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

Substantial in vitro evidence suggests that nitric oxide may be a major mediator of interleukin 1 (IL-1) induced pancreatic beta-cell inhibition and destruction in the initial events leading to insulin-dependent diabetes mellitus. Using NG-nitro-L-arginine methyl ester, an inhibitor of both the constitutive and the cytokine inducible forms of nitric oxide synthase, and aminoguanidine, a preferential inhibitor of the inducible form of nitric oxide synthase, we investigated the impact of inhibiting nitric oxide production on food-intake, body weight and temperature, blood glucose, plasma insulin, glucagon, corticosterone and leukocyte- and differential-counts in normal rats injected once daily for 5 days with interleukin 1 beta (IL-1 beta) (0.8 microgram/rat = 4.0 micrograms/kg). Inhibition of both the constitutive and the inducible forms of nitric oxide synthase prevented IL-1 beta-induced fever, hyperglycaemia, hypoinsulinemia, and hyperglucagonemia, and partially prevented lymphopenia and neutrophilia, but had no effect on IL-1 beta-induced anorexia and changes in plasma corticosterone. Preferential inhibition of the inducible form of nitric oxide synthase using two daily injections of 5 mg/rat of aminoguanidine prevented IL-1 beta-induced hyperglycaemia and hypoinsulinaemia, and slightly reduced the pyrogenicity of IL-1 on 3 out of 5 days. Higher doses of aminoguanidine (100 mg/rat) prevented lymphopenia and neutrophilia. We conclude that nitric oxide produced by the inducible form of nitric oxide synthase, mediates the IL-1 beta-induced inhibition of insulin release and that the effect of IL-1 beta on temperature, pancreatic alpha-cells, and leukocyte differential counts seems to be mediated by nitric oxide produced by the constitutive form of nitric oxide synthase.
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PMID:Interleukin 1 beta induces diabetes and fever in normal rats by nitric oxide via induction of different nitric oxide synthases. 753 59

Corticosteroids are extensively prescribed in advanced cancer for various specific indications (e.g. spinal cord compression), for pain relief, as hormone therapy and to stimulate appetite and wellbeing. Choice of corticosteroid is dictated largely by local fashion, and times of administration are more traditional than pharmacological. Corticosteroids have many potential disadvantages, some life-threatening (e.g. masked septicaemia). Others are seriously debilitating (e.g. myopathy, avascular bone necrosis). Oropharyngeal candidiasis is a common complication. Corticosteroids are withdrawn in about 5% of patients because of unacceptable adverse effects, including moon-face and diabetes mellitus. Corticosteroid hypersensitivity occurs, and the succinate salts have been associated with bronchospasm. Steroid pseudorheumatism may occur with high dose therapy or when tailing off after a prolonged course. Important drug interactions with corticosteroids relate to salt and water retention, and decreased glucose tolerance. Some anticonvulsants cause an increased clearance of corticosteroids and, with dexamethasone, up to a 50% reduction in the anticipated effect. The benefit of corticosteroids in terms of increased appetite, mood and activity has been demonstrated in several controlled trials. The effect may well be time-limited in most patients. In several studies, corticosteroids have resulted in an analgesic-sparing effect. Some centres use very high doses of dexamethasone in cases of spinal cord compression, although the justification for these is not obvious. Corticosteroids are used to help relieve nerve compression pain and in symptomatic raised intracranial pressure. Corticosteroids are also injected locally into or around bone metastases, particularly ribs and the sacro-iliac joints. Epidural injections are used for patients with troublesome intractable low back pain. Corticosteroids are now used less often in hypercalcaemia because of poor response rates. More benefit is obtained, however, if high dosages are used, e.g. prednisolone 60 to 80 mg/day. Dexamethasone is widely used as an antiemetic in association with chemotherapy. Some centres use dexamethasone by continuous subcutaneous infusion in selected patients when the oral route is not feasible. The choice of starting dose of a corticosteroid is largely arbitrary. It is important, however, not to miss a possible treatment benefit by prescribing too low a dose. For most patients, an initial dosage of prednisolone of 30 to 60 mg/day (dexamethasone 4 to 8 mg/day) is appropriate. In patients with anorexia, there are several alternative options that should be considered. There is evidence to suggest that patients with advanced cancer receiving a corticosteroid are not as closely monitored as other patients. There is a need to state clearly in writing the reason(s) for prescription and to review after 1 or 2 weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The risks and benefits of corticosteroids in advanced cancer. 781 99

