Adolescents and young adults with type 1 diabetes are at risk for poor health outcomes, including poor glycemic control, acute and chronic complications, and emergency department admissions. During this developmental period, adolescent and young adult patients also experience significant changes in living situation, education, and/or health care delivery, including transferring from pediatric to adult health care. In recent years, professional and advocacy organizations have proposed expert guidelines to improve the process of preparation for and transition to adult-oriented health care. However, challenges remain and evidence-based practices for preparing youth for adult health care are still emerging. Qualitative research suggests that adolescent and young adult patients rely on health care providers to guide them through the transition process and appreciate a gradual approach to preparing for adult-oriented health care, keeping parents in supportive roles into young adulthood. Patients also benefit from specific referrals and contact information for adult care providers. Promising models of transition care include provision of transition navigators, attendance at a young adult bridge clinic, or joint visits with pediatric and adult care providers. However, much of this research is in its early stages, and more rigorous trials need to be conducted to evaluate health outcomes during transition into adult health care. The purpose of this review is to provide an overview of the transition process, patient and health care provider perceptions of transition care, and emerging evidence of successful models of care for engagement in adult-oriented health care. Recommendations and resources for health care providers are also presented.
Pompe disease, also referred to as glycogenosis type II, is a rare, autosomal recessive disorder that results from the deficiency of the glycogen-degrading enzyme acid alpha-glucosidase. The classical form presents shortly after birth with muscle hypotonia, cardiac, and respiratory failure resulting in a fatal outcome. The late onset of Pompe disease has a very variable onset and disease presentation that often causes a delayed diagnosis. Until now enzyme replacement therapy with alglucosidase alfa is the only causative therapy option for Pompe patients that can slow down disease progression. However, uncertainty remains about the efficacy regarding survival and quality of life in Pompe patients under this very cost-intensive treatment. This paper provides a systematic review of the literature stressing different aspects of enzyme replacement therapy in infantile and late onset Pompe patients.
Prader-Willi syndrome ( PWS) represents the most common form of genetic obesity. Thanks to the advances in medical care and technology, many persons with PWS live longer and survive to adulthood. Currently, because of the many physical and behavioral manifestations, transitional health care is not easy for these patients and is considered a very important issue. Moreover, very few studies have examined these transitional problems in young adults with PWS. In recent years, there has been great interest in improving transition planning and support for young people with PWS reaching adulthood. In this article, we underline the main clinical problems in transition and give some advice to make this period less difficult and easier for adolescents with PWS. Special attention should be paid to obesity, diabetes mellitus, hypertension, osteoporosis, and sleep apnea during the period of transition. In PWS, for an effective transition from childhood to adulthood, a multidisciplinary team is needed, and should maintain the same approach to food, environment, and psychiatric issues. For comprehensive care, it is necessary to involve adult endocrinologists and other medical specialists in conjunction with the pediatric team. Parental involvement is, however, a great help for supervising adolescents with PWS during this particular period.
This study investigated the possible correlation between blood biochemical profiles and bone mineral density (BMD) in the Chinese Han population. We conducted a cross-sectional analysis using participants randomly selected from the Health Screening Center of Taihe Hospital, Hubei University of Medicine, which included a total of 285 individuals, varied in ages from 31 years to 63 years. The height, weight, and body mass index (BMI) of each subject were measured, as well as fasting blood glucose (FBG), triglycerides, total cholesterol, blood uric acid (UA), blood urea nitrogen, and blood creatinine. We evaluated BMD at the wrist (grams per centimeter square) using a dual-energy X-ray absorptiometry scan. The mean ages of female and male groups were 45.32 +/- 8.24 years and 46.76 +/- 9.01 years, respectively. The mean age of the study population was 46.14 +/- 8.79 years, which is similar to the general population. The mean BMI values were 22.08 +/- 2.38 kg/m(2) and 24.50 +/- 2.67 kg/m(2) in the female and male population, respectively, representing a statistically significant difference (P < 0.05). No significant differences in levels of FBG total cholesterol, or triglycerides were seen among the male and female population. Multiple linear regression analysis was performed using BMD as outcome variables and BMI, blood UA, FBG, total cholesterol, triglycerides, urea nitrogen, and blood creatinine as covariates, and the regression equation was established as Y=0.00017X1+0.001066X2+0.010017X3+0.168251. Positive correlation was identified between BMD and FBG and BMI and blood UA, suggesting that lipid metabolism imbalance might have neither positive nor negative effect on BMD. There might be an association between UA and BMD (P<0.05). In conclusion, these findings suggested that weak positive correlations existed between BMI and FBG and blood UA and BMD in this middle-aged Chinese Han population.
