Type 2 diabetes mellitus and fracture risk factors,most promising cure for type 1 diabetes uk,type 2 diabetes treatment guidelines 2013 ppt online,type 2 diabetes joint pain - Reviews


More than 180 million people worldwide suffer from type 2 diabetes, a disease that more than doubles the risk of death, mainly from cardiovascular disease.1 Interestingly, the medical literature provides evidence of a convergence between diabetes, a metabolic disease, and potential mechanisms accounting for osteoporosis.
There is a constant turnover of bone through bone remodeling, via a biphasic process occurring throughout the skeleton over a period of approximately 3 months.4 It includes destruction (resorption) of preexisting bone, a function exerted by a specialized bone-specific cell, the osteoclast, followed by de novo bone formation, a function exerted by another bonespecific cell, the osteoblast.
The relatively recent observation of a convergence between bone and energy homeostasis suggests that energy metabolism and bone mass are regulated by the same hormones, such as leptin (Figure 1),7 adiponectin,8 neuropeptide Y,9 and substance P.10 A remarkable feature of most types of hormonal regulation is that they are controlled by feedback loops, such that the cells targeted by a hormone send signals influencing the hormone-producing cells. Type 1 diabetes, also called insulin-dependent diabetes mellitus, is characterized by little or no insulin production and hyperglycemia.
Active, uncarboxylated osteocalcin produced in osteoblasts is secreted into serum and triggers insulin secretion in pancreatic β-cells. The mechanisms contributing to type 1 diabetic bone loss are unknown, but several theories have been put forward. Type 2 diabetes, also called non–insulin-dependent diabetes mellitus, develops when cells become resistant to insulin signaling, and accounts for more than 90% of diabetes cases. The most convincing evidence that osteoporosis is a complication of diabetesmellitus comes fromepidemiological studies that have shown an increased risk of fragility fractures.
Oral antidiabetic drugs are commonly used to improve glycemic control, but there are concerns that some may increase the risk of cardiovascular events.40 Moreover, several epidemiological studies have investigated the effects of antihyperglycemic treatment on fracture risk in diabetes. As these findings support the hypothesis of a class effect of thiazolidinediones in increasing fracture risk in women with type 2 diabetes mellitus, letters to health care providers have been issued by the manufacturers.44,45 However, doubts still exist about the clinical relevance of this phenomenon, and more studies are needed to address a number of still pending questions,21,46 such as the precise mechanism of action of these agents (Figure 4). The figure represents a suggested model of potential deleterious effects of diabetes on bone based on in vitro findings, animal studies, and observational human data. Physicians should carefully check for the existence of risk factors for osteoporosis and fractures in their patients before putting them on thiazolidinedione treatment, and an adequate clinical follow-up of treated patients is strongly recommended.
The prevalence of diabetes mellitus is increasing rapidly in the population, with the implication that adverse outcomes of the condition are likely to grow in importance as well.
Future studies should contribute to a more thorough understanding of the mechanisms of diabetic bone loss, enabling the development of newer and more effective drugs.
PUBS is a rare disorder causing discolouration of urine and urine collection bags due to the presence of indigo and indirubin pigment produced by tryptophan metabolism. A 65 year old bed ridden female, with a history of type 2 diabetes mellitus and dementia with old fracture of left femur who had an indwelling urinary catheter in place for last 3 months, presented to us in the emergency department with the complaints of nausea, vomiting, decreased oral intake, chronic constipation and purplish discolouration of the urine bag and tubing (Figure 1). PUBS was first described by Barlow and Dickson in 1978,2 after purple urine was found in a patient who had prolonged urinary catheterization.
The postulated hypothesis regarding aetiopathogenesis of PUBS is believed to be related to metabolites of dietary tryptophan (Figure 3).7 The normal flora in the intestine metabolises tryptophan to indole which is absorbed into the portal circulation via the gut wall. A strong association of PUBS with constipation and intestinal obstruction has also been described. Now, despite the common occurrence of urinary tract infection with all the risk factors of PUBS, it is interesting to note the rarity of this syndrome. Most of the patients with PUBS remain asymptomatic, its clinical course is usually benign and therefore only changing the urinary catheter and urinary bag usually are enough to solve the problem.
Both type 1 diabetes and type 2 diabetes have been linked to increased risk of fractures, with bonemineral density being decreased in type 1 diabetes and increased in type 2 diabetes. Normally, resorption and formation of bone occur not only sequentially, but in a balanced manner in order to maintain bone mass nearly constant during most of adulthood. BMD is a strong predictor of fracture risk, but bone mineral quantity is only one component of bone strength, and various disorders, including diabetes, can be associated with poor bone quality. When applied to skeletal biology, the concept of feedback regulation suggests that bone cells exert an endocrine function. Improved glucose monitoring, insulin delivery methods, and pharmacologic treatments are increasing patient lifespan. Moreover, by increasing adiponectin synthesis in adipocytes, insulin sensitivity is enhanced.