The cytokine interleukin 1 beta (IL-1) has been implicated as a pathogenetic factor in the initial events leading to insulin-dependent diabetes mellitus. Previous studies investigating the impact of IL-1 on diabetes incidence in spontaneously diabetic rodent models have been conflicting. IL-1 induces anorexia and previous studies are hampered by the lack of pair-fed controls to the IL-1 treated animals. We report that daily injections of 4.0 micrograms/kg/day of recombinant human IL-1 (rhIL-1) for 13 weeks from 25-30 days of age did not alter the incidence of diabetes in the diabetes-prone (DP) BB rats (75%) when compared to pair-fed, vehicle treated controls (55%, p = 0.18), or to unhandled DP BB rats (80%, p = 0.71). However, IL-1 induced significantly higher blood glucose concentrations in the prediabetic period (p < 0.00005) and at diabetes onset (p < 0.00005) in the DP BB rats and caused episodes of blood glucose concentrations > 11 mmol/l in the prediabetic period in 11/20 DP BB rats compared to 4/27 diabetes-resistant (DR) BB rats and 4/28 Wistar Furth (WF) rats (both p < 0.004), compared to DP BB). Further, rhIL-1 induced fever in 11 weeks in the DP BB rats compared to 3 weeks in the DR BB and 6 weeks in the WF rats. Using high performance size exclusion chromatography specific anti-rhIL-1-antibodies were demonstrated in DR BB and WF, but not in DP BB rats. These antibodies neutralized the inhibitory effect of rhIL-1 on insulin secretion from isolated islets of Langerhans in vitro. The reduced pyrogenic and endocrine effect of rhIL-1 in the DR BB and WF rats compared to the DP BB rats could be explained by the impaired ability of the DP BB rats to produce anti-rhIL-1-antibodies. In conclusion, administration of rhIL-1 modulated the prediabetic period, and produced higher blood glucose concentrations at diagnosis, but did not change the diabetes incidence in DP BB rats. The results are not in conflict with the hypothesis that IL-1 is a pathogenetic factor in IDDM, caused by high local concentrations of rat IL-1 in the islets during early insulitis. The results also show the necessity of pair-feeding of the control group to the rhIL-1 group when interpreting data from experiments investigating rhIL-1 effects on diabetes development in animal models.
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PMID:Interleukin-1 beta (IL-1) does not reduce the diabetes incidence in diabetes-prone BB rats. 806 Nov 61

Two diabetic dogs were presented for anorexia, persistent fever, and poor control of hyperglycemia. Both had neutrophilia with left shift, hypoalbuminemia, and increased serum alkaline phosphatase (SAP) activity. Radiography indicated intrahepatic gas densities in 1 dog and a hepatic mass in the other. Abdominal sonography demonstrated multiple well-demarcated hypoechoic hepatic lesions consistent with abscesses. Both dogs were successfully treated by surgical resection of the abscessed liver lobes in conjunction with antibiotics and supportive therapy. Good control of hyperglycemia was achieved in both dogs after recovery. Intracellular and extracellular Gram-negative rod-shaped bacteria were abundant in the abscesses from both dogs. These cases suggest an association between diabetes mellitus and hepatic abscessation.
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PMID:Hepatic abscesses associated with diabetes mellitus in two dogs. 806 55

From 1982 to 1991, we experienced 76 patients with Mycoplasma pneumoniae pneumonia which were confirmed by serologic tests. There were 32 (42%) male and 44 (58%) female patients. One patient had underlying disease of diabetes mellitus while the other patients were in good health. The age ranged from 9 months old to 72 years old. All the patients complained of fever and coughing; 63% had dry cough and 37% had sputum production. Upper respiratory tract complaints such as rhinorrhea, sore throat, or earache were noted in 57% of the patients. Fifty-five percent of the patients had GI symptoms of anorexia, nausea, vomiting, or diarrhea. Other complaints included myalgia/arthralgia (29%), headache (30%), and general malaise (32%). Dyspnea (17%) and chest pain (20%) were occasional complaints. Seventy-one percent of the patients had WBC counts < 10000/cu mm and 29% > 10000/cu mm. The mean value of C-reactive protein (CRP) was 53.1 micrograms/ml, while 16% of the patients had a CRP value above 100 micrograms/ml. Thirty-one percent of the patients were noted to have a transient elevation of serum transaminase. Four different patterns of infiltration were seen in chest radiographic manifestation: 1) peribronchial and perivascular interstitial infiltrates (18.4%), 2) nonhomogeneous patchy consolidations (22.4%), 3) homogeneous acinar consolidations (27.6%), and 4) mixed interstitial and alveolar infiltrates (27.6%). Interstitial infiltration was more commonly seen in pediatric than adult patients (46% vs 20%). Other features of the radiologic manifestation were as follows: unilateral lesions in 80% of patients, single lobe lesions in 77%, lower lobe predominant in 69%, pleural effusion in 7%, and radiographic deterioration in 10%. Mycoplasmal pneumonia should be considered in the differential diagnosis of community-acquired pneumonias.
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PMID:Clinical study of Mycoplasma pneumoniae pneumonia. 832 Jul 55

Acute adrenal insufficiency is a rare disorder associated with high morbidity and mortality if allowed to progress unrecognized. A constellation of nonspecific symptoms including weakness, easy fatigue, nausea, anorexia, and weight loss are typical features of adrenal insufficiency. The index of suspicion should be particularly high if the patient has hyperpigmentation; hyponatremia and/or hyperkalemia; a history of autoimmune disease (hypothyroidism, diabetes) or recent prior use of exogenous steroids or if the patient is on anticoagulant therapy. Any decline in clinical status (hypotension, fever, decreasing mental status), especially in the setting of an acute intercurrent illness, should be treated aggressively, even before laboratory confirmation of the diagnosis. Diagnostic testing is fairly straightforward and readily available. The development of purified synthetic corticosteroid preparations has provided a safe and effective means of replacement. Early awareness, recognition, and intervention remain significant steps in altering the course of acute adrenal insufficiency.
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PMID:Acute adrenal insufficiency. 832 89