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Osteogenesis imperfecta ( OI) is a rare, heritable systemic disorder of bone and -connective tissue, which in almost 90% of cases is due to mutations affecting the normal synthesis of type I collagen. In 1979, four OI phenotypes were categorized which were inherited as autosomal dominant characteristics. Individuals with OI present both genetic and phenotypic variabilities. Major characteristics of OI are bone fragility, blue sclerae, dentinogenesis imperfecta, short stature, scoliosis, and joint hyperextensibility. Both autosomal dominant and recessive inheritance are now recognized. Advances in molecular diagnosis have led to a major expansion in our understanding of the genetic basis for different OI phenotypes. To date, sequence variants in 17 genes are described as causative of OI. These genes regulate the synthesis of type I collagen pro-alpha polypeptide chains, proteins involved in type I collagen processing in the endoplasmic reticulum and proteins involved in osteoblast function. These new genetic associations have also led to uncertainty with regard to the current classification of OI phenotypes. Bisphosphonates have been widely used to improve bone mass and decrease fractures in both children and adults with OI. While effective in many but not all children when administered for 2-4 years, bisphosphonates have not proven effective in adults with OI. Studies are limited for treatment of adults with teriparatide and denosumab. Advances have been reported in the surgical management of OI. Although the role of physical therapy in the management of children and adults was previously described, this important treatment modality is significantly underutilized.
Diabetic foot ulcers are associated with substantial morbidity and mortality in diabetic patients. The aim of the study was to assess the validity and effectiveness of body mass index ( BMI) and hemoglobin A1c ( HbA1c) to predict foot ulcer healing in diabetic patients. We hypothesized that routine clinical and laboratory parameters may reliably predict the healing of diabetic foot ulcers. To validate this hypothesis, a single-center analytical study was carried out in 140 diabetic patients with foot ulceration ( from February 2014 to February 2015) in Al Qassim region of the Kingdom of Saudi Arabia. The data collection included demographics, medical diagnoses, BMI measures, ulcer healing duration, and HbA1c results. The results show that BMI and HbA1c levels were strongly associated with the process as well as duration of foot ulcer healing in the diabetic patients. Higher BMI and elevated HbA1c were associated with poor prognosis in terms of foot ulcer healing. Future studies with concomitant use of both the predictors would be an interesting strategy.
Cystic fibrosis-related diabetes (CFRD) is a common comorbidity in cystic fibrosis (CF) and portends worse clinical outcomes including lower lung function and nutritional status, and decreased survival. CFRD is distinct from other forms of diabetes, but relative insulin deficiency is a predominant feature. The catabolic effects of insulin deficiency coupled with the pro-inflammatory effects of hyperglycemia likely affect clinical outcomes. Posited mechanisms of CFRD development include collateral damage from pancreatic exocrine destruction, inherent beta-cell defect, CFTR dysfunction, and incretin deficiency or unresponsiveness. Even though CF clinical care teams are increasingly aware of its implications, CFRD screening and management remain a challenge. Promising clinical and basic research in the fields of diabetes and CF and the advent of novel therapeutics targeting the protein defect in CF have potential to change CFRD care. This review presents newer data on insulin defects and glucose derangements and highlights continuing challenges and unanswered questions.
