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Biomedical subjects

M M McMahon

Publications and source records attributed to M M McMahon.

At least 19 recordsLinked to original sources
PubMed1999

Metabolic acidosis and thiamine deficiency.

We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly thiamine. After thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement. Clinicians must be aware that thiamine is essential for normal glucose metabolism and that thiamine deficiency can lead to lactic acidosis. Thiamine deficiency should be included in the differential diagnosis of lactic acidosis. The recent shortage of intravenous multivitamin preparations has led to documented cases of lactic acidosis as a result of thiamine deficiency, and a previous shortage led to several deaths due to lactic acidosis as a consequence of thiamine deficiency. All patients receiving parenteral nutrition must also receive adequate vitamin supplementation.

Acidosis↗
PubMed1996

Nutrition support in hospitalized patients with diabetes mellitus.

Many physicians will manage the care of hospitalized patients with diabetes mellitus who require parenteral nutrition or enteral tube feeding. The nutritional assessment, indications for nutrition support, estimate of nutritional needs, and biochemical monitoring guidelines for critically ill patients with diabetes are similar to those for nondiabetic patients. In general, a weight loss of up to 10% of body weight is well tolerated and, in the absence of severe stress, the provision of dextrose-containing crystalloid solutions and electrolytes is adequate for as long as 7 to 10 days. Studies that demonstrate a beneficial influence of nutrition support on clinical outcome administered nutrition for a minimum of 1 week. No data have established that support for a briefer duration is of clinical benefit. An important goal in the care of the hospitalized patient with diabetes is to avoid the extremes of hypoglycemia and hyperglycemia. Herein we provide our approach to achieving glucose control in stressed hospitalized patients with diabetes mellitus who are receiving parenteral and enteral nutrition. Although evidence is increasing that hyperglycemia impairs immune function, well-designed prospective randomized trials are needed to determine the risks, costs, and benefits of achieving glucose control and of providing nutrition support to hospitalized patients with diabetes mellitus.

Blood Glucose↗
PubMed1995

Host defenses and susceptibility to infection in patients with diabetes mellitus.

The recently completed Diabetes Control and Complications Trial (DCCT) provided compelling evidence that intensive treatment of people with insulin-dependent diabetes mellitus can delay or prevent diabetic microvascular complications. Although not studied in the DCCT, patients with noninsulin-dependent diabetes mellitus likely will benefit from near-normoglycemia. Although it is difficult to prove a similar causal relation between hyperglycemia and infection (this outcome was not looked for in the DCCT), there is substantial in vitro data and evolving clinical studies that support this hypothesis. This information is presented in this article following a review of the regulation of glucose levels.

Complement System Proteins↗
PubMed1993

Nutritional support of critically ill patients.

Severe depletion of body protein stores can result from prolonged starvation or from hormonal and cytokine-mediated effects during critical illness. Recent advances in the understanding of cytokine actions have substantially refined the interpretation of the nutritional assessment of critically ill patients. In addition, the design of nutritional programs for hospitalized patients has changed considerably during the past decade. Although nutritional support of critically ill patients will not lead to positive nitrogen balance, nutrition can increase protein synthesis, enhance immune function, and beneficially modify the body's response to an illness.

Critical Illness↗
PubMed1993

C-peptide during the prolonged fast in insulinoma.

