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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Currently, for the patient with type 1 diabetes, a definitive treatment without resorting to the use of exogenous insulin can be achieved only with pancreas or islet cell transplantation. These means of restoring beta-cell mass can completely maintain essentially normal long-term glucose homeostasis, although the need for powerful immunosuppressive regimens limits their application to only a subgroup of adult patients. Apart from the shortage of donors that has limited all kinds of transplantation, however, the widespread use of beta-cell replacement has been precluded until recently by the drawbacks associated with both organ and islet cell transplantation. Although the study of recurrence of diabetes has generated attention, the fundamental obstacle to pancreas and islet transplantation has been, and remains, the alloimmune response. With a better elucidation of the mechanisms of alloengraftment achieved during the last 3 years, the stage has been set for further advances.
Best Pract Res Clin Gastroenterol 2002 Jun
PMID:Pancreas and islet cell transplantation. 1207 69

Postpartum thyroiditis (PPT) is the occurrence, in the postpartum period, of transient hyperthyroidism and/or transient hypothyroidism, with most women returning to the euthyroid state by 1 year postpartum. The prevalence of PPT varies from 1.1 to 16.7%, with a mean prevalence of 7.5%. Women with type I diabetes mellitus have a three-fold increase in the prevalence of PPT. PPT is an autoimmune disorder which is a transient form of Hashimoto's thyroiditis occurring postpartum as a consequence of the immunologic flare following the immune suppression of pregnancy. Women experience symptoms in both the hyperthyroid and hypothyroid phase, but the association between PPT and postpartum depression remains undefined. Approximately 25% of women with a history of PPT will develop permanent hypothyroidism in the ensuing 10 years. Treatment for the hyperthyroid phase, when required, is a short dose of beta-blockers. Women with a TSH greater than 10 mU/l, or between 4 and 10 mU/l with symptoms or attempting pregnancy, require thyroid hormone replacement. Whether or not to screen for PPT remains controversial.
Best Pract Res Clin Endocrinol Metab 2004 Jun
PMID:Postpartum thyroiditis. 1515 42

Type 1 diabetes mellitus is preceded by autoimmunity against the insulin-producing islet beta cells. Autoantibodies against islet antigens such as insulin, glutamic acid decarboxylase, and the protein tyrosine phosphatase-like molecule IA-2 are found in most patients with type 1 diabetes and are now established markers for the clinical diagnosis and the preclinical phase of this disease. The development of islet autoantibodies and diabetes is influenced by genetic and environmental factors, and the detection and characterization of islet autoantibodies in euglycemic members of affected families identifies some individuals who have a markedly elevated risk for type 1 diabetes. This ability to accurately predict diabetes risk in non-diabetic subjects will prove very useful for targeted recruitment of participants of interventional studies aimed at preventing the progression to type 1 diabetes in subjects at risk.
Best Pract Res Clin Endocrinol Metab 2005 Mar
PMID:Diabetes-related antibodies in euglycemic subjects. 1582 25

Islet autoimmunity is made evident by the appearance of islet-cell antibodies directed against insulin (IAA), glutamic acid decarboxylase (GADA), protein tyrosine phosphatase IA-2 (IA-2Ab) and other autoantigens. IAA and IA-2Ab are predominantly detected in childhood type 1 diabetes mellitus (T1DM), while frequency of GADA is not affected by age. In adult-onset T1DM patients, GADA is the immune marker of higher diagnostic sensitivity. In adult diabetic patients not requiring insulin treatment for at least 6 months after diagnosis, GADA identifies the so-called latent autoimmune diabetes in adults (LADA). In over 80% of cases, LADA patients develop insulin dependency within a few years after the diagnosis and have an increased risk for the development of other organ-specific autoimmune diseases. High GADA titers identify a subgroup of LADA patients with low body mass index (BMI), low C-peptide levels and increased frequency of T1DM-related HLA class II haplotypes. GADA assay should be offered to every diabetic patient, and in cases of positivity screening for other autoimmune diseases should be carried out.
Best Pract Res Clin Endocrinol Metab 2005 Mar
PMID:Diabetes-related antibodies in adult diabetic patients. 1582 26

