Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the Tampere region in Finland, the incidence of childhood coeliac disease was 1:1,096 between 1964 and 1973 and 1:3,214 from 1974 to 1983. The clinical picture of coeliac disease had changed to milder forms, resulting in an upward shift of age at diagnosis. Coeliac disease was found in older children and adolescents, manifesting itself mostly in minor abdominal symptoms, short stature, delayed puberty, anaemia and joint complaints, and in children with diabetes mellitus. Long breast-feeding seemed to postpone the symptoms but the introduction of gluten was of no significance. The low incidence for 1974 to 1983 was thought to be due to the estimated 20 cases born in 1979 to 1983 who were not detected. We do not believe that coeliac disease has disappeared but that it will be found during the next decade in the patients who were not diagnosed in school age and adolescence.
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PMID:Changing pattern of childhood coeliac disease in Finland. 338 34

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)
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PMID:[Adult celiac disease and type 1 diabetes: a severe and sometimes unknown genetic association]. 342 65

The relationship between increased risk in relatives over population prevalence (lambda R = KR/K) and probability of sharing zero marker alleles identical by descent (ibd) at a linked locus (such as HLA) by an affected relative pair is examined. For a model assuming a single disease-susceptibility locus or group of loci tightly linked to a marker locus, the relationship is remarkably simple and general. Namely, if phi R is the prior probability for the relative pair to share zero marker alleles identical by descent, then P (sharing 0 markers/both relatives are affected) is just phi R/lambda R. Alternatively, lambda AR, the increased risk over population prevalence to a relative R due to a disease locus tightly linked to marker locus A, equals the prior probability that the relative pair share zero A alleles ibd divided by the posterior probability that they share zero alleles ibd, given that they are both affected. For example, for affected sib pairs, P (sharing 0 markers/both sibs are affected) = .25/lambda S. This formula holds true for any number of alleles at the disease locus and for their frequencies, penetrances, and population prevalence. Similar formulas are derived for sharing one and two markers. Application of these formulas to several well-studied HLA-associated diseases yields the following results: For multiple sclerosis, insulin-dependent diabetes mellitus, and coeliac disease, a single-locus model of disease susceptibility is rejected, implying the existence of additional unlinked familial determinants. For all three diseases, the effect of the HLA-linked locus on familiality is minor: for multiple sclerosis, it accounts for only a 2.5-fold increased risk to sibs over the population prevalence, compared to an observed value of 20; for coeliac disease, it accounts for approximately a 5.25-fold increased risk to sibs, while the observed value is on the order of 60; for insulin-dependent diabetes mellitus, it accounts for a 3.42-fold increased risk in sibs, while the observed value is 15. In all cases, the secondary determinants must be outside the HLA region. For tuberculoid leprosy, an unlinked familial determinant is also implicated (increased risk to sibs due to HLA = 1.49; observed value = 2.38). For hemochromatosis and Hodgkin's disease, there is little evidence for HLA-unlinked familial determinants. With this formula, it is also possible to examine the hypothesis of pleiotropy versus linkage dis-equilibrium by comparing lambda AS with the increased risk to sibs due to the associated allele(s).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessing the role of HLA-linked and unlinked determinants of disease. 346 4

We treated two patients with dermatitis herpetiformis and Addison's disease, and one patient with celiac disease without the rash, but with Addison's disease and juvenile diabetes. In two of the patients, the concomitant diseases also included a thyroid disease. The predisposing factors to the multiple endocrine disorders in these patients with gluten-sensitive skin and/or small intestinal disease remained unknown. Two of the three patients had HLA-B8, none was known to have affected relatives, and the Addison's disease appeared before, at the same time, or after the patients contracted dermatitis herpetiformis or celiac disease.
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PMID:Dermatitis herpetiformis and celiac disease associated with Addison's disease. 360 72

Jejunal biopsy was performed without selection in 110 of 201 children with insulin-dependent diabetes mellitus; serum reticulin antibody, antigliadin antibody by enzyme-linked immunosorbent assay, and serum IgA were studied in all 201 children. Seven children had severe jejunal villous atrophy, giving a prevalence of celiac disease of at least 3.5%. Of the serum tests used, antigliadin antibody with ELISA was the most sensitive. Four patients adhered to a gluten-free diet, and their jejunal structure became normal; three had subsequent gluten provocation, and the jejunal mucosa relapsed in every one. Six had HLA-B8 and -DR3 antigens, and one had B15 and -DR4 phenotypes. In most patients, a gluten-free diet had little effect on insulin dosage, urinary excretion of glucose, or serum level of hemoglobin A1.
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PMID:Celiac disease in insulin-dependent diabetes mellitus. 370 14

