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

Two maintenance hemodialysis patients receiving deferoxamine to chelate iron and aluminum developed intestinal mucormycosis. One patient had pulmonary mucormycosis as well. The patients lacked the usual predisposing factors to mucormycosis, ie, diabetes and acidosis, but both had liver disease. The role of siderophores such as deferoxamine in promoting certain infections is discussed with reference to this particular clinical setting.
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PMID:Intestinal mucormycosis in hemodialysis patients following deferoxamine. 360 86

Because of the organ and enzyme specificity of the metabolism of galactose, evaluation of various kinds of liver disease can be done by measuring the formation of labeled breath CO2 from carbon-labeled galactose in vivo. As shown earlier with uniformly 14C- or 13C-labeled galactose, a further study of alcoholic cirrhotic patients and controls with cheaper 1-14C-galactose indicates a superior discriminatory value of this test compared with common liver function tests. The oxidation test is easier to perform and more acceptable to patients than the standard galactose tolerance blood test. Output of 14CO2 showed slight correlations with serum albumin and 99mTc-sulfur colloid scan grade, but not with other function tests (SGOT, alkaline phosphatase, bilirubin). Comparison with five-year clinical outcome (two groups: with or without known liver-related death) in 29 of 43 total cirrhotic patients (U-14C or 1-14C-galactose) showed a low (75% probability) significance of prognosis for the galactose oxidation test, but none for any of the other tests. A two-part test of oxidation of 14C-galactose (with and without an acute dose of ethanol) in 19 possibly or likely alcoholic (but non-cirrhotic) persons indicated, by correlation with other liver function tests and drinking history, some possibly enhanced sensitivity of the two-part versus the single test for recognizing early liver damage. A preliminary study of the single galactose oxidation test in 7 patients with Type II diabetes suggests moderate impairment of oxidation, which might be applied to evaluate the hepatic disorder in diabetes.
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PMID:Impaired oxidation of carbon-labeled galactose by alcoholic or diabetic liver in vivo. 367 Oct 97

The aminopyrine breath test is a valuable quantitative liver function test. However, it may be influenced by factors not related primarily to liver disease. For instance, it has been published that diabetes affects microsomal demethylation of aminopyrine in vitro. The relevance of these findings for the in vivo situation, however, is ill defined. Aminopyrine disposition was evaluated, therefore, by performing an in vivo-in vitro comparison of its kinetics in control, diabetic and insulin-treated diabetic rats. Diabetes was induced by streptozotocin (75 mg/kg i.v.). A tracer dose of [14C]aminopyrine was injected i.p. (40 mu Ci/kg, 0.7 mg/kg) and the kinetics of 14CO2 in breath as well as disappearance of aminopyrine in blood were followed simultaneously for 2 hr. Diabetes increased the 14CO2 elimination rate constant in breath by 90%, whereas total recovery of 14CO2 in breath was decreased by 30% (P less than .001). Aminopyrine clearance in blood was doubled in diabetic rats compared to control (48.9 +/- 11.3 vs. 21.4 +/- 3.3 ml/min X kg, P less than .001). This was due to an increased volume of distribution (1.99 +/- 0.31 in diabetic rats vs. 0.96 +/- 0.11 liters/kg in control). In vitro aminopyrine kinetics in hepatic microsomal preparations showed a 52% higher Vmax of aminopyrine demethylase in D (P less than .001), whereas Km remained unchanged. The diabetes-induced changes were reversible by insulin. It is concluded that diabetes alters the aminopyrine breath test by interfering with demethylation rate and distribution of aminopyrine, and by changing the fate of the cleaved C1-fragments.
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PMID:Altered liver function in diabetes: model experiments with aminopyrine in the rat. 380 88

To determine whether platelet prostaglandin production in patients with liver cirrhosis was as impaired as platelet aggregation, serum thromboxane production was studied in 52 patients with liver cirrhosis; 12 patients had consumed more than 80 gr of alcohol/day, for more than ten years; 13 patients had also had diabetes mellitus for more than two years. A reduced thromboxane synthesis by platelets of liver disease patients was observed; the parallel decrease of both platelet thromboxane and serum PGE2 formation may also suggest a decrease in arachidonic acid availability for prostaglandin and thromboxane production. A smaller reduction of thromboxane and PGE2 formation in cirrhotics with diabetes mellitus or chronic alcohol intake was also observed.
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PMID:Platelet thromboxane production in liver cirrhosis. 386 39

