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

This study sought to determine, firstly, the relative frequency of lymphocytes and macrophages and, secondly, the percentage of lymphocytes containing interferon-gamma in inflamed islets (insulitis) of patients with type 1 (insulin-dependent) diabetes. Autopsy pancreases of 12 patients who had died of recent-onset type 1 diabetes and one pre-diabetic patient who had died of cardiomyopathy were examined immunohistochemically. In the 87 islets that were studied, the lymphocyte macrophage ratio was 9.7:1 and approximately 40 per cent of the lymphocytes contained interferon-gamma. Interferon-gamma release in the insulitis process may be involved in the pathogenesis of type 1 diabetes.
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PMID:Insulitis in type 1 (insulin-dependent) diabetes mellitus in man--macrophages, lymphocytes, and interferon-gamma containing cells. 174 3

The paper proposes a new classification to describe the normal senile heart and its pathological forms: "small aortic heart" (nonhypertrophic-dilatative myocardiopathy and its ischemic form) and "large aortic heart" (hypertrophic-dilatative myocardiopathy and its ischemic form). The statistical distribution of 241 elderly patients with diabetes mellitus using this classification was compared to a control group of 92 elderly non-diabetic subjects. The results reveal the significant epidemiological incidence of ischemic cardiopathy with small aortic heart in diabetic patients compared to the control group in which more ischemic hypertrophic-dilatative cardiopathies were present. This observation supports the hypothesis that senile diabetic cardiopathy begins with a metabolic block with reduced contractile energy, and the overlying important ischemic component leads to the development of the small-size clinical phenotype.
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PMID:[The heart, the elderly, and diabetes mellitus. Epidemiologic study of 333 ambulatory clinical cases]. 174 77

What then are the lessons to be learned about prevention and treatment of hemochromatosis? Early diagnosis is essential. The best indicator would be testing of serum iron and total saturation followed by a serum ferritin if elevated. Once these indices are abnormally high, MRI and or a liver biopsy should confirm the stage of the iron over-loaded state. If indeed the patient is not iron-overloaded (normal liver biopsy in the face of high saturation and ferritin level) phlebotomies should be performed until these indices are normal and then maintained at a normal level. This should entail four to six phlebotomies a year. Family members should also be screened and managed in a like manner. HLA typing may be a partially helpful screening device. The abnormal gene is closely linked on chromosome 6 with HLA histocompatibility loci. Now, by means of HLA typing, we can identify heterozygote carriers and homozygous (abnormal) among first degree relatives of patients with hemochromatosis. Unfortunately, HLA typing can only be used within a given family and cannot be used to screen the general population. It is estimated that 70% of hemochromatoics have the antigen HLA-A3; however, so does 28% of the (well) general population. Patients with unexplained cirrhosis, arthritis, liver disease, diabetes, impotency, cardiomyopathy and neurological symptoms should be screened in a like manner. Routine health practice profile chemistries must include a serum iron and iron saturation, and if high followed by a serum ferritin. Once diagnosed, therapy must be maintained with phlebotomy for the life time of the patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemochromatosis: diagnosis and treatment. 179 61

Considering the important role of the phosphocreatine energy shuttle in contractile function of the heart we decided to study the different components of this shuttle in STZ-induced diabetic rat heart with a known diabetic related cardiomyopathy. Diabetes produced a gradual decline in total CK activity, reaching a maximum of 35-40% decrease after 4 weeks of diabetes, in both atria and ventricles. All of the CK isoenzymes including the mitochondrial CK (CKm) were reduced but to a different extent in these two tissues. The percentage reduction in diabetic ventricles was BB greater than MB greater than CKm greater than MM and in atria was CKm greater than BB greater than MB greater than MM. A major difference between atrium and ventricle was the greater loss of CKm in diabetic atria than diabetic ventricle (75% in atria vs 32% in ventricle). The B subunit seemed to be the one that was affected the most followed by CKm isoenzyme and then the M subunit. The bound myofibrillar CK isoenzyme, expressed as units of activity/mg of myofibrillar protein, was not affected by 4 weeks of diabetes. The high energy phosphates were also reduced in diabetic heart with a greater reduction in phosphocreatine (43-45%) and a smaller change in ATP (27%). Mitochondrial oxidative phosphorylation with alpha-ketoglutarate was reduced (55%) in diabetic heart, whereas, there was no difference when succinate was used as substrate. These changes were reversible by 4 weeks of insulin treatment. The loss of CKm, phosphocreatine and the reduction in mitochondrial oxidative phosphorylation, could result in an inefficient phosphocreatine energy shuttle which could contribute to the cardiac functional defects associated with diabetes.
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PMID:Alteration of the phosphocreatine energy shuttle components in diabetic rat heart. 180 23

