Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.20 (alpha-glucosidase)
4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Trypsin/creatinine clearance ratio--a recently proposed screening test for pancreatic cancer--was assessed in 45 subjects (17 control subjects, 15 patients with pancreatic cancer, and 13 with chronic pancreatitis). A statistically significant increase of the ratio was detected not only in pancreatic cancer, but also in chronic calcifying pancreatitis. Thus, the previously reported clinical usefulness of the test in pancreatic cancer diagnosis was not substantiated by the present data. Although not fully investigated as yet, reasons for an abnormal ratio are probably independent of the neoplastic or inflammatory nature of the pancreatic disease. Science renal enzyme excretion (alpha-glucosidase, gamma-glutamyltranspeptidase, leucine aminopeptidase) was not found to be invariably elevated when trypsin/creatinine clearance ratio was increased, tubular damage cannot be assumed as constituting the only reason for an altered clearance ratio.
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PMID:Role of trypsin/creatinine clearance ratio in the differential diagnosis of chronic pancreatic disease. 616 44

The catalytic activities of neutral and acid alpha-glucosidase were selectively determined in human urine. Urinary excretion of neutral and acid alpha-glucosidase in reference subjects was found to be in the range 1.61 to 20.36 microkat/mol creatinine and 7.47 to 33.60 microkat/mol creatinine, respectively. Urinary excretion of both enzymes was not related to sex, age or diuresis. A continuous assay was introduced to improve the determination of neutral alpha-glucosidase.
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PMID:Excretion of neutral alpha-glucosidase, determined with a continuous assay, and of acid alpha-glucosidase in the urine of human reference subjects. 635 66

cis-Diamminedichloroplatinum (DDP) and ifosfamide (IPP) are effective cytostatic agents with a considerable nephrotoxicity. Because of the known synergism of both drugs in animals the combination has been studied in man with disseminated testicular cancer. Nature and extent of nephrotoxicity of DDP in combination with vinblastine, bleomycin and with or without IPP was investigated. The renal involvement was studied during volume expansion and mannitol diuresis. In addition to total kidney function (creatinine clearance and renal electrolyte handling), tubular function has been determined by quantitative assessment of urinary albumin, beta 2-microglobulin, maltase and leucine aminopeptidase excretion. The urinary protein pattern was also analyzed by microgradient electrophoresis to determine low and high molecular weight proteins. The total protein excretion was raised in the groups of patients with DDP and IPP to a 5-fold of the normal (976 +/- 96 mg/24 h) versus a 4-fold increase (756 +/- 102 mg/24 h) without IPP. This was mainly due to renal tubular involvement. For example, IPP raised the tubular toxicity induced by DDP considerably with a 200-fold increase of the beta 2-microglobulin excretion versus only a 10-fold increase without IPP (p less than 0.02). All lesions were reversible and caused no lasting impairment of kidney function. It is concluded that combination regimens including DDP and IPP can be used without a major risk of acute or chronic renal insufficiency. However, urinary protein excretion should be monitored to make certain that the tubular function improves between or after the treatment courses.
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PMID:Nephrotoxicity of cis-diamminedichloroplatinum with or without ifosfamide in cancer treatment. 638 88

Distinct correlation was found between the activity of neutral alpha-glucosidase in urine and the degree of kidney impairment in 76 patients and in 15 healthy persons. In the patients with non-impaired kidney functions the activity of the enzyme in urine varied within the normal limits (from 12 to 39 microM/hr/mmole of creatinine; normal value being 14.6-15.9 microM), in the patients with moderately expressed disfunction of kidney--from 40 to 79 microM/hr/mmole of creatinine. The enzymatic activity, exceeding 80 microM/hr/mmole of creatinine (up to 227 mM), was observed in cases of severe impairment of the kidney functions. High activity of alpha-glucosidase, correlating with the severity of kidney impairment was found in urine of patients with pyelonephritis albeit the content of protein was quite normal. Interrelationship between the activity of alpha-glucosidase in urine and the state of kidney functions enables to conclude that the enzymatic activity depends on the degree of kidney impairment under various pathological conditions and that estimation of the enzyme activity in urine may be important for diagnosis of kidney diseases as well as for the control of treatment efficiency.
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PMID:[Neutral alpha glucosidase in human urine as a marker of kidney impairment]. 639 Sep 53