Objective: The aim of this study was to determine 25-hydroxyvitamin D concentrations in healthy employees of the Universidad de Ciencias Medicas, Costa Rica.Methods: Levels of 25-hydroxyvitamin D, calcium, phosphorus, intact parathyroid hormone (iPTH), and creatinine were measured in 80 people. Solar ultraviolet radiation exposure and 25--hydroxyvitamin D intake were estimated using a previously designed questionnaire. Participants were 52 women aged (mean +/- standard deviation) 35.8 +/- 10.0 years old, body mass index of 27.1 +/- 5.9 kg/m(2), and 26 men aged 36.4 +/- 10.8 years old, body mass index of 27.5 +/- 5.0 kg/m(2).Results: All participants were normocalcemic, eight females were postmenopausal, three were hypertensive; none had renal, gastrointestinal, or thyroid disease. The level of 25-hydroxyvitamin D was 23.9 +/- 7.0 ng/dL and iPTH 40.1 +/- 17.5 pg/dL. A level of 25-hydroxyvitamin D >= 30 ng/dL was seen in 17% of the population. The eight participants with iPTH higher than 67 ng/dL, had 25-hydroxyvitamin D of 18.9 +/- 4.8 ng/dL. Two participants who received 25-hydroxyvitamin D and calcium supplements were excluded.Conclusion: The 25-hydroxyvitamin D insufficiency and deficiency found in healthy employees from an academic center in Costa Rica may be due to working long hours in-doors and solar ultraviolet radiation exposure. It is unknown whether secondary hyperparathyroidism seen in nearly 10% of this population, may have long-term effects on bone health.
Congenital hyperinsulinism (CHI) is the most common cause of persistent hypo- glycemia in pediatric patients and is associated with significant risk of hypoglycemic seizures and developmental delays. CHI results from mutations in at least nine genes that play a role in regulating beta-cell insulin secretion. Thus, patients with CHI have dysregulated insulin secretion that is unresponsive to blood glucose level. Each different genetic etiology of CHI is associated with particular clinical characteristics that affect management decisions. Given the broad phe- notypic spectrum and relatively rare prevalence of CHI, it is important that patients with CHI be evaluated by clinicians experienced with CHI and the multiple subspecialty services that are necessary for the management of the disorder. In this review, we summarize the pathophysiology and genetic causes of CHI and then focus primarily on the most common genetic cause (muta- tions in the ATP-gated potassium (K ATP ) channel) for further discussion of diagnosis, medical and surgical management, and potential acute and chronic complications. We provide insight from relevant published studies and reports, in addition to anecdotal information from our center's clinical experience in caring for over 400 patients with CHI. Careful assessment of each patient's individual pathophysiology is necessary to determine the appropriate treatment regimen, and continued close follow-up and monitoring of disease- and treatment-related complications are essential. Although significant improvements have been made in the past several years with regard to diagnosis and management, given the continued high morbidity rate in patients with CHI, improved diagnostic techniques and new therapeutic options would be welcomed.
Type 1 diabetes (T1D) is caused by the autoimmune destruction of the insulinproducing pancreatic beta-cells. People with T1D manage their hyperglycemia using daily insulin injections; however, this does not prevent the development of long-term diabetic complications such as retinopathy, nephropathy, neuropathy, and various macrovascular disorders. Currently, the only "cure" for T1D is pancreas transplantation or islet-cell transplantation; however, this is hampered by the limited number of donors and the requirement for life-long-immunosuppression. As a result, the need for alternative therapies is vital. One of the strategies employed to correct T1D is the use of gene transfer to generate the production of an "artificial" beta-cell that is capable of secreting insulin in response to fluctuating glucose concentrations that normally occurs in people without T1D. The treatment of many diseases using cell and gene therapy is generating significant attention in the T1D research community; however, for a cell therapy to enter clinical trials, success and safety must first be shown in an appropriate animal model. Animal models have been used in diabetes research for over a century, have improved our understanding of the pathophysiology of diabetes, and have led to the discovery of useful drugs for the treatment of the disease. Currently, the nonobese diabetic mouse is the animal model of choice for the study of T1D as it most closely reflects disease development in humans. The aim of this review is to evaluate the success of cell and gene therapy to reverse T1D in animal models for future clinical application.
