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

Gastroparesis is delayed gastric emptying of either solids or liquids, which occurs in the absence of mechanical obstruction. Although associated with many diseases, the most frequent cause of gastroparesis is diabetes mellitus. It is estimated that up to 50% of diabetic patients may have this problem. Symptoms of gastroparesis include postprandial nausea, epigastric pain/burning, bloating, early satiety, excessive eructation, anorexia and vomiting. The vomiting associated with gastroparesis often has the following two features: (1) emesis of undigested foods ingested more than four hours previous; and (2) emesis of undigested foods in the middle of the night or in the morning prior to eating breakfast. It is important to recognize and treat gastroparesis not only to decrease symptoms but also to prevent bezoar formation and nutritional deficiencies as well as to improve glycemic control in brittle diabetics. The purpose of this article is to review the physiology of gastric emptying and to use this information to understand the pharmacological therapies for this debilitating problem.
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PMID:Gastroparesis: current management. 878 40

A 9-year-old male Doberman Pinscher was referred to the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, for polyuria/polydipsia, anorexia, and vomiting. Laboratory examination of blood and urine revealed hyperglycemia, glucosuria, and acidosis. Diabetes mellitus was diagnosed but was very resistant to subsequent insulin treatment. At the owners' request, the dog was euthanatized and a postmortem examination was performed. In addition to hepatic, pancreatic, and renal changes compatible with diabetes mellitus, an acidophilic adenoma of the adenohypophysis was found. Immunohistochemical staining for growth hormone, adrenocorticotropic hormone, and prolactin showed a strong immunolabeling for growth hormone within the cytoplasm of the tumor cells. Although growth hormone level was not measured in the plasma, our findings suggest that the diabetes mellitus in this dog was caused by excess growth hormone secreted by the pituitary neoplasm.
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PMID:Diabetes mellitus in a dog with a growth hormone-producing acidophilic adenoma of the adenohypophysis. 881 49

In this paper a new immunological model of anorexia and bulimia nervosa will be presented in which the inflammatory cytokines are conceived as the fundamental regulators of body metabolism. This conception differs from the conventional view in which the inflammatory cytokines are perceived primarily as peptide molecules utilized by the immune system to control infection, inflammation and tissue or neuronal damage. Given that the inflammatory cytokines are also fundamental regulators of body metabolism, when they become dysregulated they create physiological chaos which results in the development of a number of autoimmune, metabolic and psychiatric disorders. In this proposed immunological model of anorexia and bulimia nervosa, elevated tumor necrosis factor-alpha features as the primary cause of these conditions. Pathophysiological parallels are drawn between anorexia nervosa and cancer cachexia in terms of the causal role the cytokines, neuropeptides and neurotransmitters play in the manifestation of shared symptoms. These shared symptoms include elevated tumour necrosis factor-alpha, down-regulated interleukin-2 and interleukin-4 and depletion of lean body mass. Furthermore, the following neuropeptides are dysregulated in both anorexia nervosa and cancer cachexia: vasoactive intestinal peptide, cholecystokinin, corticotropin-releasing factor, neuropeptide Y, peptide YY and beta-endorphin. In addition, in anorexia and bulimia nervosa, secretion of the neurotransmitter serotonin is inhibited while norepinephrine is enhanced. It will be argued that the causal interplay between the cytokines, neuropeptides and neurotransmitters initiates a cascade of biochemical events which may result in either anorexia or bulimia nervosa, or cancer cachexia. The extent to which these inflammatory cytokines, neuropeptides and neurotransmitters are causally efficacious in the pathogenesis of other autoimmune disorders, such as diabetes mellitus and rheumatoid arthritis, will also be addressed.
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PMID:The role of tumor necrosis factor-alpha in the pathogenesis of anorexia and bulimia nervosa, cancer cachexia and obesity. 896 Dec 38