C-Peptide, a marker for insulin secretion, is purported to be elevated in patients with insulinoma but diagnostic criteria have not been established. Thirty-seven patients with histologically confirmed insulinoma studied preoperatively, 19 normal subjects, and 2 patients who subsequently acknowledged self-administration of insulin underwent the prolonged fast (< or = 72 h) according to a standard protocol. Plasma glucose, C-peptide, and insulin were measured every 6 h until plasma glucose was less than or equal to 3.3 mmol, then hourly until Whipple's triad was demonstrated or until 72 h without symptoms was reached. At the termination of the fasts, plasma was analyzed for sulfonylurea. Statistical analysis was by rank sum test. Data are expressed as median (range). The durations of fasts were 20 (2.5-68) h for patients with insulinomas and 72 h for normal subjects. At the end of fasts plasma glucose, C-peptide, and insulin concentrations were 2.2 (1.4-2.9) vs. 3.6 (2.7-5.5) mmol, P < 0.001; 0.60 (0.20-1.92) vs. 0.13 (0.07-0.43) nmol, P < 0.001; and 126 (35-840) vs. 35 (35-126) pmol, P < 0.001, respectively, for insulinoma patients and normal subjects. All plasma samples were negative for sulfonylurea. Insulinoma patients had C-peptide values at the end of the fasts greater than or equal to 0.20 nmol whereas normal subjects and patients with insulin factitial hypoglycemia had C-peptide concentrations less than or equal to 0.10 nmol when plasma glucose was less than or equal to 2.8 mmol. Insulinoma is confirmed in a sulfonylurea negative patient with Whipple's triad during the prolonged fast and a concomitant C-peptide concentration greater than or equal to 0.20 nmol.

Adolescent↗
PubMed1991

Functioning insulinoma--incidence, recurrence, and long-term survival of patients: a 60-year study.

For the 60-year period from 1927 through 1986, we assessed the incidence, recurrence, and long-term survival among all Mayo Clinic patients with histologically confirmed functioning insulinoma. With use of the complete medical record system at Mayo and the comprehensive epidemiologic data base of residents of Olmsted County, Minnesota, we found 224 patients in whom an initial pancreatic exploration at Mayo had confirmed the presence of insulinoma. The median age (and range) of these patients at surgical diagnosis was 47 (8 to 82) years, and 59% were female patients. During the study period, eight cases of insulinoma occurred among residents of Olmsted County; their age and gender distributions were similar to those of the total cohort. The incidence of insulinoma among residents of Olmsted County increased during the study period to a stable level during the last 2 decades of 4 cases per 1 million person-years. For the total cohort, 7.6% had multiple endocrine neoplasia type I (MEN I), and 5.8% had malignant insulinoma. The risk of recurrence was greater among patients with MEN I (21% at 10 and 20 years) than in those without MEN I (5% at 10 years and 7% at 20 years). Although survival of the total cohort was not significantly impaired, it was significantly worse than expected for patients with malignant insulinoma (29% versus 88% expected at 10 years postoperatively). We conclude that insulinoma is less rare than previously suspected. After successful surgical removal, the long-term risk of recurrent insulinoma is relatively high in patients with MEN I; for patients with benign disease, the long-term survival is normal.

Adolescent↗
PubMed1991

Comparison of extracellular and net glucose oxidation measured isotopically and by indirect calorimetry during high and low glucose turnover.

To determine the extent to which glucose oxidation measured by indirect calorimetry reflects glucose oxidation measured isotopically, subjects were studied during a 6-h hyperinsulinemic euglycemic clamp (1 mU.kg-1.min-1) and during infusion of saline. [6-14C]glucose was infused on both occasions. Breath was collected for determination of the specific activity of carbon dioxide, oxygen consumption, and carbon dioxide production. Glucose turnover during hyperinsulinemia was approximately eightfold higher than during saline infusion. During the final 1.5 h of the hyperinsulinemic glucose clamp, oxidation measured isotopically remained slightly but consistently lower (P less than 0.05) than that measured by indirect calorimetry (13.8 +/- 1.1 vs 16.5 +/- 1.7 mumol.kg-1.min-1, respectively). In contrast, during the saline infusion, glucose oxidation measured isotopically did not differ from that measured by indirect calorimetry (8.3 +/- 0.6 vs 7.2 +/- 2.8 mumol.kg-1.min-1, respectively). We conclude that although net glucose oxidation measured isotopically was slightly lower than that measured by indirect calorimetry, both techniques provide similar estimates of glucose oxidation over a wide range of glucose disposal.

Adult↗
PubMed1990

The physiology of nutritional assessment and therapy in protein-calorie malnutrition.

