycemia overnight, 12 healthy IDDM patients received human Ultralente insulin (0.2 U/kg) alone and in combination with each of the following treatments in random sequence immediately before ingesting a 750-Cal American Diabetes Association breakfast: 1) 0.15 U/kg human Regular insulin (Regular 0.15 group), 2) 0.15 U/kg Lispro insulin (Lispro 0.15 group), 3) 0.1 U/kg Lispro insulin (Lispro 0.1 group), and 4) an equimolar (1:1) mixture of Lispro and Regular insulins (0.15 U/kg; 1:1 Mix group). Glucose and hormonal parameters were assessed for 8 h after the meal. Peak postprandial glucose was increased in the Regular insulin group compared to that in all groups that incorporated Lispro insulin (P < 0.001). Glucose area under the curve (AUC) was decreased in the Lispro 0.15 group compared to that in the Lispro 0.1 group, and glucose AUC was decreased in the Lispro 0.15 and 1:1 Mix groups compared to that in the group given Regular insulin (P < 0.001). Mean plasma glucose concentrations during the final hour of study were increased in the Ultralente group compared with those in all other treatment groups and were increased in the Lispro 0.1 group compared with those in the Regular, Lispro 0.15, and 1:1 Mix groups (P < 0.05). Insulin AUC was significantly reduced in the Lispro 0.1 group compared to those in all other short acting insulin groups (P < 0.001), and time to peak insulin was more rapid in the two Lispro groups than those in all other treatment groups (P < 0.01). The glucagon response was significantly greater in the Ultralente group compared to those with all other treatments. There was no difference in the development of hypoglycemia between the groups. This study demonstrates that the reductions in plasma glucose effected by Lispro insulin are consistent and stable for 8 h after meal ingestion when Lispro insulin is used in combination with human Ultralente insulin. These findings suggest that improvement in overall glycemia, as assessed by glycosylated hemoglobin, may be achievable with Lispro insulin if adequate doses are administered.

Adult↗
PubMed1997

Meal composition is a determinant of lispro-induced hypoglycemia in IDDM.

OBJECTIVE: Lispro is a newly FDA-approved analog of human insulin that will be widely used in patients with IDDM. This insulin, however, may have an increased potential for hypoglycemia because of its very rapid subcutaneous absorption, especially in a setting of decreased carbohydrate intake. Using a short-term prospective randomized parallel group-study design, we studied the incidence of hypoglycemia when lispro was given before breakfast compared with regular human insulin. Since carbohydrate intake is a determinant of postprandial glycemia, we administered three isocaloric meals characterized by low, average, and high carbohydrate content. RESEARCH DESIGN AND METHODS: Two groups of six IDDM subjects were randomized to receive 0.15 U/kg of lispro or regular human insulin subcutaneously before the ingestion of three 500-kcal breakfast meals of differing carbohydrate content on separate days. Lispro was administered at mealtime, and regular insulin was administered 30 min before mealtime. RESULTS: Postprandial plasma glucose concentrations were decreased in the lispro group compared with the regular-insulin group for all three meal types (P < 0.05), and hypoglycemia developed more frequently and rapidly in the lispro group, compared with the regular-insulin group by survival analysis. Additionally, peak insulin concentrations were higher (P < 0.001) and peaked more rapidly (P < 0.05) in the lispro group, compared with the regular-insulin group. CONCLUSIONS: We conclude that lispro has a tendency for early postprandial hypoglycemia compared with regular insulin in the setting of reduced carbohydrate intake. This fact should be told to patients who decide to switch from regular insulin to lispro. Health care professionals should instruct their IDDM patients to monitor glucose levels frequently after switching to lispro since adjustments in their carbohydrate intake and/or their lispro dosage may be necessary to avoid hypoglycemia.

Adult↗
PubMed1996

Diabetes mellitus: 2. Managing type II disease.

For a large and growing number of people in the United States, too much fatty food, too little activity, and an inherited tendency toward insulin resistance add up to type II diabetes. Improved diet and regular exercise are the ideal therapy. But most patients also require pharmacologic intervention to keep the disorder in check and to ward off microvascular and macrovascular and complications.

Adult↗
PubMed1996

Diabetes mellitus: 1. Improving control in type I disease.

Current consensus stresses intensive insulin therapy, with the goal of bringing blood glucose levels to near normal. Achieving and maintaining that goal involves educating the patient, encouraging regular glucose determinations, and gradually adjusting the dosage and timing of insulin administration to match the patient's glucose levels and lifestyle.

Adult↗
PubMed1995

Brittle diabetes: etiology and treatment.