Management of tuberculosis in a hospital environment is well systematized and may include chemoprophylaxis, which may be hazardous when used in psychiatric impairments. We examined retrospectively adverse events occurring during a 6-month period of antituberculosis treatment. Besides patients initially treated for active pulmonary tuberculosis, 16 other patients have benefited from chemoprophylaxis with isoniazid (INH) and/or rifampicin (RFP). All these patients (mean age 53 years) had been institutionalized for several years. Fifteen of them still received a mean of 5.4 +/- 2.2 drugs including 3.3 +/- 1.4 psychotropic agents. During antituberculous treatment, 5 patients (29 per cent) presented side effects: hyperuricaemia with pyrazinamide, neutropenia, dysphagia and anorexia, dizziness and falls, diabetes and fatal fulminant hepatitis associated with INH. Drug interactions were systemically searched for. Three probably led to clinical manifestations: they implicated INH with carbamazepine, RFP with theophylline and RFP with haloperidol. Our results suggest a greater sensitivity for adverse effects and drug interactions in psychiatric institutionalized patients. They pose the problem of the appropriateness of antituberculous chemoprophylaxis in such patients, particularly because of communication difficulties and polytherapy. The INH-RFP regimen should be avoided and the clinical and biological follow-up reinforced.
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PMID:[Adverse effects related to the use of antitubercular drugs in psychiatric centers: retrospective study at the Philippe Pinel CH in Amiens 1994]. 913 90

The management of diabetes mellitus is often complicated in patients with advanced cancer. Anorexia and nausea or vomiting make caloric intake erratic. The use of diabetogenic medications such as glucocorticoids can produce profound hyperglycemia. Many malignant tumors cause derangement in intermediary metabolism and abnormal glucose tolerance in up to one-third of patients. Both hyperglycemia and hypoglycemia impair the quality of life of dying patients. Swings in blood sugar should be avoided wherever possible, but aggressive blood sugar monitoring also impairs quality of life. This paper discusses issues in the management of diabetes in patients with advanced cancer and suggests guidelines for maintaining glycemic control without excessive interventions.
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PMID:The management of diabetes in patients with advanced cancer. 956 14

A 75-year-old female with diabetes mellitus, who was born and lived in West north Kyusyu, was admitted to our hospital, because of unconsciousness and loss of appetite. The physical examination showed neck stiffness and a high fever. The laboratory data showed accentuation of inflammatory reaction and azotemia and positive HTLV-1 antibody. The spinal fluid showed increase of cell count and amount of protein. A stool and sputum smear revealed rhabditis form larvae of the nematode. Antibiotics and ivermectin were administered for the bacterial meningitis and hyperinfection of the strongyloides, respectively. Consequently, meningitis and strongyloidiasis improved. It was considered that the patient was infected with strongyloides from her husband who serve in the army during World-War II, and hyperinfection of strongyloides resulted from the immunosuppressive state of diabetes mellitus. Ivermectin, and anti-strongyloides agent, was effective, and no side effects were seen. However, the therapeutic resistance in this case was associated with the positive HTLV-1 antibody.
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PMID:[A case of bacterial meningitis induced by strongyloidiasis]. 928 47

Pheochromocytoma usually is associated with a combination of various manifestations caused by overproduction of catecholamines. We encountered a case of an occult, catecholamine-secreting pheochromocytoma. A 70-year-old man was admitted to the hospital because of anorexia. He had been treated for diabetes mellitus for 4 years; during this period he did not have any other symptoms related to pheochromocytoma. At admission, serum epinephrine, norepinephrine, and glucose levels and urinary excretion of total metanephrine were elevated. A tumor was detected in the left adrenal region and diagnosed as pheochromocytoma. After tumor resection, the increased levels of catecholamines and glucose and the decreased urinary C-peptide were normalized. This suggests that the pheochromocytoma caused hyperglycemia without other manifestations for a long time.
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PMID:Occult extraadrenal pheochromocytoma treated as diabetes mellitus. 933 69