Group B streptococcal bacteremia outside the perinatal setting is not commonly emphasized. This report reviews all episodes of group B streptococcal bacteremia during a four and a half year period in a large community teaching hospital. Fourteen episodes occurred in neonates, four in parturient women, and 28 in other adults. Bacteremic adults were usually elderly with an average age of 68 years. Group B streptococcal bacteremia occurred in adults with various underlying diseases, including diabetes mellitus, liver disease, peripheral vascular disease, and hematologic disease, and in those receiving long-term steroid therapy. Infections causing group B streptococcal bacteremia in adults included decubitus ulcers, pneumonia, endocarditis, cellulitis, arthritis, osteomyelitis, and meningitis. Thirteen of 28 episodes of group B streptococcal bacteremia in adults were hospital-acquired. Overall mortality in adults was 70 percent. Group B streptococcal bacteremia in adults outside of the perinatal setting is associated with significant underlying diseases and has a high mortality.
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PMID:Group B streptococcal bacteremia in a community teaching hospital. 388 11

Glyburide, a second-generation hypoglycemic sulfonylurea, is 200 times as potent as tolbutamide. This increase is due to greater intrinsic hypoglycemic potency of the molecule rather than to a prolonged biologic half-life. Glyburide is inactivated by the liver to 4-trans-hydroxyglyburide and 3-cis-hydroxyglyburide; 50% of these compounds is excreted in the urine and 50% in the bile. Although the serum concentration of glyburide can be measured by radioimmunoassay and high-performance liquid chromatography, the importance of its serum concentration in the reduction of hyperglycemia is not yet established. Glyburide has a therapeutic effectiveness comparable to that of the first-generation sulfonylurea chlorpropamide; however, it has a lower frequency of adverse effects. To date it has a low frequency of clinically significant interactions with other drugs. Glyburide should not be prescribed for patients with liver disease or significant renal disease. Because glyburide is a potent hypoglycemic agent, it should be prescribed in small initial doses, particularly for elderly patients with diabetes. At the present time there is no definite evidence that it modifies the increased risk of cardiovascular disease of diabetic patients. Although glyburide is a potent stimulator of pancreatic insulin secretion after short-term administration, an additional mechanism of action during long-term administration is to decrease the resistance of muscle and liver to the action of insulin. It is a useful medication for patients with type II diabetes whose hyperglycemia is not adequately reduced by dietary management and exercise. It can be used as the initial drug in these patients or as the replacement drug for those with primary or secondary failure during therapy with first-generation sulfonylureas.
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PMID:Glyburide: a second-generation sulfonylurea hypoglycemic agent. History, chemistry, metabolism, pharmacokinetics, clinical use and adverse effects. 392 53

To determine the outcome of chronic hepatitis in ESRD we studied all 358 renal transplant recipients and 295 hemodialysis patients treated for greater than 1 year since 1970. The incidence of chronic hepatitis (elevated SGOT for greater than 1 year) was 15% (N = 54) in transplanted and 3.4% (N = 10) in dialysis patients. Forty-eight percent (26) of transplanted and 50% (5) of dialysis patients were HBsAg positive. In the transplanted group, the clinical outcome of chronic hepatitis was significantly better in HBsAg-negative compared to HBsAg-positive patients; 11% died, none from liver disease, and 32% remitted after a mean follow-up from start of liver disease of 77.3 +/- 8.2 months, whereas in the HBsAg-positive group 54% (14) died, nine from liver disease, and one remitted after a follow-up of 90.2 +/- 8.9 months. Adverse prognostic factors (age, duration of diabetes, and heart disease) present before ESRD treatment began were similar in both groups, as was duration of follow-up. Only 14% (2/14) of HBsAg-negative patients progressed to chronic active hepatitis on liver biopsy compared to 71% (15/21) of HBsAg-positive patients. Histological stability in those with serial biopsies occurred in 66% (4/6) of HBsAg-negative patients, but in only 18% (13/16) of HBsAg-positive patients with a similar duration of follow-up. No dialysis patients died from liver disease. We conclude that chronic hepatitis occurs more frequently in transplanted than dialyzed patients, and that HBsAg-negative chronic hepatitis has a more benign, clinical, and histological outcome than chronic HBsAg-positive hepatitis in renal transplant recipients.
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PMID:Chronic hepatitis in end-stage renal disease: comparison of HBsAg-negative and HBsAg-positive patients. 393 66