Insulinoma is a predominantly benign and rare neuroendocrine tumor. Patients with insulinoma typically present with neurologic symptoms from hypoglycemia, such as confusion, dizziness, and behavioral changes, as well as symptoms from a surge in catecholamine levels, such as palpitations, diaphoresis, and tachycardia. Symptomatic patients usually have glucose levels below 55 mg/dL and are relieved of their symptoms when carbohydrate is administered. The 48-hour test, performed by measuring blood glucose levels of insulin, C peptide, and proinsulin collected every 4-6 hours in fasting patients, accurately confirms the diagnosis of insulinoma in the majority of the patients. Once the diagnosis is confirmed, the next step in management involves identifying the location of the tumor and successfully removing it surgically. In the last two decades, clinicians have moved away from invasive angiography for preoperative localization. A multiphase computed tomography (CT) can be used to localize the lesion and evaluate for metastasis. If CT does not detect the lesion, selective arterial calcium stimulation test is recommended to identify the region of the lesion in the pancreas. Some argue that all preoperative localization techniques are superfluous. The combination of intraoperative ultrasound and operative palpation has led to a nearly 100% success rate. Recently, in select cases, laparoscopic enucleations and resections of insulinomas have been performed with shorter length of stay and faster recovery time. Despite advances in imaging, a little over 10% of insulinoma patients undergo reexploration for missing lesions. Patients who are not candidates for tumor resections or awaiting surgery have had symptomatic relief from diazoxide and somatostatin analogs among various medical therapies. In patients with metastatic insulinoma, progressionfree survival and overall survival are reported from newly approved chemotherapeutic agents. Liver-directed therapies, such as ablation and selective radiation, and cytoreductive surgery have also been performed for symptom control and prolonging survival.
Many studies have shown that a low-carbohydrate diet (LCD) is a safe and effective intervention to improve glycemic control. However, published data are limited regarding the use of carbohydrate restriction in the treatment and prevention of type 2 diabetes mellitus (DM) in the Native Americans, in a real-world clinical practice setting. We evaluated the efficacy of an LCD on 50 obese Native Americans with either type 2 DM or impaired fasting blood glucose (IFG) in a primary care/obesity medicine practice. The primary intervention was an LCD defined as an intake of <20 g of carbohydrates per day. The intervention involved providing an educational handout and behavioral counseling assisted by a dedicated weight loss coordinator. We evaluated the effects of this intervention on hemoglobin A1c, body weight, blood pressure, and lipid parameters. The subjects were evaluated at baseline and 6 months. The subjects underwent additional safety and counseling visits throughout the study. Subjects were considered completers if they had baseline and 6-month measurements. The mean age was 55.0 +/- 10.9 years, and 66.7% were female. Subjects had significant improvements in hemoglobin A1c (-1.4%+/- 0.9%, in subjects with DM, P<0.0001), fasting blood glucose (-15 +/- 4.9 mg/dL, in subjects with IFG, P<0.0001), and body mass index (-4.0 +/- 1.7 kg/m(2), P<0.0001). An LCD can lead to clinically and statistically significant improvement in glycemic control and body weight among obese subjects with type 2 DM or IFG over a 6-month period. The results suggest that carbohydrate restriction can be an effective real-world intervention in a primarily Native American clinical practice. However, further studies are needed to assess long-term compliance and potential weight regain.
