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Query: UMLS:C0011849 (
diabetes
)
277,896
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Seventy patients with non-insulin dependent diabetes (NIDD) were studied for the chlorpropamide-alcohol flush (CPAF), first degree family history of
diabetes
, macroangiopathy and for peripheral neuropathy. Positive CPAF challenge tests were found in 65% of the tested subjects and in 77% if there was a family history of
diabetes
. Signs of macroangiopathy (loss of foot pulses) were significantly (p less than 0.05) less common in the CPAF positive than in the CPAF negative diabetics with a duration of
diabetes
of ten years or less. With a longer duration this difference between the two groups was reduced. Also signs of peripheral neuropathy (abnormal vibration sense) were less common (p less than 0.05) in the CPAF positive diabetics than in the CPAF negative. Previously a low prevalence of retinopathy in teh CPAF positive non-insulin dependent diabetics has been reported. We have shown that this is also true of peripheral macroangiopathy and peripheral neuropathy.
Chlorpropamide
-alcohol flushing seems to be related to a relative protection against late complications in
diabetes
and the test might be used to find patients at risk.
...
PMID:Chlorpropamide-alcohol flushing in relation to macroangiopathy and peripheral neuropathy in non-insulin dependent diabetes. 695 48
The 11 derivatives of beta-cytotropic sulphonylureas commonly used in the treatment of
diabetes mellitus
were tested in vivo in the highly sensitive sister-chromatid exchange test.
Chlorpropamide
and tolbutamide gave a positive reaction with a clear dose-response in Chinese hamsters and mice. The two compounds gave a mutagenic response neither in the Salmonella/mammalian-microsome mutagenicity test (with and without microsomal activation) nor in the chromosomal aberration test. In the micronucleus test, chlorpropamide was positive in 3 strains of mouse, tolbutamide in one strain. In Chinese hamsters and in rats the micronucleus test was negative with both compounds.
...
PMID:Mutagenicity of sulphonylureas. 699 Feb 52
To determine the effect of chronic sulfonylurea therapy on islet function in noninsulin-dependent
diabetes mellitus
(NIDDM), studies were performed in 18 untreated NIDDM patients before and after 12-16 weeks of chlorpropamide therapy. Fasting plasma glucose (FPG) fell with chlorpropamide therapy from 249 +/- 16 to 157 +/- 8 mg/dl (mean +/- SEM; P less than 0.001), and basal insulin increased from 17 +/- 2 to 24 +/- 3 microU/ml (P less than 0.001). The percent change in basal insulin correlated with the pretreatment FPG (r = 0.62; P less than 0.01) and inversely with the change in FPG during chlorpropamide (r = -0.57; P less than 0.025). Thus, patients with the highest pretreatment FPG showed the largest relative increase in basal insulin and the largest fall of FPG with chlorpropamide therapy. In nine patients, arginine-stimulated acute insulin responses (AIR) were studied at each of three plasma glucose (PG) levels both before and during chlorpropamide treatment. AIR at FPG was not different before and during treatment. However, when PG during treatment was matched by glucose infusion to the pretreatment FPG, the AIR was clearly increased during chlorpropamide therapy (176 +/- 65 vs. 49 +/- 11 microU/ml; P less than 0.02). When AIR is plotted against PG for each individual, the slope of the regression line generated (slope of glucose potentiation) is a measure of that patient's islet sensitivity to glucose. The logarithm of the slope of glucose potentiation correlated inversely with FPG (r = -0.92; P less than 0.001).
Chlorpropamide
treatment increased the slopes of potentiation from 0.26 +/- 0.11 to 1.47 +/- 0.70 (P less than 0.01). We conclude that chronic chlorpropamide therapy augments both basal and stimulated insulin secretion in NIDDM and that this may be an important mechanism of the drug's hypoglycemic effect. The data support the hypothesis that the hyperglycemia of NIDDM is related to islet insensitivity to glucose and that chlorpropamide treatment improves this impairment.
...
PMID:Chronic chlorpropamide therapy of noninsulin-dependent diabetes augments basal and stimulated insulin secretion by increasing islet sensitivity to glucose. 704 53
A 65-year-old woman with adult-onset
diabetes
treated with chlorpropamide (
Diabenese
) had a toxic optic neuropathy that resolved with discontinuation of chlorpropamide therapy. Visual loss occurs in diabetics for a variety of reasons, and accurate diagnosis is necessary to institute appropriate therapy. The possibility of a drug-induced optic neuropathy should be considered in the differential diagnosis of visual loss in diabetics.
...
PMID:Chlorpropamide-induced optic neuropathy. 705 67
Chlorpropamide
-alcohol flushing (CPAF) has been advanced and challenged as a specific marker for familial noninsulin dependent diabetes mellitus. The previous studies assay flushing reactions employing arbitrarily defined critical threshold values of rise and rate of rise in facial temperature. Since these methods ignore the curvilinear relationship between skin temperature and cutaneous blood flow, errors of analysis obtained, Further, the role of baseline facial temperature is obfuscated. The method of malar thermal circulation index derived from the relationship between skin temperature and cutaneous blood flow provides a more accurate assay method and permits the characterization of the role of baseline facial temperature. Baseline facial temperature is less in subjects with CPAF and noninsulin dependent
diabetes
than in normal subjects. The lower baseline facial temperature alone may account for the reported differences in the parameters of the CPAF test.
...
