[Patient education and self-surveillance in diabetes mellitus].
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Biomedical subjects
Publications and source records attributed to B Willms.
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Blood sugar self-control was assessed in 20 in-patients using a new blood sugar test strip, Haemo-Glukotest 20--800. Comparative estimations of 445 strip tests with values obtained by the hexokinase method showed good correlations particularly in the low range below the renal threshold. Nearly 70% of measurements were assessed correctly in this range. Mean deviations of test strip results from the corresponding laboratory value were 0.61 to 0.89 mmol/l (11--16 mg/dl). Haemo-Glukotest 20--800 is thus well suited for blood glucose self-control particularly in the range below the renal threshold. In a survey most patients estimated the importance of blood sugar to be more than that of urinary sugar.
The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. Blood glucose and serum immunoreactive GIP (IR-GIP) were measured after an oral load of 100 g glucose or 100 g fat was given and during an infusion of one of the following: saline, glucose, glucose plus insulin, or insulin. The infusion of insulin alone (in the presence of elevated glucose levels) or together with glucose significantly suppressed the IR-GIP rise after fat ingestion, but it did not alter the GIP response to oral glucose. Intravenous infusion of glucose had a slight but significant inhibitory effect on fat-stimulated increase of IR-GIP, which cannot be related to endogenous insulin release in these insulin-deficient diabetics. It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. This could explain the existence of a negative feedback control between insulin and GIP secretion for fat but not for glucose-induced GIP release.
The therapeutic efficacy of thioctic acid was studied in patients with peripheral diabetic neuropathy. In a double-blind study ten diabetics were treated with thioctic acid or a placebo for 21 days. In a second study ten diabetics were also treated with thioctic acid intravenously (i.v.) for 21 days. Before and on the 11th and 21st day of treatment, we examined the clinical neurological state, the vibration sense according to biothesiometry, the nerve conduction velocity, and the degree of diabetic control. In addition the patients were asked about neuropathic complaints. The therapeutic efficacy of oral or i.v. thioctic acid could not be verified by measurements of the nerve conduction velocity or the vibration sensibility. No effect of oral thioctic acid on subjective complaints was observed. However, i.v. treatment with thioctic acid resulted in a distinct improvement of subjective complaints.
One-hundred and nine patients consecutively admitted to our hospital underwent a standardized sustained hand grip test, the Valsalva maneuver, and the Schellong test in a study of autonomic diabetic neuropathy of the cardiovascular system. The correlation between autonomic diabetic neuropathy of the cardiovascular system and the duration of diabetes, the age of the diabetic patient, the forms of treatment, and other neuropathic or vascular complications of diabetes was studied. Autonomic diabetic neuropathy of the cardiovascular system is a complication of long-term insulin-dependent diabetes and is dependent on the duration of the disease. The responses to the Valsalva maneuver in 17 poorly controlled diabetics before and after establishing good control of the diabetes showed no change in the Valsalva ratio. Short-term changes in diabetic control seem to have no effect on the Valsalva ratio as an indicator of autonomous nervous system involvement. The so-called "10 second Valsalva ratio" is a simple and reproducible method of evaluating the Valsalva maneuver.
Serum insulin was measured after maximal stimulation in 213 patients with apparent secondary failure of treatment with sulfonylureas. The maximal increase of serum insulin was 327% of baseline in patients treated with oral drugs alone and 175% in patients switched to insulin. The control of diabetes in the patients treated with oral drugs alone was investigated 2 to 3 years later by a questionnaire and correlated to the insulin values measured earlier. Following conclusions were drawn: Sulfonylurea treatment is indicated if the increase of serum insulin is more than 300%. If the increase of serum insulin is below 200%, insulin treatment is necessary now or in the near future. The determination of serum insulin after maximal stimulation in patients with apparent secondary failure of sulfonylurea treatment has a diagnostic as well as a prognostic value.
Marked weight loss with cachexia together with severe depression and pain from symmetrical peripheral neuropathy were noted in a 66-year-old man, known to have had diabetes for six years, which required insulin on admission to hospital. The patient died of bronchopneumonia after one year. The severe neuropathy was proven both neurophysiologically and at necropsy. There was no diabetic retinopathy and no histological evidence of renal glomerulosclerosis. There was no evidence of a malignant tumour either clinically or at necropsy.