Analysis of type 1 diabetic bone remodeling serum markers suggests that bone turnover is unaltered or decreased, while bone formation is decreased, as indicated by reduced serum levels of osteocalcin and histomorphometric studies.16,17 The potential contributors to type 1 diabetic bone phenotypes are listed in Table I.
Diet, obesity, and reduced physical activity are several of the factors that are thought to contribute to the development of type 2 diabetes. Diabetes and hip fracture share common risk factors (eg, physical inactivity, advanced age); in contrast, obesity, a risk factor for diabetes, is associated with a lower risk of fractures, and any apparent modification in fracture risk by diabetes is likely to reflect a confounding effect of these and other extraneous factors.
Moreover, the meta-analysis found no significant increase in vertebral or distal forearm fractures in these patients.3 At present, there is no clear explanation for this apparent contradiction. Potential mechanisms contributing to low bone mass and increased fracture susceptibility in diabetes mellitus.
Optimizing therapies that prevent bone loss or restore bone density will allow diabetic patients to live longer, with strong healthy bones. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractType 1 diabetes mellitus (T1DM) has been inconsistently associated with low bone mineral density (BMD) and increased fracture risk. Vestergaard, “Discrepancies in bone mineral density and fracture risk in patients with type 1 and type 2 diabetes—a meta-analysis,” Osteoporosis International, vol.


This condition is most commonly associated with alkaline urine, female gender, constipation and urinary tract infection.1 Although this condition is benign, it can be distressing for patients, family members, and health care workers who are unaware of this entity. Chronic constipation alters gut motility and prolonged transit time, resulting bacterial overgrowth in the colon.
Aggressive investigations like urine culture or septic work up and treatment with antibiotics are usually not necessary. It often occurs in chronically catheterized and constipated patients who have significant underlying comorbidities. Case analysis of purple urine-bag syndrome at a long-term care service in a community hospital.
Insulin has an anabolic effect on bone, and the qualitatively different effects of type 1 and type 2 diabetes on bone mass are consistent with the opposite insulin-secretory states (hypoinsulinemia vs hyperinsulinemia). Nevertheless, despite a large body of accumulated data on the skeletal effects of diabetes, many questions remain unresolved, with biochemical and imaging studies producing conflicting findings. This qualifies bone remodeling as a true homeostatic function controlled by cytokines acting locally and hormones acting systemically. However, as a result, there is a parallel increase in the risk of complications due to extended exposure to diabetes.
Available data concerning an association between reduced BMD and type 2 diabetes are equivocal. An increased risk of falling in diabetic patients35 could account for the elevated hip fracture risk in the face of normal or elevated BMD. Although fractures may now be prevented thanks to the availability of effective treatments, no clear rationale exists for treating patients with type 2 diabetes with antifracture agents able to increase BMD, and our knowledge base is not strong enough for a more effectively tailored prophylaxis to be designed for this group.
Adiponectin and AMP kinase activator stimulate proliferation, differentiation and mineralization of osteoblastic MC3T3-E1 cells. Critical interplay between neuropeptide Y and sex steroid pathways in bone and adipose tissue homeostasis.
Substance P stimulates bone marrow stromal cell osteogenic activity, osteoclast differentiation, and resorption activity in vitro. Early manifestation of type 1 diabetes in children is a risk factor for changed bone geometry. The lumbar bone mineral density is affected by long-term poor metabolic control in adolescents with type 1 diabetes mellitus. Diabetes interferes with the bone formation by affecting the expression of transcription factors that regulate osteoblast differentiation.
Bone mineral density measured by dual energy x-ray absorptiometry in patients with non-insulin- dependent diabetes mellitus.
Diabetic osteopenia and circulating levels of vitamin D metabolism in Type 2 (noninsulin-dependent) diabetes. Diabetes mellitus and the incidence of hip fracture: results from the Nord-Trondelag Health Survey. Prospective study of type 1 and 2 diabetes and risk of stroke subtypes: The Nurse’s Health Study.
Elevated hip fracture risk in type 1 diabetic patients: a population-based cohort study in Sweden.
Hip and distal arm fracture rates in peri- and post-menopausal insulin-treated diabetic females.
Glycation of collagen: the basis of its central role in the late complications of ageing and diabetes. Effects of glucose and its modulation by insulin and estradiol on BMSC differentiation into osteoblastic lineages.
Reductions in degree of mineralization and enzymatic collagen cross-links and increases in glycation-induced pentosidine in the femoral neck cortex in cases of femoral neck frature. Relationships between serum adiponectin levels versus bone mineral density, bone metabolic markers, and vertebral fractures in type 2 diabetes mellitus.
Risk of cardiovascular disease and all cause mortality among patients with type 2 diabetes prescribed oral antidiabetes drugs: retrospective cohort study using UK general practice research database. Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective PioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial.
