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Biomedical subjects

J M Falko

Publications and source records attributed to J M Falko.

At least 73 records · Page 4Linked to original sources
PubMed1979

Hyperlipoproteinemia and multifocal neurologic dysfunction in systemic lupus erythematosus.

Two patients with systemic lupus erythematosus, including one with neuropathologic findings, had recurrent multifocal neurologic dysfunction and hyperlipoproteinemia. The lipoprotein disturbances were complex and variable over time. Deficient lipoprotein lipase was found in both patients and appeared to be related temporally to neurologic deterioration. One of these patients had neurologic disease and lipoprotein abnormalities 2 1/2 years before SLE could be documented serologically. These studies suggest that lipoprotein lipase deficiency may be a marker for the endothelial disorder causing cerebral vasculopathy in SLE.

Adolescent↗
PubMed1977

Stimulation of pancreatic secretion of water and electrolytes by furosemide.

The effect of furosemide on secretin-stimulated pancreatic secretion was examined in 12 normal subjects using a perfusion method to quantitate pancreatic output. During continuous secretin infusion (0.9 U per kg per hr), secretory volume rose to a steady state level of 32.5 +/- 10.2 ml per min. When a bolus injection of furosemide (20 mg) was given during continuous secretin infusion, mean secretory volume increased further to a maximum value of 110 +/- 14.7 ml per min. Similarly, the outputs of bicarbonate, sodium, and chloride increased significantly after furosemide, compared to values obtained with secretin infusion alone. Total bilirubin output fell after furosemide, suggesting that the effect of furosemide on secretory volume and electrolyte output was not due to a stimulatory effect on bile flow. Furosemide also had no effect on duodenal water transport. These observations demonstrate that furosemide stimulates pancreatic secretion of water and electrolytes, possibly via inhibition of pancreatic ductal absorption of sodium.

Adult↗
PubMed1976

The insulinotropic effect of endogenous gastric inhibitory polypeptide in normal subjects.

Intravenously administered porcine GIP is insulinotropic in man. This study was designed to investigate the effects of simultaneous fat ingestion, a potent stimulus for GIP release, and intravenous glucose infusion upon endogenous serum GIP and insulin concentrations in normal subjects. Seven normal volunteers were studied on three separate occasions following: a) the ingestion of 67 grams of emulsified corn oil, b) constant intravenous infusion of glucose, and c) simultaneous administration of corn oil and glucose as in parts (a) and (b) of the study. Serum glucose, insulin (IRI), and GIP concentrations were measured at intervals between 15 and 180 minutes following each stimulus. With corn oil, mean serum GIP concentrations increased from a fasting level of 290 +/- 40 (SE) pg/ml to 1936 +/- 402 pg/ml at 60 minutes without a significant change in serum IRI or glucose concentrations. The infusion of intravenous glucose alone was associated with no rise in serum GIP levels despite a substantial increase in serum IRI and glucose concentrations. With the combined stimuli, mean serum GIP increased less (P is less than .05) between 30 and 90 minutes, and total integrated incremental GIP was significantly less (P is less than .025) than that after corn oil ingestion alone. Following the combined stimuli, incremental insulin levels were higher (P is less than .05) between 15 and 90 minutes, total integrated incremental insulin was greater (P is less than .025), and glucose homeostasis was significantly enhanced (P is less than .05) at 120 and 180 minutes compared with the effects on insulin of glucose infusion alone. We conclude that the potentiation of glucose-stimulated insulin secretion induced by the ingestion of fat is associated with serum GIP levels that are within the insulinotropic range. The augmented secretion of insulin may be mediated partially or completely by endogenous GIP. The lower serum GIP concentrations observed following the combined stimuli suggest a feedback inhibition of GIP release which is perhaps mediated by insulin.

Adult↗
PubMed1976

Inhibition of intestinal iron absorption by laundry starch.