Rats were made severely uremic with partial nephrectomy (24-hour creatinine clearance 10% of normal). Jejunal dipeptidase activities (substrates: glycyl-L-leucine, L-alanyl-L-proline, and L-methionyl-L-methionine), disaccharidase activities (maltase, sucrase, trehalase, and lactase) and morphology were studied. A highly significant increase in glycyl-L-leucine and L-methionyl-L-methionine dipeptidases was found in uremic rats compared with controls. Proline dipeptidase activities were unaltered. Disaccharidase activities showed a slight increase in sucrase in uremic rats; otherwise no change was found.
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PMID:Small intestinal dipeptidases and disaccharidases in experimental uremia in rats. 677 73

The glomerular filtration rate (creatinine clearance), glomerular permeability (qualitative and quantitative proteinuria), tubular reabsorption (k-lambda chains of immunoglobulins and lysozyme) and indexes of tubular cell lysis (alpha-glucosidase and gamma-glutamyltranspeptidase) were measured in the urine of 10 patients with moderate, uncomplicated essential hypertension during placebo therapy and after captopril given at increasing doses of 25, 50, 100 and 200 mg twice daily, the first three doses being given for 3 days and the last one for 4 weeks in all patients and for an additional 6 months in 5 patients. During placebo therapy, proteinuria was absent in eight patients and detectable (glomerular and selective) in two; selective proteinuria appeared in two and a decrease in selectivity was observed in two patients with previous proteinuria after 4 weeks of captopril therapy. No proteinuria was detectable in the five patients followed up to 6 months, not even in the one in whom a decrease in glomerular selectivity had occurred after 4 weeks. The glomerular filtration rate was unchanged as were lysozyme and gamma-glutamyltranspeptidase values, while light chains were always undetectable. Alpha-glucosidase showed some increase; however, increments were transient and always much lower than those observed with known tubular toxic drugs. These data show that under our experimental conditions captopril caused no evident changes in glomerular and tubular function.
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PMID:Effect of captopril on renal function in patients with essential hypertension. 704 2

The biguanide metformin (dimethylbiguanide) is an oral antihyperglycaemic agent widely used in the management of non-insulin-dependent diabetes mellitus (NIDDM). Considerable renewal of interest in this drug has been observed in recent years. Metformin can be determined in biological fluids by various methods, mainly using high performance liquid chromatography, which allows pharmacokinetic studies in healthy volunteers and diabetic patients. Metformin disposition is apparently unaffected by the presence of diabetes and only slightly affected by the use of different oral formulations. Metformin has an absolute oral bioavailability of 40 to 60%, and gastrointestinal absorption is apparently complete within 6 hours of ingestion. An inverse relationship was observed between the dose ingested and the relative absorption with therapeutic doses ranging from 0.5 to 1.5 g, suggesting the involvement of an active, saturable absorption process. Metformin is rapidly distributed following absorption and does not bind to plasma proteins. No metabolites or conjugates of metformin have been identified. The absence of liver metabolism clearly differentiates the pharmacokinetics of metformin from that of other biguanides, such as phenformin. Metformin undergoes renal excretion and has a mean plasma elimination half-life after oral administration of between 4.0 and 8.7 hours. This elimination is prolonged in patients with renal impairment and correlates with creatinine clearance. There are only scarce data on the relationship between plasma metformin concentrations and metabolic effects. Therapeutic levels may be 0.5 to 1.0 mg/L in the fasting state and 1 to 2 mg/L after a meal, but monitoring has little clinical value except when lactic acidosis is suspected or present. Indeed, when lactic acidosis occurs in metformin-treated patients, early determination of the metformin plasma concentration appears to be the best criterion for assessing the involvement of the drug in this acute condition. After confirmation of the diagnosis, treatment should rapidly involve forced diuresis or haemodialysis, both of which favour rapid elimination of the drug. Although serious, lactic acidosis due to metformin is rare and may be minimised by strict adherence to prescribing guidelines and contraindications, particularly the presence of renal failure. Finally, only very few drug interactions have been described with metformin in healthy volunteers. Plasma levels may be reduced by guar gum and alpha-glucosidase inhibitors and increased by cimetidine, but no data are yet available in the diabetic population.
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PMID:Clinical pharmacokinetics of metformin. 874 35