Following the application of simple serological tests for the diagnosis of coeliac disease (CD) in the 1980s, it gradually became clear that the prevalence of CD in different countries in the Middle East, North Africa and India is almost the same as that in Western countries. The prevalence of CD in at-risk populations in these regions is reported to range between 3 and 20% and the prevalence in people with type 1 diabetes is approximately 3-5%. Clinical manifestations of CD vary markedly with age, the duration and the extent of disease. Clinical studies showed that presentation with non-specific symptoms or no symptoms is as common in the Middle East as it is in Europe. Wheat has been the major staple food in these regions for many centuries and it is possible that the continuous and high level of exposure to wheat proteins has induced some degree of immune tolerance, leading to milder symptoms, which are misdiagnosed as irritable bowel syndrome or unexplained gastrointestinal disorders. A high index of suspicion for CD should be maintained in all developing countries for patients who present with chronic diarrhoea or iron deficiency anaemia. The best method for diagnosing CD in patients with diarrhoea is the panel of coeliac serological tests followed by small-bowel biopsy. In the absence of supplies for a gluten-free diet in Middle Eastern countries, maintaining this diet represents a real challenge to both patients and clinicians.
Best Pract Res Clin Gastroenterol 2005 Jun
PMID:Coeliac disease in developing countries: Middle East, India and North Africa. 1592 41

Demographic trends with longer life expectancy and a lifestyle characterized by low physical activity and high-energy food intake contribute to an increasing incidence of diabetes mellitus and osteoporosis. Diabetes mellitus is a risk factor for osteoporotic fractures. Patients with recent onset of type 1 diabetes mellitus may have impaired bone formation because of the absence of the anabolic effects of insulin and amylin, whereas in long-standing type 1 diabetes mellitus, vascular complications may account for low bone mass and increased fracture risk. Patients with type 2 diabetes mellitus display an increased fracture risk despite a higher BMD, which is mainly attributable to the increased risk of falling. Strategies to improve BMD and to prevent osteoporotic fractures in patients with type 1 diabetes mellitus may include optimal glycemic control and aggressive prevention and treatment of vascular complications. Patients with type 2 diabetes mellitus may additionally benefit from early visual assessment, regular exercise to improve muscle strength and balance, and specific measures for preventing falls.
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PMID:Osteoporosis in patients with diabetes mellitus. 1750 67

Children and adolescents with poorly controlled type 1 diabetes mellitus (T1DM) are at risk for decreased bone mass. Growth hormone (GH) and its mediator, IGF-1, promote skeletal growth. Recent observations have suggested that children and adolescents with T1DM are at risk for decreased bone mineral acquisition. We examined the relationships between metabolic control, IGF-1 and its binding proteins (IGFBP-1, -3, -5), and bone mass in T1DM in adolescent girls 12-15 yr of age with T1DM (n = 11) and matched controls (n = 10). Subjects were admitted overnight and given a standardized diet. Periodic blood samples were obtained, and bone measurements were performed. Serum GH, IGFBP-1 and -5, glycosylated hemoglobin (HbA(1c)), glucose, and urine magnesium levels were higher and IGF-1 values were lower in T1DM compared with controls (p < 0.05). Whole body BMC/bone area (BA), femoral neck areal BMD (aBMD) and bone mineral apparent density (BMAD), and tibia cortical BMC were lower in T1DM (p < 0.05). Poor diabetes control predicted lower IGF-1 (r(2) = 0.21) and greater IGFBP-1 (r(2) = 0.39), IGFBP-5 (r(2) = 0.38), and bone-specific alkaline phosphatase (BALP; r(2) = 0.41, p < 0.05). Higher urine magnesium excretion predicted an overall shorter, lighter skeleton, and lower tibia cortical bone size, mineral, and density (r(2) = 0.44-0.75, p < 0.05). In the T1DM cohort, earlier age at diagnosis was predictive of lower IGF-1, higher urine magnesium excretion, and lighter, thinner cortical bone (r(2) >or=0.45, p < 0.01). We conclude that poor metabolic control alters the GH/IGF-1 axis, whereas greater urine magnesium excretion may reflect subtle changes in renal function and/or glucosuria leading to altered bone size and density in adolescent girls with T1DM.
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PMID:IGF-1 and IGF-binding proteins and bone mass, geometry, and strength: relation to metabolic control in adolescent girls with type 1 diabetes. 1884 35