The pathogenesis of iron deficiency anemia associated with amylophagia is usually attributed to dietary iron lack. However, large quantities of starch may inhibit intestinal iron absorption. Accordingly, studies were carried out to determine the effect of laundry starch on the intestinal absorption of inorganic and hemoglobin iron. In vitro, laundry starch bound 19 to 80% of the available 59FeSO4 and 34 to 68% of the available 59Fe-hemoglobin. Binding of both forms of iron was pH-dependent, with maximal binding at pH 7.0. In vivo, laundry starch significantly inhibited mucosal uptake of 59FeSO4 from isolated duodenal loops. In nonanemic rats, administration of laundry starch (100 mg) 1 hr before a 100-mug dose of 59FeSO4 significantly decreased the absorption of 59FeSO4, as compared to saline or low iron chow controls (6.2 +/- 2.0 versus 14.9 +/- 2.1 and -1.8 +/- 1.7, respectively, P less than 0.001). In anemic rats the absorption of either a 100-mug dose of 59FeSO4 or a 500-mug dose of 59Fe-hemoglobin was also significantly decreased by prior administration of laundry starch. The data obtained indicated that laundry starch (1) binds appreciable quantities of inorganic and hemoglobin iron in vitro; (2) inhibits the mucosal uptake or inorganic iron by isolated intestinal loops; (3) inhibits the intestinal absorption of inorganic iron in normal nonanemic rats, and (4) blunts the compensatory increase in inorganic and organic iron absorption in anemic rats.

Anemia, Hypochromic↗
PubMed1976

Primary hyperparathyroidism and anemia.

The frequency of anemia associated with primary hyperparathyroidism is uncertain. When anemia does occur, its mechanisms are obscure. Two patients with primary hyperparathyroidism and moderate normochromic, normocytic, reticulocytopenic anemia were studied in detail. Both had results of ferrokinetic studies that were consistent with the anemia of chronic disease; one had low serum iron concentrations and reduced normoblastic iron incorporation. Anemia in both patients resolved after parathyroidectomy. Clinical records of 100 nonuremic patients with primary hyperparathyroidism were reviewed and three other anemic patients were found. The cause of anemia in two of these individuals was bleeding in the upper gastrointestinal system, and the third had folate deficiency attributable to chronic alchoholism.

Adenoma↗
PubMed1975

Silent pancreatic pseudocyst. An unusual cause of extrahepatic biliary obstruction.

Extrahepatic biliary obstruction due to mechanical obstruction of the common bile duct is a relatively rare complication of pancreatic pseudocyst. When jaundice does occur, clinical or laboratory evidence of associated primary hepatobiliary disease or acute pancreatitis has invariably been present. The patient described had a 3-month history of painless juandice, 40-lb weight loss, pruritus, and hepatomegaly, but no clinical or biochemical evidence of acute or chronic pancreatitis. After initial evaluation, including an abdominal echogram and a transhepatic cholangiogram, carcinoma of the head of the pancreas was diagnosed preoperatively. At laparotomy, a small pancreatic pseudocyst obstructed the terminal portion of the common bile duct. This case illustrates that a pancreatic pseudocyst should be considered in the differential diagnosis of obstructive jaundice, even in the absence of clinical evidence of pancreatitis or pseudocyst formation.

Adult↗
PubMed1975

Gastric inhibitory polypeptide (GIP) stimulated by fat ingestion in man.

Ten normal volunteers ingested emulsified corn oil and the immunoreactive GIP, insulin (IRI) and nonesterified fatty acid (NEFA) responses were measured. Serum GIP levels increased after the ingestion of corn oil in all subjects, rising from a mean fasting level of 272 pg/ml to 856 +/- 272 pg/ml (P less than 0.05) by 30 minutes. The peak mean serum GIP concentration of 1,345 +/- 291 pg/ml occurred at 60 minutes; and mean serum GIP levels at 180 minutes remained significantly elevated over fasting values. Serum IRI, glucose and NEFA concentrations did not change during the 180 minutes of study. No changes in serum GIP concentrations occurred when, for control purposes, six volunteers ingested water on another day. We conclude: 1) Fat is a potent stimulus for the release of GIP in normal individuals. 2) Endogenously released GIP is not insulinotropic under the conditions of this study.

Adult↗
PubMedDate not supplied

Case report. Congestive heart failure complicating the hungry bone syndrome.

A patient with the hungry bone syndrome following parathyroidectomy for hyperparathyroidism developed congestive heart failure, probably due to the myocardial depressant effects of hypocalcemia and hypomagnesmia. Calcium and magnesium alone were instrumental in relieving his symptoms, decreasing his heart size, and clearing the pulmonary congestion. A mechanism for the pathogenesis of hypocalcemia and hypomagnesemia induced heart failure is proposed.

