Gene R. Pesola

Insulin secretion and action in patients with pancreatic cancer

The authors investigated insulin secretory capacity and insulin action in 11 preoperative patients with pancreatic carcinoma and 15 age‐matched and weight‐matched healthy subjects (C). Five patients were classified as diabetic (D), two as impaired glucose tolerant (IGT), and four as nondiabetic (ND). Postabsorptive serum insulin levels (mean ± SE, in uU/ml) in D (12 ± 2), IGT (17 ± 7), and ND (10 ± 2) were comparable. After administration of 100 g of oral glucose, peak insulin achieved in D (60 ± 11) was lower than in IGT (101 ± 26) and ND (83 ± 20), whereas peak insulin levels in IGT and ND were significantly (P < 0.05) higher than in C (45 ± 6). Comparable insulin response to nonglucose stimuli was documented in all subjects using the slow arginine infusion test with mean serum insulin of 27 ± 4 in D, 28 ± 6 in IGT, 34 ± 10 in ND, and 32 ± 5 in C. In six patients (P) and six controls, insulin action was assessed by the euglycemic hyperinsulinemic clamp technique, with glucose turnover rates estimated by [3‐3H]glucose infusion. Steady‐state plasma glucose concentrations were maintained at 92 ± 3 (P) and 91 ± 1 mg/dl (C). After insulin infusion at the rate of 1.0 mU/kg/min, comparable high physiologic insulin levels were observed in P (73 to 104 uU/ml) and in C (81 to 103 uU/ml). Postabsorptive rates of endogenous glucose appearance (Ra) were higher in P (2.86 to 3.02 mg/kg/min) than in C (1.50 to 2.80 mg/kg/min). At high physiologic insulin concentrations, negative Ra values were documented in all subjects, and complete suppression of Ra was assumed. Total body glucose use (M) was consistently lower in P (3.90 to 6.40 mg/kg/min) than in C (6.98 to 10.40 mg/kg/min), consistent with a state of insulin resistance. Patients with pancreatic cancer manifest insulin resistance by virtue of a decrease in total body glucose use (M) and decreased insulin response to glucose due to either inherent beta cell dysfunction or decreased islet cell mass. The latter is not identifiable by histologic morphology.

Relationship between glucose oxidation and FFA concentration in septic cancer-bearing patients

Glucose oxidation is inhibited in severely ill patients. The present investigation was designed to study the relationship between glucose tissue uptake, glucose oxidation, and FFA concentration in septic cancer-bearing patients. The influence of glucose infusion alone (3.9 mg x kg-1 x min-1), followed by a euglycemic clamp with the same glucose load, on oxidation of glucose, plasma FFA concentration, and lipid oxidation were measured in eight septic cancer-bearing patients. During infusion of 3.9 mg glucose x kg-1 x min-1 glucose tissue uptake was 4.6 +/- 0.3 mg x kg-1 x min-1, glucose oxidation 0.5 +/- 0.2 mg x kg-1 x min-1, FFA concentration 377 +/- 52 mumol x L-1, and lipid oxidation 2.0 +/- 0.2 mumol x kg-1 x min-1. During the euglycemic clamp glucose tissue uptake was 4.4 +/- 0.3 mg x kg-1 x min-1, glucose oxidation rose to 1.8 mg x kg-1 x min-1 (.001 less than P less than .01), FFA concentration dropped to 202 +/- 23 mumol x L-1 (P less than .001), and lipid oxidation to 1.2 +/- 0.2 mumol x kg-1 x min-1 (.001 less than P less than .01). Nonprotein respiratory quotient rose from 0.73 +/- 0.02 to 0.85 +/- 0.02 (.001 less than P less than .01); 11% +/- 5% of the total amount of glucose taken up by the tissues was oxidized during infusion of glucose alone and increased to 42% +/- 6% during the euglycemic glucose clamp. It is concluded that in septic cancer-bearing patients glucose oxidation is inhibited during infusion of 3.9 mg glucose x kg-1 x min-1, even when expressed as percentage of glucose tissue uptake. With insulin, glucose tissue uptake was not influenced, but glucose oxidation expressed as percentage of glucose tissue uptake was normalized.

Pulmonary embolus-induced disseminated intravascular coagulation.

Pulmonary embolus as a cause of disseminated intravascular coagulation has only recently been recognized. The hemorrhagic disorder reported in the past was associated with little or no bleeding. We report a case of pulmonary embolus associated with life-threatening disseminated intravascular coagulation.

Thermodilution cardiac output: Proximal lumen versus right ventricular port

ObjectiveTo assess the accuracy of thermodilution cardiac output measurements from the right ventricular port vs. the central venous port. In addition, waveform patterns were evaluated in 50 right-heart catheters to determine the actual location of the right ventricular port. DesignCentral venous port cardiac output measurements were compared with right ventricular port cardiac output measurements using the same right-heart catheter. SettingThe general ICU of Memorial Sloan-Kettering Cancer Center. PatientsForty-seven critically ill cancer patients with 60 different right-heart catheters were evaluated. InterventionFour injections of 10 mL of iced normal saline were made through each port, with the results of the last three injections averaged. Cardiac output determinations from both ports were completed in < 10 min. The order of port injection was random. ResultsNo difference was noted between cardiac output determinations from the two ports (paired t-test). Twenty-five of 50 right-heart catheters were in the right ventricle, with the other 25 in the right atrium. A comparison of ports in the 25 catheters that were in the right ventricle showed no difference with a significant (p < .01, r2 = .94) correlation. ConclusionThermodilution cardiac output measurements using 10 mL of iced saline can be determined accurately using the right ventricular port if the central venous port becomes nonfunctional. (Crit Care Med 1991; 19:563)

Primary Ciliary Dyskinesia With Central Pair Agenesis: A Rare Cause of Adult Bronchiectasis

The etiology of bronchiectasis is undetermined in one half of adults. Consideration of primary ciliary dyskinesia (PCD), a diagnosis made in childhood, may not occur in adults without dextrocardia. A 37-year-old man with recurrent sinusitis, cough, and sputum production was noted to have bronchiectasis on chest computed tomography. A work-up for tuberculosis, human immunodeficiency syndrome infection, cystic fibrosis, &agr;-1 antitrypsin deficiency, and collagen vascular disease was negative. There was no family history of chronic lung disease but the mother and father were distant relatives. A maxillary sinus biopsy was performed to rule out PCD and it came back positive with central pair agenesis on transmission electron microscopy. PCD with central pair agenesis does not occur with dextrocardia and has never been clinically described in an adult. Definitive diagnosis requires ciliary biopsy and cross-sectional examination with electron microscopy. All adults with idiopathic bronchiectasis should be considered for ciliary biopsy.