Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative importance and behaviour of plasma and platelet plasminogen activator inhibitor (PAI-1) in disease has not hitherto been examined. In this study the concentration of PAI-1 in the plasma and platelets of patients with a variety of disorders was examined using a specific ELISA and a functional assay. Mean plasma PAI-1 was elevated in groups of patients with diabetes mellitus, hypertension, alcoholic cirrhosis, angina and myocardial infarction. Plasma PAI-1 was raised in the post-operative phase and the PAI-1 released after surgery was not derived from platelets. In all groups PAI-1 in the platelet pool reflected the platelet count, except in type II diabetes mellitus and chronic renal failure, where a reduced quantity of PAI-1 antigen per platelet was found. In severe chronic renal failure, abnormal platelets and diminished platelet PAI-1 may contribute to the haemorrhagic tendency sometimes seen in this disorder. Plasma PAI-1 represents a larger proportion of total circulating PAI-1 in disease than it does in healthy individuals; PAI-1 per platelet is abnormal only in a minority of disorders. Plasma and platelet pools of PAI-1 vary independently in disease and both merit consideration in evaluating the importance, if any, of PAI-1 in thrombosis or haemorrhage.
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PMID:The platelet and plasma pools of plasminogen activator inhibitor (PAI-1) vary independently in disease. 220 5

A 49-year-old man with an 11 year history of NIDDM presented hypercalcemic and with acute on chronic renal failure. His only symptoms were mild anorexia and nausea. Four years previously he had been diagnosed as having lipoid pneumonia, with classical histological findings. On this admission, serum parathyroid hormone was suppressed and 1,25 dihydroxyvitamin D levels elevated. The cause of his hypercalcemia presumably was ectopic 1 hydroxylation of 25 hydroxyvitamin D in the chronic granulomata in his lungs. It should be emphasised that any chronic granulomatous disease, and not just sarcoidosis, may be a cause of hypercalcemia.
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PMID:Hypercalcemia and lipoid pneumonia. 263 65

The hyperglycemia usually observed in patients undergoing heart surgery with extracorporeal circulation (EC) represents a difficult therapeutic problem. We studied the effects of several regimens of insulin therapy on serum glucose (SG) in 24 noninsulin dependent diabetic patients (NIDDs). The patients were randomly divided in five groups; group A received on IV bolus of 10.0-50.0 U/h according to glycosuria; groups B, C, D and E were given a continuous iv insulin infusion of 2.5, 5.0, 7.5 and 10.0 U/h respectively. In 10 non-diabetic patients (NDP) SG levels were also measured, but insulin was not given. A mean of 5.0 l/m2 of body surface of fluids containing 300 g of glucose were administered to all patients during surgery. At the operations SG levels rose progressively soon after the anesthesia was started, reached the highest values during the period of EC, and decreased slowly in blood samples taken after the EC phase and by 24h. This patterns was shown by all groups studied statistically significant lower SG levels, however, were observed in patients of group C, whose values were similar to those seen in the NDP group. Groups D and E had slightly higher SG levels than those of group C. An additional NIDDM patient with advanced chronic renal failure (CRF), had a tendency to hypoglycemia even during the EC period in response to relatively low doses of insulin (2.5 U/h), given by a continuous iv infusion and, although the insulin administration was stopped, his SG levels remained well below the mean values of the other patients for the rest of the operation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Perioperative management of the diabetic patient in cardiac surgery with extracorporeal circulation]. 293 94

Diabetes mellitus is a significant health problem in south Auckland. A retrospective case note review of all diabetic admissions to Middlemore Hospital in 1983 was performed to establish a database to identify current problem areas and permit ongoing analysis. Three hundred and seventeen admissions from 225 patients using 6086 hospital days were reviewed: 204 diabetes-related admissions occupied 4040 days. One hundred and nine patients were male. One hundred and fifty-seven patients were European, 45 were Maori and 21 were Polynesian. European patients were older (mean age 64 years) and lighter (mean weight 69kg) than the non-European patients (mean age 56 years, mean weight 83kg). One hundred and eighty patients had noninsulin dependent diabetes mellitus: European patients were discharged on insulin treatment in 38% of admissions compared with 17% for nonEuropean patients. The patterns of admission were similar for all racial groups except for admissions for chronic renal failure where 21 of 22 admissions were by nonEuropean patients. A comparative cost analysis was performed: admissions for peripheral vascular disease contributed 34% to the calculated total cost of diabetes-related admissions despite only accounting for 17% of admissions. Further research, especially in the nutritional field, is necessary before realistic cost-benefit interventions can be devised and implemented.
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PMID:Diabetic patient discharges from Middlemore Hospital in 1983. 345 13