Adult↗
PubMedDate not supplied

Limitations in usefulness of single dose intermediate acting insulin: a rapid response pattern in some type I diabetics.

Ten Type I insulin-dependent diabetics who were receiving single daily injections of intermediate acting insulin were studied to assess time-response characteristics of this therapy on 24-hour profiles of both glucose and free insulin. Nine of ten patients had undetectable postprandial levels of C-peptide. All patients had insulin antibodies typical of chronically treated Type I diabetes. Mean peak free insulin levels occurred four hours post injection with free insulin rising from 12.3 +/- 1.6 microU/ml to 26.5 +/- 1.4 microU/ml; p less than 0.01. The glucose nadir for the 24-hour profile also occurred at four hours after injection with glucose declining from 199 +/- 29 mg/dl fasting to 155 +/- 5 mg/dl; p less than 0.05. There was significant negative correlation between mean glucose and free insulin throughout the first six hours after insulin injection (r = -0.74; p less than 0.02); no correlation occurred 8 to 12 hours post injection. Two of the ten patients had hypoglycemic symptoms within four hours after their morning insulin. Although free insulin levels remained above basal for 20 hours, single dose intermediate insulin therapy never really controlled postprandial glucose levels after breakfast or lunch. These data suggest there may be limitations in managing Type I diabetics with single dose intermediate insulin. Furthermore, some patients on intermediate acting insulin may have a more rapid than anticipated maximal hypoglycemic response, often within four hours.

Adult↗
PubMedDate not supplied

The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose.

To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). Serum insulin, glucose, and GIP were measured. In each of the 3 h after sugar ingestion the integrated insulin response to (S) was greater than to (G) with the 3-h total being 104% greater. The integrated glucose response to (S) was slightly greater than to (G) in the first and second hours but the differences were not significant. Integrated GIP response to (S) was greater than to (G) in hours 2 and 3. Although significant insulin and glucose responses to (F) occurred in hour 1, G + F led to insulin and glucose responses similar to G. G + F led to greater GIP levels than G in hour 3. These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. This may result from delayed gastric emptying and glucose absorption. The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP.

Adult↗
PubMedDate not supplied

The effects of physiologic amounts of simple sugars on lipoprotein, glucose, and insulin levels in normal subjects.

Using a crossover design, eight healthy volunteers randomly received physiologic amounts (1/3 of each subject's total carbohydrate intake) of either fructose or sucrose as the primary source of simple sugar, incorporated into isocaloric diets comprised of typical American foods. After 7 and 14 days of consuming either of the two sugars, no change occurred in fasting glucose or insulin levels. In addition, total triglyceride, total cholesterol, low-density-lipoprotein (LDL) cholesterol, and high-density-lipoprotein (HDL) cholesterol concentrations were unaltered. Since our study used conventional foods in normal eating patterns rather than contrived formulas or excessive amounts of simple sugar, our data indicate that there is no difference between sucrose or fructose on various lipid components or glucose and fasting insulin levels in the "real world" in normal subjects.

Adult↗
PubMedDate not supplied

Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients.

Patients with type II diabetes mellitus (type II DM patients) are characteristically obese, hyperinsulinemic, and non-ketosis prone. Recently, we have encountered several obese type II DM patients with either diabetic ketoacidosis or significant ketonuria after insulin withdrawal. There was no evidence of infection, stress, or starvation to explain their ketonuria. Therefore, we assessed serum connecting peptide (C-peptide) response to oral glucose in 14 obese, insulin-treated type II DM patients: 6 with and 8 without episodes of spontaneous ketonuria. The group presenting with ketonuria had low to absent basal and stimulated serum C-peptide responses. The nonketonuric group had higher basal C-peptide (P less than 0.01) concentrations that increased significantly (P less than 0.001) after oral glucose compared with those of the ketonuric group. Clinical characteristics and biochemical control were similar in both groups. Our findings confirm that obese type II diabetes mellitus is a heterogeneous disease with variable fasting and stimulated C-peptide responses. Spontaneous ketonuria could be a feature in the clinical presentation of the patients especially in the presence of both low fasting and stimulated C-peptide levels. The significance of these findings is unclear but suggests individualization in the management of type II DM patients and cautious withdrawal of insulin therapy in such patients. Furthermore, serum C-peptide levels alone cannot be recommended to classify patients into either type I or type II diabetes mellitus.

Aged↗