PMID:Chlorpropamide-alcohol flushing, malar thermal circulation index, and baseline malar temperature. 712 Dec 66
Chlorpropamide
alcohol flushing (CPAF) in non-insulin-dependent diabetics (NIDDs) has been reported to be associated with a lower tendency to develop late complications. The flush was thought to be mediated by enkephalins and prostaglandins. Early studies could not correlate CPAF to increased levels of acetaldehyde in blood and the flush was not regarded as an antabuse-like reaction. In this study, the increase of plasma acetaldehyde during the flush in 13 CPAF positive diabetics was significantly (P less than 0.005) higher than in the 13 CPAF negative diabetics during a CPAF challenge test. The increase of plasma acetaldehyde was reduced to the level of CPAF negative diabetics in three CPAF positive diabetics when they were exposed to alcohol without premedication with chlorpropamide and they did not flush. The normal breakdown of ethanol to acetic acid via acetaldehyde appears to be inhibited by chlorpropamide in the flushers. Acetaldehyde measurement is an objective method to study the chlorpropamide alcohol flush and it appears superior to the measurement of skin temperature.
Diabetes
1981 Sep
PMID:Increase of plasma acetaldehyde. An objective indicator of the chlorpropamide alcohol flush. 726 73
Chlorpropamide
-induced hypoglycemia is often overlooked, misdiagnosed, and mistreated, because of the atypical, insidious, and intermittent clinical picture and because of the normal serum glucose level in some of the patients when arriving at the hospital. These facts are demonstrated in three case reports. Since the correction of low glucose levels in the cerebrospinal fluid occurs hours after its correction in the serum, examining and at times following the cerebrospinal fluid glucose levels in patients with chlorpropamide-induced neuroglycopenia will enable physicians to diagnose and cure more patients. A high index of suspicion should exist in the presence of any atypical encephalopathy, mainly in the elderly diabetic patient treated with chlorpropamide and suffering from impaired cerebral, hepatic, or renal function. By suspecting and identifying neuroglycopenia, disabling residual deficits and even death could eventually be prevented.
Diabetes
Care
PMID:The significance of the cerebrospinal fluid examination in the management of chlorpropamide-induced hypoglycemia. 738 45
A 55-year-old gentleman, after being treated for a short time with a diet and with
Chlorpropamide
, was switched to purified porcine insulin due to ketonuria and ketoacidosis. After a year the patient developed immunological insulin resistance (mean daily insulin dose: 3.72 U/kg body weight; anti-insulin antibodies 78%). In order to lower anti-insulin antibodies human recombinant DNA insulin was introduced into further therapy. Contrary to expectations, the patient did not reduce whatsoever his anti-insulin antibodies and his daily insulin dose increased up to 5.63 U/kg body weight. Introduction of combined immunosuppressive therapy (prednisone plus azathioprine) together with plasmapheresis resulted in rapid lowering of daily insulin requirement and reduction in anti-insulin antibodies. Immunosuppressive therapy was continued with 10 mg of prednisone and a year later the patients insulin daily requirement was 0.66 U/kg BW while his antibodies were 18%. The possible causes of insulin resistance to human recombinant DNA insulin are discussed as well as the advantage of combined immunosuppressive therapy together with plasmapheresis that was used for rapid lowering of insulin daily requirement and anti-insulin antibodies titer.
Diabetes
Res Clin Pract 1993 Jan
PMID:Immunological resistance to human biosynthetic insulin--effects of immunosuppression and plasmapheresis. 847 23
Chlorpropamide
(
CPM
) has been reported to produce impaired water excretion due to the enhancement of renal vasopressin (ADH) action and/or due to centrally enhanced ADH release, but it is still unknown whether
CPM
gives rise to ADH release with a subsequent hyponatremia in
diabetes mellitus
(DM), which, in turn, causes an impairment of the central nervous system. In 3 patients with DM, who developed hyponatremia during the treatment with
CPM
, an acute water load (WL) was carried out in the presence and absence of the drug, and plasma ADH was determined with plasma and urine osmolalities. Moreover, in 2 cases, MRI scans of the brain were taken. In all the patients, acute WL tests failed to suppress completely ADH release in response to changes in plasma osmolality in the presence of
CPM
, which, in turn, resulted in the impaired water excretion. In the absence of
CPM
, an acute WL normally suppressed plasma ADH leading to the diuresis. MRI scans illustrated the presence of central pontine myelinolysis. It is likely that
CPM
might stimulate ADH release in DM with a subsequent hyponatremia and brain damages.
...
PMID:Chlorpropamide-induced ADH release, hyponatremia and central pontine myelinolysis in diabetes mellitus. 892 90
Diabetes mellitus
is a debilitating hormonal disorder in which strict glycemic control and prevention of associated complications are of crucial importance. This study was designed to evaluate the hypoglycemic effect of methanolic extract of mature, green fruits of Musa paradisiaca (MEMP) in normal (normoglycemic) and streptozotocin (STZ)-treated, diabetic (hyperglycemic) mice, using chlorpropamide as the reference antidiabetic agent. MEMP (100-800 mg/kg p.o.) induced significant, dose-related (p < 0.05-0.001) reductions in the blood glucose concentrations of both normal and diabetic mice.
Chlorpropamide
(250 mg/kg p.o.) also produced significant (p < 0.01-0.001) reductions in the blood glucose concentrations of normal and diabetic mice. The results of this experimental study indicate that, in the mammalian model used, MEMP possesses hypoglycemic activity. Although the precise mechanism of the hypoglycemic action of MEMP is still unclear and will have to await further studies, it could be due, at least in part, to stimulation of insulin production and subsequent glucose utilization. Nevertheless, the findings of this experimental animal study indicate that MEMP possesses hypoglycemic activity, and thus lends credence to the suggested folkloric use of the plant in the management and/or control of adult-onset, type-2 diabetic mellitus among the Yoruba-speaking people of South-Western Nigeria.
...
PMID:Hypoglycemic effect of methanolic extract of Musa paradisiaca (Musaceae) green fruits in normal and diabetic mice. 1294 31
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