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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    International journal of colorectal disease 9 (1994), S. 105-109 
    ISSN: 1432-1262
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé Afin d'étudier la pathophysiologie de l'incontinence fécale en cas de diabète, deux groupes de patients diabétiques ont été analysés: 14 sujets incontinents (7 femmes et 7 hommes dont l'âge moyen est de 57±9 ans) (groupe A) et 15 sujets sans incontinence mais porteurs d'une neuropathie périphérique (6 femmes et 9 hommes dont l'âge moyen est de 54,7±8 ans). Un troisième groupe (groupe C) constitué de 10 volontaires sains a servi de groupe contrôle. Tous les sujets ont subi des investigations électroneurographiques de leur neuropathie périphérique, une mesure du temps de latence du nerf honteux interne, une manométrie anorectale et des tests de sensibilité rectale. Tous les patients du groupe A présentent une neuropathie somatique périphérique. La pression maximale de rétention est plus basse dans le groupe A que dans le groupe C (P〈0,025) et peut être maintenue moins longtemps dans le groupe A que dans le groupe B (P〈0,0005) ou que dans le groupe C (P〈0,0005). Les seuils de sensibilité rectale sont plus élevés dans le groupe A que dans les groupes B et C. Le temps de latence du nerf honteux interne est allongé chez 92,9% des patients étudiés dans le groupe A et 73,3% des patients du groupe B (A vs B,P〈0,005); la différence est encore plus significative en comparaison avec le groupe C (A vs CP〈0,0005, B vs CP〈0,005). Nos constations suggèrent que la neuropathie somatique joue un rôle important dans la genèse de l'incontinence chez les patients diabétiques, en combinaison avec des altérations du seuil de sensibilité rectale en tant que symptôme d'une atteinte autonome.
    Notes: Abstract To investigate the pathophysiology of faecal incontinence in diabetes mellitus, two groups of diabetic patients were studied: 14 subjects (7 females and 7 males, mean age 57±9 years) with faecal incontinence (Group A) and 15 subjects (6 females and 9 males, mean age 54.7±8 years) without faecal incontinence but affected by somatic peripheral neuropathy. A third group (C) of 10 healthy volunteers was used as controls. All subjects underwent electroneurographic evaluation of peripheral neuropathy, pudendal nerve terminal motor latency, anorectal manometry and rectal sensitivity tests. All the patients of group A had somatic peripheral neuropathy. Maximum squeeze pressure was lower in A compared to C (P〈0.025) and sustained for a shorter period in A compared with B (P〈0.0005) and C (P〈0.0005). All rectal sensitivity thresholds were higher in A compared with B and C. Pudendal Nerve Terminal Motor Latency was prolonged in 93% of patients studied in group A and in 73% of patients in group B (A vs BP〈0.005), with a significant difference in comparison with C: A vs CP〈0.0005, B vs CP〈0.005. Our findings suggest that somatic neuropathy plays an important role in faecal incontinence in diabetic patients, combined with sesation threshold impairment as a feature of an autonomic involvement.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; biguanides ; metformin ; insulin receptors ; insulin therapy ; artificial pancreas ; Biostator
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of metformin on Type 1 (insulin-dependent) diabetes has been assessed with the artificial pancreas. Fourteen Type 1 diabetic patients of normal body weight received in addition to their usual insulin therapy 850 mg metformin or placebo three times a day for 4–6 weeks. The sequence was placebo-metformin in eight patients and metformin-placebo in the other six. On the last day of metformin or placebo treatment, an artificial pancreas was used for about 36 h to assess insulin requirement. There was a 25.8% reduction in insulin requirement during metformin management despite slightly lower blood glucose levels (5.25±0.20 versus 5.98±0.18 mmol/l, P〈0.01). Maximum reduction (about 50%) occurred 2 h after both lunch and dinner. There was no nocturnal effect. A marked decrease in specific insulin binding before metformin was found (0.56 + 0.27% to 107 monocytes versus 2.82±0.75 of control subjects) and significant increase after metformin (1.36±0.36%, p〈0.05). There were no significant changes in blood lactate, total and HDL-cholesterol, triglycerides and C-peptide levels. These results show that insulin receptor binding is diminished in Type 1 diabetes, perhaps as a consequence of higher peripheral blood insulin levels and that metformin can improve binding, and so reduce the amount of insulin needed to reach euglycaemia. The insulin sparing effect is greatest after meals, and interference with intestinal absorption of sugars may also be important. It follows that metformin could be usefully administered to Type 1 diabetic patients with unimpaired liver and renal function to reduce their insulin requirement.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 39 (1994), S. 1633-1637 
    ISSN: 1573-2568
    Keywords: anti-endomysium antibodies ; celiac disease ; gluten intolerance ; diabetes mellitus ; IDDM ; IgA-EmA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We screened for celiac disease, by means of IgA class anti-endomysium antibodies (EmA), 383 consecutive adults with insulin-dependent diabetes mellitus (IDDM). Two control populations entered the study as well: 151 adults with biopsy proven celiac disease, as true positives; and 520 controls (healthy and diseased) as true negatives. IgA-EmA positivity was found in 145 of 151 (96%) celiac disease patients but in none of the controls (100% specificity). EmA were positive in 12 of 383 (3.13%) IDDM patients: 10 of these positives underwent intestinal biopsy, which showed either partial or total villous atrophy. Only one patient presented with gastrointestinal complaints, but severe iron deficiency was found in all. The IDDM celiac patients were started on a gluten-free diet: four refused both the diet and the follow-up protocol. Approximately one year after gluten withdrawal no significant change in the degree of diabetes control was observed, while an increased requirement for insulin was observed in three of four patients who strictly complied with the diet. The prevalence of biopsy-proven celiac disease among adult IDDM patients (1:38), eight times higher than that recently estimated for the general Italian population and the absence, except in one case, of gastrointestinal symptoms emphasizes the benefit of screening programs on populations at risk.
    Type of Medium: Electronic Resource
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