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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A newborn infant, small for her gestational age with macroglossia and transient insulinopenic diabetes mellitus is described. Two similar cases have been found in the literature. Flat glucose tolerance test results were found in the mother, the mechanism of which was not disclosed; there was no evidence of hyperinsulinism or malabsorption syndrome and the response of plasma growth hormone, and cortisol, and of urinary epinephrine to insulin-induced hypoglycemia was adequate. It is suggested that the triad of intrauterine growth retardation, macroglossia, and transient neonatal diabetes mellitus constitutes a distinct clinical entity. The link to the maternal abnormalities of carbohydrated homeostasis remains speculative.
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PMID:Macroglossia, transient neonatal diabetes mellitus and intrauterine growth failure: a new distinct entity? 111 Aug 57

The diagnosis of pancreatic disease is difficult. The first step is clinical suspicion, based on the symptoms and signs. If pancreatic disease is suspected, investigation is necessary to prove this diagnosis. Investigation aims to answer two questions: a) is there pancreatic disease and b) if so, what type? The first question may be answered by demonstrating abnormal pancreatic function, using pancreatic function tests, whereas the second is answered by using techniques to demonstrate structural (anatomical) abnormalities of the pancreas. a) The methods to establish abnormal pancreatic function consist of 1. tests to demonstrate abnormal digestive capability, 2. tests to study pancreatic exocrine secretion, and 3. tests to study endocrine secretion. The tests of group 1 are: chemical fat balance study before and during enzyme replacement therapy, faecal nitrogen balance study, and the demonstration of either the malabsorption of vitamins A, D and K or the sequelae of their malabsorption (low serum calcium, high alkaline phosphatase, prolonged prothrombin time, etc.). Abnormal vitamin B12 absorption also may be present. 2. The tests designed to study pancreatic exocrine secretion are determination of the presence or absence of proteolytic enzymes in the stool, the secretion test, the pancreozymin stimulation test and the Lundh test. The serum amylase and lipase values are of little help in assessment of pancreatic function. 3. The tests to study endocrine function are the glucose tolerances test (which frequently gives abnormal results in pancreatic disease), and radioimmunoassays for insulin and gastrointestinal hormones (which may be increased in patients with functioning tumours of the islet cells). b) The techniques used to establish structural abnormalities of the pancreas are: duodenal cytology (during secretin tests), radiological techniques (abdominal survey films, barium meal, hypotonic duodenography, roentgenography of the biliary tract, barium enema, and angiography,) gastroscopy, duodensocopy, endoscopy and retrograde pancreatography, echography, scan and laparotomy. The relative value of these tests is discussed.
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PMID:Diagnosis of chronic pancreatic disease. 127 46

The influence of insulin on plasma and bone mineral homeostasis was studied in the BB rat model, which develops an autoimmune form of diabetes at the age of about 100 days. Untreated diabetes of short duration resulted in hypercalciuria and intestinal calcium malabsorption despite increased free concentrations of serum 1,25-dihydroxyvitamin D. The concentrations of two vitamin D-dependent calcium-binding proteins were also decreased: a low duodenal calbindin-D 9K concentration corresponding to the low intestinal active calcium absorption and a low serum osteocalcin concentration, corresponding to a low bone formation and highly correlated with serum IGF-I concentration. Indeed, on bone histology a very low number of osteoblasts and low osteoblast activity (osteoid formation and mineral apposition rate) were observed. Similar abnormalities persisted in rats with long-standing diabetes resulting in markedly decreased bone mass and increased brittleness of bone. Diabetes therefore resulted in low-turnover osteoporosis. Several hormones (testosterone, growth hormone and 1,25-dihydroxyvitamin D) and growth factors (IGF-I and its binding proteins) with known effects on bone were markedly decreased in diabetic rats. A continuous infusion of testosterone, GH or 1,25-(OH)2D3 for 14 d by miniosmotic pumps could not improve the biochemical or histomorphometric abnormalities. Insulin infusion for 2 weeks, however, rapidly increased and overcorrected the number of osteoblasts, normalized serum osteocalcin and IGF-I concentrations but could not yet normalize bone mineralization. Continuous infusion of IGF-I alone did not improve the osteoblast number of osteocalcin but markedly stimulated bone mineralization. From these data we can conclude that both insulin and IGF-I are potent bone growth factors but with different mode of action. In human type 1 diabetes, a similar decrease in serum osteocalcin and IGF-I was observed. A reduction of regional bone mass, both in long and trabecular bones, is frequently observed in human diabetes. Cumulative data from case control studies indicate that the life-time fracture risk is increased in diabetes.
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PMID:Diabetic bone disease. Low turnover osteoporosis related to decreased IGF-I production. 146 60