Dear Healthcare Provider Letter, re: clinical trial observation of an increased risk of fractures in female patients who received long-termtreatment with Avandia (rosiglitazone maleate) tablets for type 2 diabetes mellitus.
86 consecutive T1DM cases and 140 unrelated age and sex matched healthy nondiabetic controls were included in the study.
Though the condition is benign, it should draw immediate attention to the possibility of an underlying urinary tract infection.
Physical examination revealed mild palor and features suggestive of left lower limb deep vein thrombosis. PUBS has been shown to be associated with female gender, constipation, advanced age, chronic urinary catheterisation, urinary tract infection and use of plastic urinary catheter and bag.


Urinary bacteria produce an enzyme indoxylsulphatase, breaking down the indoxylsulphate into indoxyl.
The existence of an elevated fracture risk in type 2 diabetes, despite the underlying hyperinsulinemia, has led to speculation about differences in bone quality between type 1 diabetes and type 2 diabetes. This is likely to be due in large part to the complex pathophysiology of diabetes, the diversity of skeletal sites examined, the multitude of techniques used for measuring bone mass, and variations in the duration, severity, and treatment of diabetes in the different studies.
Attention has been recently focused on diabetic bone pathology, as type 1 diabetes was found to be clearly associated with bone loss and suppressed bone formation.
This pathway is negatively regulated by the Esp-encoded phosphatase in osteoblasts, which inactivates osteocalcin by posttranslational γ-carboxylation. Type 2 diabetes mellitus in the literature has been reported to be associated with increased,18 unchanged,19 or decreased20 BMD. Additional research is needed to better define the determinants of bone strength in diabetic individuals, including the abnormal properties of bone that might respond to treatment of diabetes itself. Relative fracture risk in patients with diabetes mellitus, and the impact of insulin and oral antidiabetic medication on relative fracture risk.
Observation of an increased incidence of fractures in female patients who received long-term treatments with Actos (pioglitazone HCl) tablets for type 2 diabetes mellitus.
After history and examination, BMD and body composition were assessed by dual energy X-ray absorptiometry (DXA).
The postulated hypothesis for this unusual event is probably a chemical reaction involving tryptophan from food in the gut. Her urine bag was filled with purple coloured urine along with purplish discolouration of the tubing and the bag. Higher bacterial load in urine, in combination with the above factors, facilitates the development of PUBS. Furthermore, a certain concentration of the pigments may be required for the precipitants to become visible. For asymptomatic patients, treatment should be aimed at the underlying medical problem rather than purple bag itself and to reduce the likelihood of this problem, it is important that the drainage bags and indwelling catheters may need to be changed on a regular basis.
This could be explained by the fact that increased blood glucose levels are associated with increased urinary calcium loss, resulting in a negative calcium balance.
This paper reviews our current understanding of the pathogenetic bases of bone disease in diabetes. However, most large-scale epidemiological studies indicate normal or above-normal BMD.21 Possible contributing factors to the higher BMD of type 2 diabetes mellitus are listed in Table II.
Conversely, the differences between type 1-diabetic- and age-associated bone loss stress the importance of selecting condition-specific individualized treatments for osteoporosis. The mixture of these two substances produces purple urine in the urinary catheter and collection bag. The presence of alkaline urine and also the type of materials used to manufacture the urinary catheter and bag may be important factors.
There is also speculation about the role of the resistance to parathyroid hormone observed in diabetes, and its effect on calcium and bone turnover. A concern is that existing bone loss in type 1 diabetic patients could compound the fracture risk associated with conditions such as menopause and aging. Because in type 1 diabetes the bone defect results predominantly from a decrease in bone formation, anabolic therapies appear likely to be the most effective treatment. Falls associated with diabetes-related comorbidities are another possible cause of low-trauma fractures. Urine microscopy revealed 4-5 leucocytes, 3-4 red blood cells and calcium oxalate and phosphate crystals, bacteria 3+ and albumin 2+. Adequate glycemic control and prevention of diabetic complications are the mainstay of therapy to lower fracture risk, with the caveat that thiazolidinediones increase fracture risk in postmenopausal women with type 2 diabetes.
In conclusion, bone health is an important consideration in diabetes, and caution should be exercised in prescribing thiazolidinediones to postmenopausal women with low bonemass and patients with prior fragility fracture.
This article reviews the current state of knowledge on the association between diabetes and bone health.
Hu, “Systematic review of type 1 and type 2 diabetes mellitus and risk of fracture,” American Journal of Epidemiology, vol. Cauler, “Diabetes mellitus, bone mineral density, and fracture risk,” Current Opinion in Endocrinology, Diabetes and Obesity, vol. Sjostrom, “The International Physical Activity Questionnaire (IPAQ): a study of concurrent and construct validity,” Public Health Nutrition, vol.



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