A report is presented of five aged patients with hemorrhagic colon ulcer, which was strongly suspected to be a side effect of non steroidal anti-inflammatory drugs (NSAID). All patients were suffering from orthopedic diseases and NSAIDs were administered for pain: Zaltoprofen for one patient and slow-releasing diclofenac for the other four. Four patients had being treated underlying diabetes mellitus and three of them were being treated with sulfonylurea. Appetite loss was the earliest symptom, 1-2 weeks after administration of NSAID began. Diarrhea occurred 1-2 weeks after appetite loss, and finally hemorrhagic stool developed 1-2 weeks after that. Acute gastric mucosal lesion, hemorrhagic colon ulcer and colitis were diagnosed in all patients by emergency gastro-duodenocolonoscopy. NSAID and oral diet were ceased, and intravenous hyperalimentation was instituted when the patients revealed severe anemia due to bleeding. All patients could take an oral diet after a few weeks. In conclusion hemorrhagic colon ulcer must be prevented in patients treated with NSAID especially those who are aged and have a history of diabetes mellitus.
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PMID:[Hemorrhagic colon ulcer as a side effect of non-steroidal anti-inflammatory drugs in five aged patients]. 943 Sep 88

Lectins are a family of proteins that stimulate cellular responses after binding to carbohydrate chains on plasma membranes. In the study described here, a mixture of lectins--pokeweed mitogen (PKW)--was shown to have insulinomimetic effects in mice. After receiving PKW (15 mg/kg intraperitoneally [IP]), serum glucose declined from 154 +/- 3 to 23 +/- 10 mg/dL by 24 hours later. Anorexia developed, and by 3 days, there was a significant decline in body weight. Carcass weights were 10% lower, and epididymal fat pad weights were 45% lower. When given for 16 days, PKW 3 mg/kg every other day caused a sustained 10% weight loss. Severe combined immune deficiency (SCID) mice were sensitive to PKW, showing that B and T lymphocytes were not required for the effects to develop. Cytokine antagonists attenuated the hypoglycemia and anorexia, but only by 50%. Further study showed that PKW has insulin-like effects in vitro. Glucose uptake was stimulated when murine C2C12 myotubes were exposed to an enriched fraction of PKW. These results demonstrated that PKW has both insulin-like activity and weight-reducing effects when administered to mice. The development of therapy for adult-onset diabetes or obesity based on lectins from pokeweed may be possible.
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PMID:The metabolic effects of pokeweed mitogen in mice. 944 Apr 81

Loss of lean body mass is common in patients with acute or chronic renal failure but the mechanisms causing this loss are only beginning to be understood. One mechanism involves an inability of uremic patients to activate the critical metabolic responses that maintain protein balance when dietary protein is limited. Metabolic responses to dietary protein restriction include a sharp reduction in the degradation of essential amino acids and protein; changes in protein synthesis are less reliable. If uremia prevents suppression of essential amino acid or protein degradation when dietary protein is reduced by anorexia, negative nitrogen balance and loss of lean body mass will ensue. One complication of uremia, metabolic acidosis, stimulates the degradation of branched-chain amino acids and proteins and therefore blocks the ability of the patient to respond to a low-protein diet. The mechanisms require glucocorticoids and involve increased activity of branched-chain keto acid dehydrogenase and the ubiquitin-proteasome proteolytic pathway; there also is increased transcription of genes encoding components of enzymes involved in the pathways. Besides acidosis, a low insulin concentration and cytokines activate the ubiquitin-proteasome proteolytic pathway. Understanding how proteolysis is activated, including how these genes are stimulated, is important because the same pathways are activated in diabetes, cancer, sepsis, burns, starvation, and muscle denervation. Activation of the ubiquitin-proteasome pathway leads to reduced lean body mass.
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PMID:Robert H Herman Memorial Award in Clinical Nutrition Lecture, 1997. Mechanisms causing loss of lean body mass in kidney disease. 949 77


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