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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-five patients (25 male and 20 female) over 12 years of age with cystic fibrosis have been studied clinically, radiologically and physiologically. Their mean age at the first visit was 17 years; they were followed for a mean period of 4 years and attended at least every six months. The first symptom which developed before the age of five in 42 of the 45 patients was respiratory. Thirty-two of the 45 patients had severe lung disease (Group III) at the start of the study of the seven patients died during the study. Cough and sputum were almost universal, 23 had haemoptyses and eight pneumothoraces. Staphylococcus pyogenes, Haemophilus influenzae and Pseudomonas aeruginosa were the common pathogens isolated from sputum and the increasing prevalence of the latter was again confirmed. Acquisition of the mucoid strain of pseudomonas signified poor prognosis. Established infection was never eradicated. Forty-three patients had evidence of pancreatic insufficiency; in all but one patient the symptoms were mild and five patients abandoned dietary restriction and pancreatin without ill effect. Seven patients had symptoms of partial bowel obstruction (meconium ileus equivalent) but only one required surgical relief. The liver was enlarged in seven patients and the spleen was felt in three. Three patients had diabetes mellitus. The influence of cystic fibrosis on growth and development is reported--the growth spurt is late in the majority but growth failure is not confined to those with severe lung infection or malabsorption and in these circumstances remains unexplained. Mean weight was low in relation to height and puberty was delayed in both sexes.
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PMID:Cystic fibrosis in adolescents and adults. 82 Oct 91

Very frequently in acute and chronic pancreatitis, the surgical treatment is indispensable. The disease itself is accompanied by metabolic disturbances, protein deficiency, hepatic lesion, by diabetes and malabsorption syndrome. Following the laboratory parameters we were able to perform partial or total hyperalimentation, correction of acid-base dis-equilibrium and to obtain the positive nitrogen balance, and in this way keep the patients in optimal conditions pre- and postoperatively.
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PMID:[Metabolic disorders and current treatment of the surgical patient with pancreatitis]. 85 52

Subtotal pancreatectomy in the rat was performed by a new method. Except for a small remnant along the splenal hilus, the gland was completely removed. Exocrine pancreatic insufficiency was confirmed by fat and nitrogen malabsorption. A moderate diabetes mellitus was seen. Insulin substitution or diet restriction was unnecessary. The absorption of vitamin B12 after oral administration of 10 ng 57CoB12 was 5.0 +/- 0.2 (ng 57CoB12 +/- S.E.M.) in unoperated rats and 5.1 +/- 0.1 in pancreatectomized rats (p greater than 0.5). Pancreatic extract (PE) (100 mg) increased the absorption of 57CoB12 in unoperated rats (p less than 0.01), but not in pancreatectomized rats (p greater than 0.2). PE (300 mg) reduced the absorption in unoperated rats (p less than 0.01). The results indicate that an optimal amount of pancreatic secretion may stimulate the absorption of vitamin B12.
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PMID:The absorption of vitamin B12 after subtotal pancreatectomy in the rat. 99 34

Chronic pancreatitis has to be treated in the first line by medical means. Dietary procedures, absolute abstinence from alcohol, compensation of malabsorption and treatment of diabetes will do in most cases. Surgery is indicated in cases resistent to this form of therapy of when complications arise (cysts, persistent jaundice, portal hypertension). The patient has to be given high caloric parenteral nutrition preoperatively. Pancreato-jejunostomy with an Y shaped loop and surgical removal of various amounts of pancreatic tissue are the only efficient surgical procedures. In cases of dilatation of the pancreatic duct drainage has to be performed. Results of surgery are satisfactory in 2/3 of cases.
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PMID:[Medical and surgical management of chronic pancreatitis (author's transl)]. 100 87

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

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

The SeHCAT test was used to investigate possible bile acid malabsorption in 166 patients presenting to a district general hospital with chronic diarrhoea of uncertain cause. Eighty-four (51%) patients had impaired SeHCAT retention. These included 23 of 28 patients with a possible type I abnormality (terminal ileal resection or disease, previous pelvic radiotherapy), 20 of 74 with a possible type II abnormality (idiopathic diarrhoea), 32 of 45 with a possible type III abnormality (post-cholecystectomy, post-vagotomy), and 9 of 19 with diarrhoea associated with diabetes. Patients with severe bile acid malabsorption demonstrated a good response to cholestyramine whereas the response in patients with a mildly abnormal SeHCAT retention was variable. Bile acid malabsorption is an important cause of diarrhoea in patients presenting with unexplained chronic diarrhoea.
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PMID:Use of the SeHCAT test in the investigation of diarrhoea. 140 91

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

Gastrointestinal dysfunction due to autonomous neuropathy is a complication described in various diseases such as diabetes mellitus, multiple sclerosis, and familial amyloidosis with polyneuropathy. We present the results of a prospective investigation of bile acid malabsorption in 17 patients with familial amyloidosis by means of 75Se-labelled homocholic-tauro acid (SeHCAT). The diagnosis was in all cases verified by the DNA test for mutation of transthyretin in position 30. Small-intestinal biopsy specimens were examined for deposits of amyloid, and the presence of gastric retention was evaluated by gastroscopy. In addition, the patients were investigated for bacterial overgrowth by means of the bile acid breath test (BABT). A high frequency of abnormal BABT results (44%) was encountered. However, 65% also had abnormal low SeHCAT values, indicating bile acid malabsorption. Only two patients had abnormal BABT and normal SeHCAT results, indicating bacterial contamination of the small intestine. Bile acid losses increased with the duration of gastrointestinal symptoms. Significantly lower SeHCAT values were encountered in patients with gastric retention, whereas the occurrence of amyloid deposits in small-intestinal biopsy specimens was without effect on SeHCAT retention. Bile acid malabsorption is frequently encountered in familial amyloidosis with polyneuropathy and seems to be more closely associated with gastrointestinal motility dysfunction than with amyloid deposits in the intestinal mucosa.
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PMID:Bile acid malabsorption caused by gastrointestinal motility dysfunction? An investigation of gastrointestinal disturbances in familial amyloidosis with polyneuropathy. 150 82

Diarrhea is a common gastrointestinal problem in diabetes, and its prevalence has been underestimated. The cause of diabetic diarrhea is unknown, but it is probably related to gastrointestinal motility disturbances secondary to diabetic autonomic neuropathy. Other causes (especially primary malabsorption syndromes and islet cell tumors) must be excluded. Treatment of diabetic diarrhea is largely symptomatic and only moderately effective. Antidiarrheal agents may ameliorate acute episodes. Broad-spectrum antibiotics and clonidine hydrochloride (Catapres) have had some success in long-term control. Most recently, subcutaneous administration of somatostatin analogues has been shown to be helpful, the main side effects being drowsiness and vomiting.
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PMID:Diabetic diarrhea. An underdiagnosed complication? 160 50


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