This paper reviews the effects of renal insufficiency on the pharmacokinetics of oral antidiabetic drugs. Of the 3 groups of drugs currently available for the treatment of non-insulin-dependent diabetes mellitus (NIDDM), the sulphonylureas and metformin are, in general, well-tolerated and generally safe. In patients with chronic renal insufficiency, however, care must be exercised in the use of many of these drugs, as accumulation, either of the active drug or of active metabolites, can lead to serious adverse effects such as hypoglycaemia or, with metformin, lactic acidosis. The sulphonylurea drugs, to a greater or lesser degree, are metabolised in the liver to a variety of active or inactive compounds which, in general, are excreted by the kidneys. In addition, varying amounts of parent compound may depend on renal elimination. As a result, sulphonylurea drugs such as tolazamide, acetohexamide, chlorpropamide and glibenclamide (glyburide) are more likely to cause significant hypoglycaemia, as the metabolism of these drugs, compared with other commonly prescribed sulphonylureas, can lead to the accumulation of either the parent drug or the active metabolite in the presence of renal insufficiency. Tolbutamide, glipizide, gliclazide and gliquidone are much less likely to cause hypoglycaemia as their metabolites are either inactive or have minimal hypoglycaemic potency. Metformin is dependent on renal excretion and is not significantly metabolised. As a result, caution is required when treating patients with renal insufficiency where metformin accumulation can occur, with the danger of lactic acidosis. Although the correlation between creatinine clearance (CLCR) and total oral clearance of drug is weaker than the correlation between CLCR and renal clearance (CLR) of metformin, it is clear that renal insufficiency is associated with most cases of metformin-induced lactic acidosis. For this reason, clinicians in general would regard a raised plasma creatinine as a contraindication to metformin treatment. Acarbose, an alpha-glucosidase inhibitor, and a relatively new agent for treating NIDDM, is likely to be safe in patients with impaired renal function, as the drug is not significantly absorbed from the gut, but data on this subject are lacking.
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PMID:Pharmacokinetics of oral antihyperglycaemic agents in patients with renal insufficiency. 885 33

Quantitative estimation of urinary enzymes has been advocated as a more sensitive marker than conventional renal function tests to assess radio-contrast media induced nephrotoxicity. We studied 27 subjects with normal renal functions who underwent abdominal aortography for varied indications. Among these, 8 also required selective renal arteriography and 3 underwent arch aortography in addition. Sodium iothalamate was used as a radio-contrast medium and the average amount injected was 73 ml (45 to 120 ml) per subject. Standard renal function assessment including urinalysis, 24 hour urinary protein excretion, creatinine clearance done both before and after aortography did not show any significant alteration. Urinary excretion of tubular enzymes including leucine aminopeptidase (LAP), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT) and maltase (MAL) was estimated before and 2, 24 and 48 hours after aortography. All enzymes showed a significant rise at 2 hours. Urinary excretion of LAP, ALP and GGT peaked at 24 hours after aortography without a further change in MAL levels. Enzymuria returned to baseline values 48 hours following the procedure. It is concluded that an increase in the urinary excretion of the brush-border enzymes within 24 hours of contrast media administration may suggest an early nephrotoxicity.
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PMID:Quantitative enzymuria following aorto-renal angiography. 1099 87

Several protein-bound uremic retention solutes (including p-cresol) originate from colonic bacterial fermentation of protein. Higher colonic availability of carbohydrates drives this process towards lower production of toxic metabolites. Small intestinal alpha-glucosidase inhibitors like Acarbose (Glucobay) enhance the amount of undigested carbohydrates reaching the colon. We studied the effect of Acarbose on generation and serum concentrations of p-cresol. Nine healthy volunteers (age 25 (22-36) years) with a creatinine clearance of 89.6 ml/min/1.73 m(2) (85.5-116.4) were treated with Acarbose for 3 weeks. Dose was gradually increased to reach 300 mg/day after 1 week. Blood sampling, 24-h urine and stool collections on 3 consecutive days were performed before and during the last days of the treatment period. p-Cresol generation was estimated from mean 24-h urinary elimination. Gastrointestinal side effects, if present, were mild to moderate. Serum concentrations of p-cresol declined significantly after Acarbose treatment (before: 1.14 mg/l (0.93-3.03); after: 1.11 mg/l (0.31-1.82); P=0.047). Urinary excretion of p-cresol, reflecting its colonic generation rate, was significantly lower after treatment (before: 29.93 mg/day (6.79-75.19); after: 10.54 mg/day (1.08-30.85); P=0.031). The fecal excretion of nitrogen increased after treatment (before: 1.04 g/day (0.47-2.29); after: 1.99 g/day (0.76-3.08); P=0.047). This pilot study suggests that Acarbose treatment lowers generation and serum concentrations of the protein-bound uremic solute p-cresol. Although further confirmation is warranted, the data may point to a novel treatment option for chronic kidney disease patients in view of the potential toxic effects of p-cresol and related substances.
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PMID:Acarbose treatment lowers generation and serum concentrations of the protein-bound solute p-cresol: a pilot study. 1668 14


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