Numerous empirical studies indicate a higher frequency of eating disorders such as anorexia or bulimia nervosa in young female diabetic patients compared to the normal population. The comorbidity of the two syndromes usually leads to a continuous metabolic disorder bearing high risks of acute metabolic failure or early microangiopathic lesions. In addition to "restraint eating" as an essential element of diabetic therapy a premorbid neurotic malformation and/or poor coping strategies are further predisposing aspects for the development of an eating disorder. The inpatient treatment of a 22 year old patient suffering from both diabetes mellitus and bulimia nervosa demonstrates the association of neurotic malformation, poor coping style and the directive function of diabetic therapy.
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PMID:[Eating disorders and diabetes mellitus]. 856 Sep 50

We describe a case of hemoglobinopathy detected on admission for examination for high blood glucose levels and abnormal liver function. In 1991, it was pointed out that he had postprandial hyperglycemia. In 1994, at age 60, he had lassitude and anorexia. He was admitted to our hospital on the suspicion of diabetes mellitus and liver disease. Glycosylated hemoglobin levels was very high, but the 75 gram oral glucose tolerance test result was within the normal range. After abstinence from alcohol, his glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and gamma glutamyl traspeptidase became normal. Diabetes was excluded and abnormal hemoglobinopathy had been suspected. We analyzed his abnormal hemoglobin. In isoelectro-phoresis a fast moving variant was detected suggesting the presence of abnormal hemoglobin at the cathode. We fractionated hemolytic globin by CM-chromatography and detected an abnormal peak before the alpha chain band. Subsequently, we sequenced isolated abnormal alpha chain and detected the substitution of Ariginine for Glutamamine at position 92 (Hb J Cape Town). So far he has not demonstrated any symptoms or signs of HbJ Cape Town. Hemoglobinopathy is not uncommon in aged people.
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PMID:[A case of abnormal hemoglobin (HbJ Cape Town) with high serum levels of HbAlc]. 865 77

Metformin is an oral antihyperglycemic agent that is approved by the Food and Drug Administration for the treatment of noninsulin-dependent diabetes mellitus. It differs from the sulfonylureas in that it is does not enhance insulin secretion and normally does not produce hypoglycemia. Metformin acts to decrease preprandial and postprandial blood glucose concentrations by increasing skeletal muscle uptake of glucose, decreasing gluconeogenesis, and decreasing absorption of glucose. The addition of metformin to maximum dosages of a sulfonylurea may synergistically improve glucose control. The drug may offer other potential benefits, such as weight loss or minimal weight gain, improved blood flow in patients with peripheral vascular disease, reduction of tissue plasminogen activator inhibitor, and improved lipid profiles. It is relatively safe if taken appropriately. Its most common side effects are gastrointestinal (nausea, diarrhea, anorexia), metallic taste, and vitamin B12 malabsorption. Lactic acidosis may also occur, but it is rare if metformin is avoided in patients with contraindications to its use. With careful monitoring, the agent may be considered for the initial treatment of obese patients who fail dietary measures, and those whose disease is refractory to maximum dosages of sulfonylureas or who do not tolerate them.
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PMID:Metformin in noninsulin-dependent diabetes mellitus. 872 92

Using a validated postal questionnaire, we investigated the frequency of 24 gastrointestinal symptoms during the previous 3 months in a cohort of 110 young adult patients (54 males and 56 females, mean age 37.2 +/- 4.7 years) with onset of Type 1 diabetes mellitus at < 16 years of age. They were compared with 210 age- and sex-matched controls (104 males and 106 females). The main difference in the frequency of various symptoms between the two groups was a significant increase among the diabetic patients in upper gastrointestinal symptoms, such as loss of appetite (17.8% vs 3.6%, p < 0.001), early satiety (26.8% vs 6.1%, p < 0.001), nausea (22.7% vs 9.1%, p < 0.01) and vomiting (12.2% vs 3.0%, p < 0.01). No difference was noted in the frequency of symptoms from the lower gastrointestinal tract, apart from a significant increase in the feeling of incomplete defaecation (28.6% vs 17.0%, p < 0.04) in the diabetic patients. Patients with levels of haemoglobin A1c in the highest quartile had significantly more gastrointestinal symptoms than other diabetic patients. Further, the prevalence of symptoms was higher in females than in males. In conclusion, long-term Type 1 diabetes is accompanied by a markedly increased frequency of upper gastrointestinal symptoms, mainly in females and patients with poor metabolic control.
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PMID:Increased prevalence of upper gastrointestinal symptoms in long-term type 1 diabetes mellitus. 873 31


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