Brittle diabetes is an uncommon complication of type I diabetes. However, the seriousness of the complication and its demands on the health care system warrant aggressive intervention. Studies during the last decade demonstrate that brittle diabetes is always secondary to a specific, identifiable etiology. This etiology is rarely apparent, however, without both extensive metabolic and psychological testing. In the long term, this testing is cost-effective inasmuch as approximately 50% of brittle diabetic patients are amenable to specific therapy. Several important issues have been clarified during the last decade, during which time major attempts have been made to understand the etiology of brittle diabetes. These issues may be summarized as follows: 1. There is always a specific etiology causing the brittle diabetes. 2. There are many different causes of brittle diabetes, but the most common are psychological abnormalities. 3. Therapy should always be directed at correcting the underlying pathogenic factor(s). 4. Empirical therapy and invasive procedures are contraindicated in brittle diabetic patients. 5. Extensive evaluation of a brittle diabetic patient may require referral of the patient to a diabetes center that has the expertise and manpower to appropriately evaluate a brittle diabetic patient. 6. Close follow-up and continued evaluation of therapy are necessary to confirm the suspected etiology and prevent diabetic ketoacidosis from developing. Unfortunately, only 50% of brittle diabetic patients respond to specific etiologic treatment. Research efforts during the next decade will focus on several clinical problems. First, improved psychological interventions are needed for common causes such as manipulative behavior and factitious disease. Second, treatment of severe systemic insulin resistance is still a major therapeutic challenge. Third, impaired glucose counterregulation needs to be better understood so that treatment is possible. The ultimate goal for physicians caring for brittle diabetic patients is to have effective therapy for all causes of brittle diabetes.

Diabetes Mellitus, Type 1↗
PubMed1994

A treatable cause of recurrent severe hypoglycemia.

OBJECTIVE: To see if glucocorticoid deficiency might explain increased insulin sensitivity causing severe brittle diabetes in two type I diabetic patients. CASES: We describe two patients who developed brittle diabetes characterized by recurrent severe hypoglycemia on small daily insulin doses with severe hyperglycemia on further insulin dose reduction. In both patients, insulin requirements had fallen markedly. RESULTS: Both patients were found to have glucocorticoid deficiency. In one patient, this was a result of hypopituitarism, in which hypoglycemia was aggravated by growth hormone deficiency. In the other patient, glucocorticoid deficiency was the result of primary adrenal failure. Resolution of brittle diabetes and restoration of normal insulin doses followed steroid replacement therapy in both patients. CONCLUSIONS: These patients emphasize the importance of seeking an organic cause for recurrent severe hypoglycemia. Increasing insulin sensitivity in type I diabetic patients should alert clinicians to the possibility of glucocorticoid deficiency.

Adult↗
PubMed1993

Short-term fasting is a mechanism for the development of euglycemic ketoacidosis during periods of insulin deficiency.

To determine the etiology of euglycemic ketoacidosis, the effect of a 32-h fast on the rate of metabolic deterioration was examined in a group of 10 healthy subjects with type I diabetes mellitus. Patients were studied during 5 h of insulin withdrawal after 8 h (postprandial) and 32 h (fasted) of food deprivation. Study parameters included substrate levels, electrolytes, counterregulatory hormone levels, and rates of glucose and glycerol turnover. In the fasted state, mean peak plasma glucose concentrations were significantly lower than those in the 8-h postprandial state (13.3 +/- 1.6 vs. 17.4 +/- 1.4 mmol/L, respectively; P < 0.05), and mean rates of glucose production were also significantly lower at all time points in the fasting state. The rate of development of ketosis was significantly more rapid during insulin deficiency after a fast (8.82 +/- 0.63 vs. 6.23 +/- 0.30 micro/L.min; P < 0.05), while plasma nonesterified fatty acids and glycerol turnover showed a biphasic response to insulin withdrawal, which was also more robust after a fast. Metabolic acidosis, as reflected in the rate of decrease in serum bicarbonate concentration, was more severe after 32 h of fasting than in the postprandial state (mean nadir, 15.4 +/- 0.9 vs. 18.6 +/- 0.5 mmol/L; P < 0.001). In contrast to values in the postprandial state, serum glucagon levels rose during insulin withdrawal in the fasting state, and plasma norepinephrine levels also correlated positively with the ongoing metabolic decompensation. Other counterregulatory hormones did not differ significantly in the fasted vs. postprandial states in these short term metabolic studies. We conclude that a fast of moderate duration, such as might be expected to occur during the development of diabetic ketoacidosis, predisposes patients with type I diabetes to euglycemic ketoacidosis during periods of insulin deficiency. Furthermore, decreased rates of hepatic glucose production are responsible for the lower plasma glucose values observed during a fast. The development of ketosis continued progressively in both conditions, but the rate of rise of plasma ketones was increased in the fasted state. This accelerated development of ketosis may be attributable to the effects of elevated levels of glucagon and/or catecholamines on lipolysis.

Adult↗