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In a double blind study 16 maturity onset diabetics were treated with d-2-(6-methoxy-2-naphthyl)-propionic acid (naproxen) and tolbutamide with a view to possible interactions between both drugs. There were no significant differences between blood glucose levels after placebo and naproxen, respectively. The concentrations of tolbutamide were not significantly different, either. Thus diabetics on tolbutamide can be treated additionally with naproxen without any clinical side effect on carbohydrate metabolism.
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HLA-typing was performed in two groups of juvenile-onset diabetics, one with (n = 58) and one without (n = 109) a family history of the disease. The association of this type of diabetes with certain HLA antigens (excess of B8 and B15, shortage of B7) was confirmed. No heterogeneities could be established between the two groups. This suggests that the aetiologic basis in single and familial cases of juvenile diabetes is the same. The hypothesis, that the B8 associated gene is more penetrant than the B15 associated gene, cannot be confirmed. Haplotypes were determined in families with one and two diabetic siblings. The findings of high haplotype concordance among diabetic siblings was confirmed: concordance of 2, 1 and 0 haplotypes in 7, 5 and 3 pairs respectively. There was a low degree of haplotype concordance between diabetics and nonaffected siblings in the families with two diabetics: 2, 1, and 0 haplotypes in 2, 8 and 6 pairs respectively. This led to the hypothesis of negative selection against these HLA-linked "diabetogenic" genes. This tendency was not, however, observed in families with only one diabetic. The report of a high recombination rate in families with juvenile diabetics could not be confirmed.
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The fate of the diabetic today is essentially determined by the late complications of diabetes. Of the forms of clinical expression of diabetic microangiopathy, nephropathy and retinopathy are the most significant. Findings are presented which suggest that diabetic microangiopathy is not of genetic or immunologic origin, but is to be considered a consequence of insulin deficiency. More recently, some studies have been carried out which which strongly support the concept that metabolic control of the diabetic prevents or at least delays the development of late complications of diabetes. For this reason an optimal for control of diabetes, if at all possible with aglycosuria, should be aimed at.
The treatment of diabetes may be improved by a more physiological insulin supply and by supplements to the insulin supply. Grafting the entire pancreas or transplantation of the islet cells represents an improvement in the insulin supply. But because fo the lack of donor material and immunological difficulties, the realization of these two methods may be questionable. On the other hand the implantation of an artificial B cell seeems realizable in the foreseeable future. Such a method would be indicated in a diabetic whose life is threatened by late complications. Somatostatin is available as a supplement to insulin therapy because it eliminates the growth hormone as possible source of diabetic vascular complications and it blocks the secretion of hormones with a contrainsular effect.
Since vitamin B12malabsorption has been described in diabetics on biguanides and inhibition of bile acid absorption found in rat ileum the effect of treatment with different biguanides (phenformin, buformin, metformin) on bile acid metabolism and vitamin B12 absorption was assessed in maturity onset diabetics. Biguanides did not alter faecal weight or faecal fat excretion, but they decreased faecal bile acid excretion. All biguanides tested increased deconjugation of glycocholic acid, as determined by a simple breath test technique. Vitamin B12 malabsorption was most prominent in patients on metformin. Discontinuation of biguanide treatment, or administration of antibiotics, normalized or improved the increased deconjugation of bile acids and the Schilling test. Decreased faecal bile acid excretion, positive 14C-glycocholate breath tests, pathological Schilling tests and the reversal of pathological tests by antibiotic treatment suggest that small intestinal bacterial overgrowth, leading to binding of the intrinsic-factor-vitamin B12-complex to bacteria, is responsible for the previously observed pathological Schilling tests in diabetics on biguanides. Bile acid malabsorption, possibly responsible for the cholesterol-lowering effect of biguanides, does not occur in diabetics on biguanides. Whether qualitative changes in small intestinal bile acid composition might affect cholesterol metabolism remains to be determined.