Non-insulin-dependent diabetic (NIDD) male Wistar rats develop a cardiomyopathy approximately 9 mo after the onset of the diabetic condition. This cardiomyopathy is characterized by reduced contractility, relaxation, cardiac work, and diastolic compliance. Although the basis for these defects is not completely understood, altered cellular Ca2+ regulation appears to play a major role in their development. In both isolated sarcolemmal membrane and cardiomyocytes, significant diabetes-linked defects in Ca2+ metabolism were observed. A small, but significant, decrease in the rate of sarcolemmal ATP-dependent Ca2+ transport of the diabetic heart was observed. Also evident was a major defect in sarcolemmal Na(+)-Ca2+ exchange as determined by reduced Na(+)-dependent Ca2+ transport into vesicles and Na(+)-dependent Ca2+ efflux from 45Ca(2+)-loaded cardiomyocytes from diabetic rats. In isolated cardiomyocytes, it was observed that the relative fluorescence of fura-2 at 502 nm was higher in cells from NIDD hearts, suggestive of a higher cytosolic free Ca2+. Consistent with diabetes-linked defects in Ca(2+)-transporter activities, the accumulation of Ca2+ after depolarization with KCl was greater in the diabetic. This study demonstrates that diabetes-induced defects in Ca2+ movement by the various Ca2+ transporters lead to abnormal cytosolic Ca2+ regulation by the diabetic cardiomyocytes. This observation supports the notion that abnormal Ca2+ regulation contributes to the development of the NIDD cardiomyopathy.
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PMID:Non-insulin-dependent diabetes-induced defects in cardiac cellular calcium regulation. 182 24

Hypertensive diabetic rats develop a cardiomyopathy characterized by systolic and diastolic ventricular dysfunction, myocardial hypertrophy and fibrosis, pulmonary congestion and a very high mortality rate. Alterations in contractile proteins and sarcoplasmic reticular calcium (Ca2+) transport in diabetic myocardium and their partial reversal with verapamil suggest that calcium channel blockade may prevent death from congestive heart failure in hypertensive diabetic rats. A large group of rats with renovascular hypertension and streptozotocin diabetes were divided into four groups: untreated animals (Group 1) and animals treated with 100 (Group 2), 300 (Group 3) or 600 (Group 4) mg/kg per day of sustained release diltiazem mixed in their food. Treatment was begun shortly after the onset of hypertension and diabetes. Mortality rates after 4 months were 59% (19 of 32), 53% (17 of 32), 27% (7 of 26) and 35% (12 of 34) in Groups 1, 2, 3 and 4, respectively; the mortality rate in age-matched control rats was 5% (1 of 19). The reductions in mortality rates in Groups 3 and 4 were statistically significant. Diltiazem did not change systolic blood pressure, serum glucose concentration, heart rate or left ventricular mass. There was a trend to decreased left ventricular interstitial fibrosis and perivascular fibrosis in diltiazem-treated animals. Ventricular collagen concentration was similar in untreated hypertensive diabetic and control rats; levels were higher in hypertensive diabetic rats that died than in those that survived. There was a trend to decreased collagen concentration as diltiazem dose increased. Myosin isoenzyme distribution was not changed in Groups 3 and 4 (in comparison with Group 1). In all hypertensive diabetic groups, rats that died had a higher blood pressure, heart rate, relative left ventricular mass, lung weight and lung water than did survivors. The mortality rate was two to three times higher among rats with an initial blood pressure greater than or equal to 180 mm Hg. The beneficial effects of diltiazem on survival were most significant among rats with severe hypertension.
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PMID:Beneficial effects of diltiazem on the natural history of hypertensive diabetic cardiomyopathy in rats. 183 34