The medical records of six cases of nesidioblastosis were examined to determine the diagnostic approach, treatment, and neurologic sequelae. All six patients were male, and their ages at the onset of the disease ranged from one day to six months (mean 3.36 +/- 2.5 mo.). Initial clinical features were seizure, cyanosis, poor feeding, and apnea. Other subsequent symptoms were developmental delay, hyperactivity, and cold sweating. The Birth weight of the neonatal onset group was heavier than the postneonatal onset group (4.4 +/- 0.3 vs 3.26 +/- 0.04 kg). Before the diagnosis of hyperinsulinism, steroids of ACTH proved effective for seizure control. Initially, hyperinsulinemia (serum insulin greater than 10 microU/ml) was detected in four cases, but another two cases also showed hyperinsulinism by insulin/glucose(I/G) ratio greater than 0.3 during the fasting test. The glucagon response performed in 2 cases, showed normal and partial responses. Euglycemia was obtained by near total pancreatectomy (95% pancreatic resection)without malabsorption or persistent diabetes. In one case, nesidioblastoma coexisted with nesidioblastosis. Developmental delay was noted in three cases. In this group, the mean duration between symptom onset and operation was longer than the group without developmental delay (1.25 +/- 0.47 vs 0.38 +/- 0.19 yr).
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PMID:A study on nesidioblastosis in hyperinsulinemic hypoglycemia--diagnosis, treatment, and neurologic sequelae. 171 Sep 1

Dependent on the dosages used, digestion and absorption inhibitors or disaccharidase inhibitors, such as Acarbose, might cause malabsorption of nutrients, and hence, among other effects, affect caloric balances. This negative effect on caloric balance has actually been well documented in animal experimentation. However, in nondiabetic subjects with excessive degrees of obesity, no consistent weight reduction could be induced by disaccharidase inhibitors. Subsequently, Acarbose has been advocated for type 2 diabetic patients in dosages that might reduce postprandial hyperglycemia and insulinemia, whereas significant degrees of malabsorption should be excluded. At these dosages of the drug, there is no clinical perspective with regard to weight-reducing (side) effects of disaccharidase inhibitors. Whether a hypothetical diminution of serum insulin daily profiles during Acarbose treatment in obese type 2 diabetic patients might contribute to a normalization of the metabolic syndrome and to a facilitation of weight-reducing efforts remains speculative. At present, there does not seem to be much rationale in trying to exploit digestion and/or absorption inhibitors for weight-reduction therapies in obesity, unless they are used to enforce a negative caloric balance by malabsorption of nutrients.
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PMID:Pharmacological treatment of obesity: digestion and absorption inhibitors-clinical perspective. 172 47

In two randomized, placebo-controlled, double-blind studies, the efficacy, duration of action and tolerability of a single morning dose of 25, 50, and 100 mg miglitol (BAY m 1099), an absorbable inhibitor of intestinal alpha-glucosidases, were assessed after repetitive sucrose or maize-starch loads (50 g of carbohydrates in 400 ml of water each at 08.00, 12.00, and 17.00 h). With sucrose, miglitol reduced the postprandial rise in blood glucose, serum insulin and serum gastric inhibitory polypeptide concentrations at any dosage. This effect was dose-dependent and confined to the first carbohydrate load in the morning, thus indicating the duration of alpha-glucosidase inhibition of less than 4 h. Sucrose malabsorption, indicated by breath hydrogen responses, occurred dose-dependently with 50 and 100 mg, but not with 25 mg of miglitol. Similarly, symptoms of carbohydrate malabsorption were absent with 25 mg of the inhibitor and mild to moderate after 50 and 100 mg of miglitol. With starch as the substrate, BAY m 1099 led to a significant amelioration of glycemic and hormonal rises after the first meal, but not thereafter. A numerical dose dependency was recognized, but this was not significant at the 5% level. Symptoms of carbohydrate malabsorption were absent with 25 mg and negligible with 50 mg BAY m 1099, but occurred almost regularly with the 100-mg dose. Breath hydrogen concentrations increased gradually with the dose of miglitol administered. A single morning dose of 25-100 mg of miglitol thus may be useful for the control of postprandial hyperglycemia after breakfast. Due to the duration of action of less than 4 h, this substance should be given with the three main meals.
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PMID:Inhibition of glycemic and hormonal responses after repetitive sucrose and starch loads by different doses of the alpha-glucosidase inhibitor miglitol (BAY m 1099) in man. 178 28

