[Diabetogenic tropical pancreatitis]. / Pancréatite tropicale diabétogène.

The tropical calcifying pancreatitis and/or fibrous pancreatitis are responsible for a number of cases of juvenile insulin-dependent diabetes in the Third World countries. World wide distributed in the tropical areas of Asia, Africa and South America, they can also be observed in Europe, in migrants from these countries. Intensive epidemiological and biochemical studies are currently developed in order to shed light on the many obscure points. Classification of the typical calcifying pancreatitis and the related syndromes is a matter of debate. The pathological basis is calcification of the pancreas and echography of the gland may become a cheap convenient relatively specific tool for epidemiology. The clinical syndrome consists of chronic painful pancreatic episodes since childhood, associated with pancreatic exocrine insufficiency, followed by the onset, during adolescence, of diabetes mellitus, which is most of the times insulin dependent. Patients' history is free of chronic alcoholism, but includes constantly chronic caloric and proteic malnutrition. Although insulin dependent this diabetes in not prone to ketosis, due presumably to carnitine deficiency and relative glucagon deficiency (or suppressibility). Insulin resistance is traditionally noted, the pathophysiology of which is unknown. The mechanism of calcification appearance is also undetermined. Either a deficiency in pancreatic stone protein, or the toxic effect of cyanogen glucosides present in cassava and other tropical foodstuffs, or the malnutrition-related deficiency in sulphur-containing aminoacids may be causal factors. No valid experimental model of the disease is available.

[Adult celiac disease and type 1 diabetes: a severe and sometimes unknown genetic association]. / Maladie coeliaque de l'adulte et diabète de type 1: une association génétique sévère et parfois méconnue.

In 6 type 1 (insulin-dependent) diabetics, treated with insulin since the age of 2 to 35 years (mean 12), coeliac disease was diagnosed between the 10 th and 73 th years of age (mean 26). Five were of North African origin. Digestive symptoms and severe malnutrition were present in all of them, associated, in the two younger, with a major growth retardation and, in one, multiple pathologic fractures. Biopsy of the small intestine demonstrated, in all, total or subtotal villous atrophy. The metabolic control of diabetes was poor, with frequent hypoglycaemic attacks, induced by minute insulin doses. Severe chronic complications of diabetes were detectable in all of them. Plasma anti-reticulin antibodies were present, at high titer before starting the gluten-free diet, declining slowly after starting this diet, and negative in the patients who followed this diet. Among the genetic markers (which were determined in 4), HLA A1 was present in 4, B8 and DR3 in 3 and DR4 in 3. The DR7 was not detected. The gluten-free diet, memorized by the patients by the use of simple rules, improved the digestive symptoms, and insulin doses could then be increased. The overall prognosis remained poor, due to diabetic complications and sociologic desinsertion. Coeliac disease occurs in 1 to 2% of type 1 diabetics and 4-6% of the coeliac patients are diabetics. Diabetic subjects from North Africa are at high risk of this association. Misdiagnosis of the coeliac disease compromises the metabolic control and nutritional state.(ABSTRACT TRUNCATED AT 250 WORDS)