Serum concentrations of apolipoproteins A-I, A-II, B, C-I, C-II, C-III and E were determined by electroimmunoassay in 56 patients with chronic renal failure (CRF) in the predialytic phase. The results were compared with those obtained in asymptomatic normolipidemic subjects, patients with type IV hyperlipoproteinemia, and patients with type II diabetes mellitus. CRF patients had reduced concentrations of ApoA-I and ApoA-II, normal levels of ApoB and ApoC-I, and increased concentrations of ApoC-II and, in particular, of ApoC-III. There was a significant reduction in the levels of ApoE, especially in male patients. In comparison with type IV, hyperlipoproteinemic patients, CRF patients had lower concentrations of ApoA-I, ApoA-II, ApoB, ApoC-I and, particularly, ApoE; there was no difference in ApoC-III levels reflecting the hypertriglyceridemia common to both disorders. Similar but less marked differences were also found in comparison with type II diabetics. The findings suggest that in CRF, the accumulation of ApoC-III-enriched lipoprotein particles accompanied by a moderate hypertriglyceridemia may be caused more probably by an impaired catabolism than overproduction of triglyceride-rich lipoproteins. CRF patients with vascular disease tended to have higher serum concentrations of triglycerides, cholesterol and ApoB and lower ApoA-I/ApoC-III and ApoA-I/ApoB ratios than patients without vascular disease.
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PMID:Serum apolipoprotein profile of patients with chronic renal failure. 366 95

Utilizing an acid gel chromatography and insulin radioreceptor assay (RRA), serum levels of receptor assayable insulin-like activities were measured under various conditions. Acid gel filtration of sera on a Sephadex G-50 was adopted to separate small molecular ILAs from binding proteins before the assay by RRA. By employing 125I-pork insulin as the tracer, and pork insulin as the standard, an RRA for insulin was developed, in which kidneys of sacrificed pregnant guinea pigs were used as the source of the solubilized receptor. After gel-filtration of the sera, pooled fractions, which grossly corresponded to those of 125I-insulin marker, were assayed by RRA. The subjects consisted of fifty-nine cases: normal control subjects (n = 19), active acromegaly (6), Sheehan's syndrome (5), liver cirrhosis (7), chronic renal failure (10), non-insulin dependent diabetes mellitus (6), overt hyperthyroidism (5) and Nelson's syndrome (1). The average receptor assayable ILA of the normal control subjects was 40.2 +/- 12.2 ng/ml. As insulin RRA has a big interassay variation, receptor assayable ILA-ratio was used to minimize the variation, and each data was shown as the ratio to the average ILA of the normal controls. By this method, sera from normal adults had a mean (+/- SD) receptor assayable ILA ratio of 1.00 +/- 0.28. Four out of six cases of acromegaly revealed significantly high concentrations, and the average receptor assayable ILA-ratio of acromegaly was 1.30 +/- 0.28 (mean +/- SD, p less than 0.015). In the cases of Sheehan's syndrome, the ILA-ratio was 0.30 +/- 0.12, which was significantly low (p less than 0.001). Therefore, GH dependency was suspected from these two factors. However, the direct correlation was not indicated between GH and receptor assayable ILA. It was also considered that receptor assayable ILA was influenced not only by GH but also by some other factors. Furthermore, the subjects with liver cirrhosis indicated the low levels of receptor assayable ILA-ratio of 0.46 +/- 0.31, while the subjects with chronic renal failure showed the high ILA-ratio of 1.59 +/- 0.45 (p less than 0.05). No differences in ILA-ratio were found in the subjects with diabetes mellitus, hyperthyroidism and Nelson's syndrome, compared to the normal subjects.
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PMID:[Serum levels of receptor assayable insulin-like activity in various diseases]. 636 8

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.
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PMID:[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism]. 857 95