Studies investigating the effect of leptin on bone mass were inconsistent and some related it to the effect of insulin. We intend in this cross-sectional study to investigate the effect of leptin on bone mass in type 1 diabetic patients. We recruited 42 patients with type 1 diabetes for which we determined weight, height, HbA1c, microalbuminuria, serum leptin, bone mineral content (BMC) and density (BMD), and body composition. The patients had an average age of 20.1 +/- 0.6 years, an average body mass index (BMI) of 23.6 +/- 0.5 kg/cm(2) and an average duration of diabetes of 9.1 +/- 1.0 years. The Z-score was not correlated with HbA1c or duration of the disease, and the average Z-score was not different in patients with microalbuminuria as compared to patients with no reported microalbuminuria. On the other hand, Z-score and BMC correlated negatively with leptin (r = -0.31; p = 0.04 and -0.60, p < 0.01, respectively). These correlations persisted after adjustment for fat mass. We conclude that not metabolic control of diabetes, but serum leptin has a negative effect on bone density in young patients with type 1 diabetes. This negative effect of leptin on bone density maybe, in part, due to deficiency of endogenous insulin secretion in these patients.
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PMID:Negative effect of leptin on bone mass in type 1 diabetes. 1869 Apr 7

People with diabetes have increased risk of fracture disproportionate to BMD, suggesting reduced material strength (quality). We quantified the skeletal effects of type 1 diabetes in the rat. Fischer 344 and Sprague-Dawley rats (12 wk of age) were injected with either vehicle (Control) or streptozotocin (Diabetic). Forelimbs were scanned at 0, 4, 8, and 12 wk using pQCT. Rats were killed after 12 wk. We observed progressive osteopenia in diabetic rats. Trabecular osteopenia was caused by bone loss: volumetric BMD decreased progressively with time in diabetic rats but was constant in controls. Cortical osteopenia was caused by premature arrest of cortical expansion: cortical area did not increase after 4-8 wk in diabetic rats but continued to increase in controls. Postmortem muCT showed a 60% reduction in proximal tibial trabecular BV/TV in diabetic versus control rats, whereas moments of inertia of the ulnar and femoral diaphysis were reduced approximately 30%. Monotonic bending tests indicated that ulna and femora from diabetic animals were approximately 25% less stiff and strong versus controls. Estimates of material properties indicated no changes in elastic modulus or ultimate stress but modest ( approximately 10%) declines in yield stress for diabetic bone. These changes were associated with a approximately 50% increase in the nonenzymatic collagen cross-link pentosidine. Last, cyclic testing showed diminished fatigue life in diabetic bones at the structural (force) level but not at the material (stress) level. In summary, type 1 diabetes, left untreated, causes trabecular bone loss and a reduction in diaphyseal growth. Diabetic bone has greatly increased nonenzymatic collagen cross-links but only modestly reduced material properties. The loss of whole bone strength under both monotonic and fatigue loading is attributed mainly to reduced bone size.
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PMID:Type 1 diabetes in young rats leads to progressive trabecular bone loss, cessation of cortical bone growth, and diminished whole bone strength and fatigue life. 1933 53

Vitamin D has historically been considered to play a role solely in bone and calcium metabolism. Human disease associations and basic physiological studies suggest that vitamin D deficiency is plausibly implicated in adverse health outcomes including mortality, malignancy, cardiovascular disease, immune functioning and glucose metabolism. There is considerable evidence that low maternal levels of 25 hydroxyvitamin D are associated with adverse outcomes for both mother and fetus in pregnancy as well as the neonate and child. Vitamin D deficiency during pregnancy has been linked with a number of maternal problems including infertility, preeclampsia, gestational diabetes and an increased rate of caesarean section. Likewise, for the child, there is an association with small size, impaired growth and skeletal problems in infancy, neonatal hypocalcaemia and seizures, and an increased risk of HIV transmission. Other childhood disease associations include type 1 diabetes and effects on immune tolerance. The optimal concentration of 25 hydroxyvitamin D is unknown and compounded by difficulties in defining the normal range. Whilst there is suggestive physiological evidence to support a causal role for many of the associations, whether vitamin D deficiency is a marker of poor health or the underlying aetiological problem is unclear. Randomised controlled trials of vitamin D supplementation with an appropriate assessment of a variety of health outcomes are required.
Best Pract Res Clin Endocrinol Metab 2010 Aug
PMID:Vitamin D and pregnancy: An old problem revisited. 2083 34


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