Protein-calorie malnutrition (PCM), in the purest sense, is the result of depleted body protein stores due to semistarvation. A review of the hormonal response to simple semistarvation illustrates the elegant adaptive ability of the body to respond to an inadequate diet. By contrast, the body's metabolic response to an injury or illness stimulus is a dynamic process orchestrated by monokines and hormones. Although the injury response, strictly speaking, is not synonymous with PCM, the resultant increased energy expenditure, anorexia, and potential for skeletal muscle breakdown can result in an even more rapid depletion of body protein stores. Ultimately, the need for nutritional support depends on the amount of recent weight loss, anticipated time of insufficient oral intake, and the degree of stress. A discussion of basic concepts of anthropometry precedes examples of advantages and disadvantages of a given anthropometric parameter for selected disease states. The effects of PCM on visceral structure and function are discussed in detail so that the reader can appreciate why the metabolic response to injury may have a very different impact on the nourished compared with the malnourished patient. Particular attention is paid to the adverse effects of PCM on immune function and its antithesis, the beneficial impact of nutritional repletion on the immune system. An approach to refeeding discusses indications for initiation of nutritional support, choice of route, design of a macronutrient and micronutrient regimen, and guidelines for monitoring. Familiarity with the metabolic alterations of refeeding is key to the mitigation of potentially life-threatening complications of sudden refeeding. Appreciation of the anticipated response to nutrition is important, as the response will vary with the degree of stress. A nearly optimal response can be expected with appropriate nutrition in the nonstressed semistarved patient, whereas inefficient repletion is to be expected in the severely stressed patient. The review concludes with a discussion of the role of nutrition as a modifier of the body's metabolic response to injury.

Anthropometry↗
PubMed1990

Guidelines for refeeding the marasmic patient.

Nutritional support of the malnourished patient can be lifesaving. However, the efficacy of total parenteral nutrition in this setting depends on: a) careful estimation of energy requirements, using the Harris-Benedict equation or indirect calorimetry; b) minimizing the fluid retention which invariably complicates refeeding in marasmus; c) adequate repletion of P, K, and Mg on a daily basis; and d) accurate assessment of the rate of weight regain.

Basal Metabolism↗
PubMed1990

Overzealous resuscitation of an extremely malnourished patient with nutritional cardiomyopathy.

Overzealous resuscitation of the severely malnourished patient may be associated with life-threatening complications. A variety of electrolyte, hemodynamic, septic, and nutritional derangements may result in sudden decompensation and even death. We present a case that dramatically illustrates these complications and focuses on the key role of underlying nutritional cardiomyopathy.

Adult↗
PubMed1990

Long-term parenteral nutrition and metabolic bone disease.

Home parenteral nutrition has prevented malnutrition in patients who cannot maintain adequate nutrition by enteral feedings alone. The risk of bone and mineral abnormalities in these patients is significant for several reasons. Pre-existing skeletal disease can occur from factors known to affect the population at large as well as from malnutrition, malabsorption, and corticosteroid use related to the underlying disease process. Long-term use of infused nutrients and potential toxins can further alter bone turnover. Hypercalciuria is frequently present during HPN, yet its etiology is poorly defined. Parenteral nutrition admixture concentrations of calcium, phosphorus, protein, sodium, and dextrose may all play a role. Any development of acidosis can certainly aggravate hypercalciuria, which may be an indirect marker of abnormal bone turnover. Although increased protein intake can promote the development of acidosis-induced calciuresis, infused phosphorus and acetate can help reduce calcium excretion. Parenteral nutrition contamination by aluminum can cause a spectrum of osteomalacic bone disease similar to aluminum-associated changes seen in renal failure patients. Even with recent attempts to remove aluminum from the parenteral admixture, low-turnover bone disease can still occur. At present, HPN-related bone disease is a poorly understood entity because of its multifaceted nature. Patients receiving long-term parenteral nutrition should be considered to have an increased risk for the development of metabolic bone disease. Early monitoring for and treatment of bone disease should be considered in all patients receiving HPN.

Aluminum↗
PubMed1989

Diagnostic interpretation of the intravenous tolbutamide test for insulinoma.