Prostaglandins are ubiquitous biologically active compounds that are involved in inflammatory reactions, hemostasis, and, under certain circumstances, the maintenance of renal function. NSAIDs, which inhibit PG synthesis, are used therapeutically most often as antiinflammatory agents in conditions of inflammation and pain, mostly of a nonurologic nature. However, since NSAIDs inhibit systemic PG synthesis, administration of NSAIDs can lead to adverse side effects. For example, the gastrointestinal irritation caused by NSAIDs probably reflects removal of a cytoprotective effect of gastrointestinal PGs. Similarly, the kidney may be especially susceptible to adverse effects of NSAIDs. In diseases such as peptic ulcers, diabetes, hypertension, congestive heart failure, liver disease with ascites, and renal insufficiency, PGs seem to play a protective role in the kidney. This protective role, which results from increased synthesis of vasodilator PGs in the face of elevated vasoconstrictors, is diminished in the presence of NSAIDs. Other side effects include the antagonism by NSAIDs of the action of diuretics, such that the dose of the diuretic must be adjusted accordingly. The diuretic triamterene should not be used in conjunction with indomethacin due to several reported cases of toxicity. Another drug interaction involves the salicylates, which have been shown to diminish the uricosuric effects of probenecid and sulfinpyrazone. Likewise, since corticosteroids increase the renal clearance of salicylates, it is important to monitor the patient carefully following termination of steroid treatment in patients receiving large doses of salicylates, since this change in elimination can precipitate toxicity. In addition, the NSAIDs bind to plasma proteins and, as such, can displace or be displaced by other drugs that bind in the same manner and can result in either decreased efficacy or toxicity. Despite the fact that the kidney may not be the target of NSAID therapy, renal function may be adversely affected by NSAID treatment. It has therefore been proposed that a renal-sparing NSAID would be a very useful therapeutic agent. Sulindac (Clinoril) has been suggested to be such an agent, eg, able to inhibit systemic PG synthesis (usually monitored by measuring serum thromboxane synthesis) without an apparent effect on renal PG synthesis (monitored by measurement of urinary PGs). However, recent data have suggested that Sulindac does inhibit renal PG synthesis and does not exhibit selectivity. The reasons for the discrepancy are not clear, but may relate to the doses or time intervals examined.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indications and contraindications for the use of nonsteroidal antiinflammatory drugs in urology. 393 61

The ability to recognize diverse clinical forms of xanthomas, such as tuberous, planar, eruptive and tendinous, is important in the detection of underlying systemic disease. A variety of primary genetic disorders, as well as numerous secondary conditions such as diabetes, obstructive liver disease, thyroid disease, renal disease, and pancreatitis, can lead to hyperlipoproteinemia that results in the formation not only of xanthomas but also of life-threatening vascular atherosclerosis. An understanding of the pathogenesis of the underlying lipoprotein alterations provides a rational approach to therapy utilizing dietary manipulations and drugs. Such treatment is capable of correcting most disorders of lipid metabolism, and, if appropriate therapy is initiated at the first sign of xanthoma evolution, it may prevent progression of atherosclerosis, provide resolution of xanthomas, and in some instances prevent serious pancreatitis.
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PMID:Xanthomas and hyperlipidemias. 403 Nov 42

Modern contraceptive methods are discussed, with special emphasis on oral contraceptives, which are regarded as the most effective. They are also regarded as generally safe, although there are contraindications and the drugs should only be prescribed after careful examination. The need for selecting the drug most suitable for the individual patients, mainly on the basis of the characteristics of the menstrual cycle (suggesting a predominance of estrogen or progestin, within safety limits, such as 50 mcg of estrogen), is emphasized. The examinations required include a general clinical, gynecological, and breast examination, cytology tests, evaluation of the menstrual flow pattern, measurements of arterial pressure, weight, glucose, cholesterol and triglyceride levels, and urine tests. They should be repeated at 6-month intervals, or 3-month intervals in the case of high-risk patients (varicose veins, obesity, heavy smokers, high cholesterol and triglyceride levels, history of jaundice, slight heart condition, clinical or potential diabetes, porphyria or predisposition to uterine myoma). Oral contraceptives are contraindicated in cases presenting a history of thromboembolism, phlebitis, cerebral apoplexy; sickle cell anemia, which indicates a predisposition to thromboembolic accidents; serious liver disease or recent hepatitis; serious heart disease; hormone-dependent neoplasia (breast cancer); predisposition to uterine cancer; erythematous lupus; metorrhagia of unknown origin; psychic disorders, especially of a depressive type. They should also be avoided for 3-4 years after puberty, in order to avoid interfering with the development of the hypothalamus and with growth. A carcinogenic effect of the pill and an increase in the risk of giving birth to abnormal children can be ruled out, although the incidence of abortions due to chromosome anomalies after suspending treatment is rather high (due to the previous inhibition of ovulation, a situation similar to repeated pregnancies at short intervals, which involve the same risk).
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PMID:[Current clinical problems of contraception]. 502 53


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