Hereditary haemochromatosis is an autosomal recessive disease that is genetically expressed by excessive accumulation of iron in the tissues, resulting in cirrhosis, diabetes mellitus, cardiomyopathy and hypogonadism. As the disease may be diagnosed before the appearance of symptoms, and prevented by repeated phlebotomies, there are strong implications for adoption of a screening procedure. Determinations of transferrin saturation (TS) and serum ferritin concentration (SF) were used to screen 4302 blood donors, who were selected for follow-up studies if they fulfilled any of the following three criteria: (i) TS greater than or equal to 0.7; (ii) TS greater than or equal to 0.5 together with SF greater than or equal to 150 micrograms l-1; (iii) SF greater than or equal to 300 micrograms l-1. A total of 58 subjects who fulfilled at least one of these criteria were reinvestigated, after which 18 individuals still fulfilled at least one criterion. Fifteen subjects having SF greater than or equal to 300 micrograms l-1 were offered liver biopsy and thirteen of these accepted. In one individual, no stainable iron was detected, and two subjects did not fulfil the previously established diagnostic criteria for the diagnosis of hereditary haemochromatosis. Ten subjects who had a high TS and liver iron grade 2-4 according to Bassett were classified accordingly as homozygotes. On the basis of these results, the prevalence of haemochromatosis in Denmark was estimated to be 0.0037-0.0046.
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PMID:Screening for haemochromatosis: prevalence among Danish blood donors. 189 49

Changes in number and/or affinity of cardiac neurotransmitter receptors have been associated with myocardial ischemia and infarction, congestive heart failure, cardiomyopathy, as well as diabetes or thyroid-induced heart muscle disease. These alterations of cardiac receptors have been demonstrated in vitro on membrane homogenates from samples collected mainly during surgery or post mortem. The disadvantage of these in vitro binding techniques is that receptors lose their natural environment and their relationships with the other components of the tissue. In vitro autoradiographic techniques in human tissue offer several advantages over homogenate-binding techniques: an increase in sensitivity and the possibility of anatomic resolution allowing light microscopic mapping of relationships between the distribution of specific cell populations and neurotransmitter receptors. However, the evolution of receptor changes as the disease progresses or as the effect of a drug cannot be analyzed. With the advent of positron emission tomography it is now possible to achieve, non-invasively, quantitative determination of regional biochemical processes in the heart.
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PMID:Cardiac receptors studied by positron emission tomography. 196 75

Survival period of malignant pheochromocytoma treated only conservatively is reported to be less than one year by T. Sato. A patient of malignant pheochromocytoma with liver metastasis has been treated with alpha-methyl-p-tyrosine (alpha MPT), tyrosine hydroxylase inhibitor, in the last 5 years. Catecholamine levels markedly decreased and he has a long survival time. He lives over 17 years from the detection of malignant pheochromocytoma. alpha MPT was considered to have a role to protect a patient from cardiomyopathy induced by hyper-catecholaminemia and to have the action of inhibiting the growth of this tumor. The growth of this tumor was very slow. Since this case had insulin independent diabetes mellitus, insulin therapy was applied, however, blood glucose level was not controlled well. Then we tried midaglizol (DG-5128), alpha 2-adrenoceptor antagonist, to control diabetes mellitus and a sufficient control was obtained. C-peptide level in urine was increased concomitant with decrease of blood glucose. This fact suggested that insulin secretion was improved. It is well known that catecholamine, especially noradrenaline has an inhibiting action on insulin secretion from beta cell. This action was appeared through alpha 2-adrenergic receptor. DG-5128 has an action as alpha 2-adrenoceptor antagonist. We think an inhibiting action on insulin secretion of catecholamine was diminished through its action as adrenoceptor antagonist. Kawazu et al. reported that catecholamine levels, heart rate and blood pressure did not change by DG-5128 administration in healthy subjects. In this patient, no change was appeared either. No major complication was observed during this treatment.
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PMID:[A long survived case of malignant pheochromocytoma treated with alpha-methyl-p-tyrosine and midaglizol (DG-5128)]. 197 32

I have outlined the approach to therapy of supraventricular tachyarrhythmias practiced by a cardiologist who is not performing special studies in the cardiac electrophysiology laboratory. This review includes the list of common and rare supraventricular arrhythmias, application of diagnostic noninvasive procedures, indications for referral for special electrophysiologic studies, and brief description of drugs and procedures used in the therapy of supraventricular tachyarrhythmias. In addition to general guidelines for treatment of these arrhythmias, I have outlined specific recommendations for patients with acute myocardial infarction, angina pectoris, ventricular dysfunction and congestive heart failure, obstructive cardiomyopathy, hyperthyroidism, AV accessory pathways, chronic obstructive lung disease, diabetes mellitus, hypertension, concomitant ventricular arrhythmias, tachycardia-bradycardia syndrome, and anxiety.
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PMID:What determines the choice of treatment in patients with supraventricular tachycardia? 197 41


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