The plasma glucose and insulin responses to intravenous administration of tolbutamide in patients with insulinoma and healthy control subjects were compared to determine the sensitivity and specificity of the intravenous tolbutamide test for the diagnosis of insulinoma. The records of 406 healthy persons without concurrent disease known to affect glucose homeostasis or insulin concentrations and 41 patients with histologically confirmed insulinoma who underwent standard intravenous tolbutamide testing during the period from 1976 to 1986 were reviewed. The 5th percentile of the mean of plasma glucose levels at the 120-, 150-, and 180-minute points (G120-180) after injection of tolbutamide was 55 mg/dl for lean and 62 mg/dl for obese control subjects. With 95% specificity, the sensitivity of these criteria was 95% for lean and 100% for obese patients with insulinoma. Minimal differences were observed between men and women. At 95% specificity, the sensitivities were less for the ratio of the 180-minute plasma glucose to fasting plasma glucose level (64% in lean and 75% in obese patients), for mean of plasma insulin at the 120-, 150-, and 180-minute points (IRI120-180) (53% in lean and 36% in obese patients), for maximal insulin concentration (27% in lean and 31% in obese patients), for increase in insulin concentration above basal (18% in lean and 23% in obese patients), and for the combined criteria of the 5th percentile of G120-180 and the 95th percentile of IRI120-180 (47% in lean and 73% in obese patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma, Islet Cell↗
PubMed1989

Underestimation of glucose turnover measured with [6-3H]- and [6,6-2H]- but not [6-14C]glucose during hyperinsulinemia in humans.

Recent studies indicate that hydrogen-labeled glucose tracers underestimate glucose turnover in humans under conditions of high flux. The cause of this underestimation is unknown. To determine whether the error is time-, pool-, model-, or insulin-dependent, glucose turnover was measured simultaneously with [6-3H]-, [6,6-2H2]-, and [6-14C]glucose during a 7-h infusion of either insulin (1 mU.kg-1.min-1) or saline. During the insulin infusion, steady-state glucose turnover measured with both [6-3H]glucose (8.0 +/- 0.5 mg.kg-1.min-1) and [6,6-2H2]glucose (7.6 +/- 0.5 mg.kg-1.min-1) was lower (P less than .01) than either the glucose infusion rate required to maintain euglycemia (9.8 +/- 0.7 mg.kg-1.min-1) or glucose turnover determined with [6-14C]glucose and corrected for Cori cycle activity (9.8 +/- 0.7 mg.kg-1.min-1). Consequently "negative" glucose production rates (P less than .01) were obtained with either [6-3H]- or [6,6-2H2]- but not [6-14C]glucose. The difference between turnover estimated with [6-3H]glucose and actual glucose disposal (or 14C glucose flux) did not decrease with time and was not dependent on duration of isotope infusion. During saline infusion, estimates of glucose turnover were similar regardless of the glucose tracer used. High-performance liquid chromatography of the radioactive glucose tracer and plasma revealed the presence of a tritiated nonglucose contaminant. Although the contaminant represented only 1.5% of the radioactivity in the [6-3H]glucose infusate, its clearance was 10-fold less (P less than .001) than that of [6-3H]glucose. This resulted in accumulation in plasma, with the contaminant accounting for 16.6 +/- 2.09 and 10.8 +/- 0.9% of what customarily is assumed to be plasma glucose radioactivity during the insulin or saline infusion, respectively (P less than .01). When corrected for the presence of the contaminant, glucose turnover determined with [6-3H]glucose during insulin infusion (9.5 +/- 0.6 mg.kg-1.min-1) no longer differed from either the glucose infusion rate or that determined with [6-14C]glucose. Therefore, the underestimation of glucose turnover during insulin infusion and negative glucose production rates observed with traditional methods to analyze plasma radioactivity and commercially available tracers is the result of an artifactual increase in [6-3H]glucose specific activity. The etiology of the underestimation of glucose turnover with [6,6-2H2]glucose remains to be determined.

Adult↗
PubMed1986

Follicular carcinoma of the thyroid presenting with hematuria: a case report.

A 59-year-old woman presented with hematuria in which a subsequent workup showed follicular carcinoma of the thyroid metastatic to the urinary bladder. Soft tissue metastasis from such a carcinoma is seen most commonly in the lungs and occasionally in the liver and kidneys. This case illustrates that follicular carcinoma of the thyroid may have a variable presentation, including hematuria.

Adenocarcinoma↗