The absorbable deoxynojirimycin derivative emiglitate (BAY o 1248) is a potent competitive inhibitor of small intestinal alpha-glucosidases in man. In two similar randomized, placebo-controlled, double blind investigations, the efficacy, duration of action and tolerability of single doses of 10, 20 and 40 mg emiglitate have been assessed in healthy male volunteers after repeated sucrose or maize-starch loads at 08.00, 12.00 and 17.00 h. Even at the lowest dose used, emiglitate almost abolished the glycaemic (-88%) and hormonal responses after the first sucrose meal, simultaneously evoking significant hydrogen evolution (mean peak H2-concentration greater than 100 ppm), which was not related to the dose, and which induced unacceptable symptoms of carbohydrate malabsorption, i.e. at the dosages tested, the inhibition of glycaemic and hormonal responses was at the expense of intolerable gastrointestinal adverse effects. Flattening of postprandial responses of blood glucose, serum insulin and gastric inhibitory polypeptide was still apparent after a second sucrose load 4 h later, demonstrating long-lasting inhibition of alpha-glucosidase activity. After starch, the dose dependency of inhibition emerged more clearly than after sucrose, i.e. the reduction was less pronounced. However, emiglitate led to significant reduction of the glycaemic and hormonal rises after both the first and second starch meals. Symptoms of carbohydrate malabsorption were absent after 10 mg and were negligible with 20 mg or 40 mg emiglitate. Breath hydrogen concentration increased gradually, indicating slight but significant carbohydrate malabsorption after the highest dose of the alpha-glucosidase inhibitor. The results show that a single morning dose of 20-40 mg emiglitate might be useful in the control of postprandial hyperglycaemia after breakfast and lunch.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of sucrose- and starch-induced glycaemic and hormonal responses by the alpha-glucosidase inhibitor emiglitate (BAY o 1248) in healthy volunteers. 181 67

Little information has been reported on the metabolic characteristics of the totally pancreatectomized patient or the efficacy of medical management after radical pancreatic surgery. The prospective evaluation of 49 such patients, with 31% followed for 48 or more months, forms the basis of this report. The major immediate postoperative challenge is control of diarrhea and weight stabilization. Chronically patients have an increased daily caloric requirement (mean +/- SE, 56 +/- 1 kcal/kg), not wholly explained by moderate steatorrhea (fecal fat excretion, 16% +/- 2% of unrestricted fat intake). Despite persistent malabsorption, deficiencies in fat-soluble vitamin, magnesium, and trace element serum levels can be prevented in most patients. Pancreatogenic diabetes is characterized by (1) absence of the major glucoregulatory hormones insulin and glucagon, (2) instability, and (3) frequent hypoglycemia, with the latter parameters improving with rigorous home glucose monitoring. No patient has developed clinically overt diabetic micro- or macrovascular disease. Performance status in long-term survivors has been reasonable. However adverse chronic sequelae of the operation occur and include an unusual frequency of liver disease, characterized by accelerated fatty infiltration, and osteopenia, with an 18% reduction in radial bone mineral content noted in pancreatectomized patients studied more than 5 years after surgery.
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PMID:Metabolic consequences of (regional) total pancreatectomy. 186 20

IgA and IgG antigliadin antibodies were measured in 498 patients with insulin dependent diabetes mellitus and no history of intestinal malabsorption. Thirty patients had abnormal concentrations of antigliadin antibodies; 22 of these had an intestinal biopsy carried out and 16 of the 22 had subtotal villous atrophy suggestive of coeliac disease (prevalence 3.2%). There were no significant differences between patients with coeliac disease and diabetes and diabetic patients with normal IgA antigliadin antibodies in any of the nutritional variables measured, duration of diabetes, and mean insulin requirement. The mean age of onset of diabetes and attainment of expected height for age were both significantly lower in the patients with both diseases. Typing HLA classes I and II was done in 242 patients. The incidence of HLA-B8, DR3, and DQW2, which are commonly associated with both the diseases, is increased when both are present.
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PMID:Screening of diabetic children for coeliac disease with antigliadin antibodies and HLA typing. 203 7

We have treated 16 acromegalic patients for up to 44 months with octreotide in varying doses. Growth hormone levels were suppressed in 14 patients with associated clinical improvement. IGF-1 levels were measured in 12 and fell into the normal range in 10. Prolactin was suppressed in six hyperprolactinaemic patients but was unaltered in normoprolactinaemic acromegalic patients. Post-prandial hyperglycaemia with impaired insulin secretion was noted in all patients, and one patient required oral hypoglycaemic agents. Octreotide did not affect thyroid function. CT scans from before and after six months of treatment demonstrated minimal tumour shrinkage in only two patients. Octreotide was well tolerated with no serious haematological or biochemical disturbance and no evidence of malabsorption. Two patients developed gallstones. Octreotide is effective in acromegaly. The development of gallstones is the only serious adverse event we have encountered.
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PMID:Long-term treatment of acromegaly with a long-acting analogue of somatostatin, octreotide. 211 18


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