A 14 year-old boy with coeliac disease and poorly treated diabetes mellitus and pulmonary tuberculosis due to INH resistant BK presented with a permanent malabsorption of rifampicin. Pharmacokinetics of rifampicin was studied after oral administration and intravenous injection. Treatment of diabetes and coeliac disease did not improve the situation. Tuberculosis was cured by pyrazinamide and ethambutol.
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PMID:[Permanent malabsorption of rifampicin in a diabetic with celiac disease]. 377 4

Pancreatic carcinoma is one of the most lethal malignancies seen in humans. If cure is to be effected, radical surgery for small lesions confined to the gland must be undertaken, but the cost in morbidity and mortality is high. An otherwise fit elderly patient should not be denied the small chance of cure because of age alone, but such a patient must be frankly appraised of the significant risks and limitations of resectional therapy. The Whipple procedure remains the standard operation for lesions of the head of the gland, but pre-existing severe diabetes and technical factors may dictate that a total pancreatectomy be performed. Patients with unresectable cancers who develop biliary or enteric obstruction should be bypassed internally if otherwise healthy. If frail or infirm from other organ failure, patients may be offered relief by a percutaneous decompression with minimal risk. Pain must be dealt with in all patients with celiac blocks or liberal use of analgesics. Adjuvant forms of therapy are experimental, costly in time and money, not without serious side effects, and should be advised cautiously in elderly patients.
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PMID:Alternatives in the management of pancreatic cancer. 383 Mar 79

Subtotal villous atrophy in the proximal jejunum was observed in six patients affected by juvenile diabetes. Introduction of gluten free diet invariably led to clinical improvement, in the four patients in whom also rebiopsy was performed the jejunal mucosa exhibited improvement. In all cases gluten sensitive enteropathy was diagnosed after the onset of diabetes. Marked stunting in growth, strikingly labile carbohydrate tolerance, pronounced proneness to hypoglycaemia or development of Mauriac's syndrome were the symptoms pointing to coeliac disease. Protracted diarrhoea was seen only in two patients, pronounced deceleration in weight development occurred in none of the six children. In four patients out of six the presence of both HLA B8 and DR3 antigens was demonstrated, in a fifth patient only DR3 was present; this suggests a common genetic background of the simultaneous occurrence of the two disorders. Untreated coeliac disease aggravates preexisting diabetes. The importance of early recognition of latent coeliac disease is stressed.
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PMID:Simultaneous occurrence of diabetes mellitus and coeliac disease. 387 51

The patient presented with a diabetes at the age of 3 years. At the age of 5 years she got persistent diarrhoea, lost weight and showed symptoms or arthritis and pericarditis. She was found to have total villous atrophy of the jejunum, which did not respond to dietary treatment, total parental nutrition, prednisone and cyclophosphamide medication. She had high titres of antinuclear antibodies and elevated serum IgG, but antibodies to DNA and to ribonuclearprotein were negative. A low titre of antibodies to human intestinal epithelial cells was found. The patient died of overwhelming fungal sepsis. We propose that the intestinal damage is part of the autoimmune disease. Careful study of jejunal biopsy specimens is helpful in distinguishing this type of patient from patients with coeliac disease.
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PMID:Fatal unresponsive villous atrophy of the jejunum, connective tissue disease and diabetes in a girl with intestinal epithelial cell antibody. 400 75

Six patients with hyperphagia (ingestion of 5-11 000 Kcals/day) associated with severe malabsorption and steatorrhoea are described. The cause of the malabsorption was coeliac disease in three patients, Crohn's disease with ileal resection in two, and carcinoma of the pancreas in one patient. There was no evidence of neurological or endocrine disease (apart from mild diabetes mellitus in the patient with carcinoma of the pancreas) but three patients suffered from severe depression. This association may be commoner than previously realized and be revealed in patients with steatorrhoea of unexplained severity by careful dietary assessment. Its detection has therapeutic implications since restriction of caloric and fat intake decreased steatorrhoea without weight loss in several of the patients described.
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PMID:Hyperphagia in intestinal disease. 453 69


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