The aim of this study was to determine the clinical significance of serum and urinary insulin-like growth factor I (IGF-I) in renal disease and diabetes mellitus. In renal portion, we measured their concentrations in patients with chronic renal disease (serum creatinine < 2.0 mg/dl) (CRD. n = 22) and those with chronic renal failure (serum creatinine > or = 2.0 mg/dl) (CRF, n = 26) and compared with normal healthy controls (C. n = 20). Serum concentrations growth hormone (GH) and IGF-I did not differ among these groups. Urinary IGF-I level was significantly increased in CRF (4.0 +/- 0.5 ng/mg creatinine) compared with CRD (2.8 +/- 0.6 ng/mg creatinine) and C (1.8 +/- 1.0 ng/mg) creatinine). Urinary IGF-I did not correlate with either serum GH or serum IGF-I. Urinary IGF-I, but not serum IGF-I, demonstrated a significant negative correlation with creatinine clearance. In diabetic portion, 29 patients with noninsulin dependent diabetes mellitus (NIDDM), whose serum creatinine were within normal range, and age-matched 12 subjects were enrolled. Serum IGF-I in NIDDM (130 +/- 11 ng/ml) was significantly lower than that in controls (201 +/- 11 pg/ml). In contrast, urinary IGF-I level in NIDDM (1.93 +/- 0.31 ng/mg creatinine) did not differ from that in controls (2.00 +/- 0.31 ng/mg creatinine). In NIDDM, urinary IGF-I had poor correlation with both serum IGF-I and albuminuria. The data in renal patients suggest the possible participation of renal IGF-I in the progression of renal disease, while in NIDDM with normal serum creatinine the role of renal IGF-I may be less in the early diabetic nephropathy.
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PMID:Serum and urinary levels of insulin-like growth factor I in patients with chronic renal disease and diabetes mellitus: its clinical implication. 879 28

Nephropathy is a frequent complication of long-term diabetes. Strong evidence exists that genetic predisposition plays a major role in the development of diabetic nephropathy. The role of the angiotensin I-converting enzyme gene (ACE) in the susceptibility to nephropathy in diabetes, especially in non-insulin dependent diabetes mellitus (NIDDM), remains unclear. This study examines the association of two ACE polymorphisms: a 287-bp insertion/deletion (I/D) in intron 16 and PstI (A/G substitution in intron 7; alleles P/M) with renal complications in 941 NIDDM patients. From this group, for further analysis 127 patients were selected with overt proteinuria or chronic renal failure, 335 patients with microalbuminuria, and a control group of 254 normoalbuminuric patients with a diabetes duration of at least 10 yr. No significant differences in the distribution of ACE I/D and PstI genotypes or allele frequencies were observed between the examined groups. The results of this study strongly suggest that there is no association between the ACE gene I/D and PstI polymorphisms and nephropathy in NIDDM.
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PMID:Angiotensin I-converting enzyme gene polymorphisms: relationship to nephropathy in patients with non-insulin dependent diabetes mellitus. 972 75

In order to investigate the influence of aldehyde dehydrogenase 2(ALDH2) genotype in the pathogenesis of nephropathy due to non-insulin dependent diabetes mellitus (NIDDM), genotyping of ALDH2 was measured using the PCR-RFLP method in patients with NIDDM on chronic hemodialysis (HD). The results were as follows; 1) The frequency of active ALDH2 was 63% and that of inactive ALDH2 was 37%. 2) The percentage of active ALDH2 was significantly higher in patients with alcohol tolerance than that in those without it (38%). 3) The estimated amount of alcohol consumption in the past was 506 +/- 720 g/week in the active ALDH2 group, and 156 +/- 288 g/week in the inactive ALDH2 group, showing a significant difference between the two groups. 4) Interdialytic body weight gain was larger in patients with active ALDH2 than in those with inactive ALDH2. Since the frequency of active ALDH2 was similar to that in patients without nephropathy, these results do not support the hypothesis that ALDH2 gene polymorphism is involved in the development and persistence of chronic renal failure due to NIDDM. However, salt and water craving in dialysis patients may be influenced partially by an active ALDH2 gene.
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PMID:[Aldehyde dehydrogenase 2(ALDH2) gene polymorphism in NIDDM patients with chronic renal failure]. 975 91


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