Congenital hypothyroidism (CH), the most common pediatric endocrine disorder with an estimated prevalence of 1: 2,000 to 1: 4,000, is an under-recognized problem in countries without routine newborn screening (NBS) programs. Thyroid dysgenesis (TD) is the most common cause of primary CH accounting for approximately 85% of all cases; most of the remaining patients have dyshormonogenesis. Transient CH and CH with eutopic gland, are increasingly being identified after introduction of routine NBS. The clinical features of CH are often subtle resulting in delayed diagnosis and eventually poor intellectual outcome. In developed countries, detection by NBS and early initiation of treatment has largely eliminated the intellectual disability caused by this disorder. The lower screening thyroid stimulating hormone (TSH) cutoff and changes in birth demographics in some countries have been associated with an increase in the reported incidence of CH. However, the additional cases detected by the lower TSH cutoff tend to have either milder or transient hypothyroidism. Diagnosis of CH is made on the basis of serum concentrations of TSH and thyroxine (T4). Thyroid ultrasound, radionuclide scintigraphy, serum thyroglobulin (TG) levels and specific genetic tests help ascertaining the exact etiological diagnosis. Non-availability of later tests should not deter the pediatrician from initiation of treatment. Age at initiation of treatment and starting dose of levothyroxine are critical factors that determine the long-term outcome. Higher doses of levothyroxine at 10-15 mu g/kg/day are required in infants, with titration based on T4 and TSH levels, which are repeated frequently. Coexistence of other congenital anomalies in children with CH adds to the morbidity. Approximately 70% of babies worldwide are not born in an area with an established NBS program and hence are not detected and treated early. Consequently, the economic burden of mental retardation due to CH remains a significant public health challenge in countries without NBS. The health burden owing to CH continues to be high even in countries with well-developed NBS.
Background: Lifestyle with less physical activity and higher consumption of sugar and fat has transformed obesity to an epidemic, which poses a risk for the development of type 2 diabetes. This study was aimed to assess type 2 diabetes mellitus and its associated factors among government employees in Harar Eastern Ethiopia.Materials and methods: A cross-sectional study was conducted on 714 employees working in ten government offices from May 2013 to July 2013. The WHO STEPwise approach to chronic disease risk factor surveillance questionnaire was used. An overnight fasting capillary blood was analyzed for blood glucose concentration using a commercially available electronic glucose monitor (SensoCard Plus). Participants with fasting blood sugar level >= 126 mg/dL were checked with a more specific glucose oxidase method using a compact automated clinical chemistry analyzer. Logistic regression was used to examine the factors associated with type 2 diabetes mellitus, and a P-value,0.05 was used to declare statistical significance.Results: A total of 50 (7%) participants were found to have a fasting blood sugar level of >= 126mg/dL after an overnight fasting. Of these, 1.5% were known diabetic cases. There was a statistically significant association between hip circumference (crude odds ratio [COR] = 2.32; 95% confidence interval [CI] = 1.27, 4.22), waist circumference (COR [95% CI] = 1.94 [1.05, 3.58]) and type 2 diabetes. Participants who consumed fruits and vegetables for >= 3 days/ week were less likely to have type 2 diabetes mellitus (adjusted odds ratio [AOR] = 0.49; 95% CI = 0.27, 0.91). A ten- point increase of systolic blood pressure increases the likelihood of developing type 2 diabetes mellitus by 6%, AOR (95% CI) = 1.057 (1.027, 1.087).Conclusion: Behavioral change communication on the need for healthy lifestyle, with a special emphasis on fruits and vegetables consumption and regular checkup for blood sugar level is recommended for prevention and early detection of type 2 diabetes mellitus.
Pegvisomant (PEG) is a genetically engineered growth hormone (GH) analog able to bind and block the GH receptor. PEG blocks all metabolic effects of GH hypersecretion, normalizes insulin-like growth factor I (IGF-I) level and paradoxically produces an increase in GH secretion. When PEG was commercialized, there were some concerns regarding whether the increased GH secretion could cause growth of the residual tumor or cause the overcoming of receptor blockade with loss of efficacy. PEG commercialization was followed by the onset of two main prospective observational studies aiming to evaluate the safety and outcome of PEG long-term treatment: the German Pegvisomant Observational Study and ACROSTUDY. These observational studies, along with several independent studies have provided comprehensive information regarding the actual use, efficacy and safety of long-term treatment with PEG. The efficacy of PEG in clinical setting is somewhat lower than that reported in the pivotal studies, nevertheless PEG normalizes IGF-I levels ranging between 65% and 97% of cases. Side effects in observational studies were uncommon and rarely caused discontinuation of treatment. Liver dysfunction developed in 2.5% of cases, was usually transient and no permanent liver damage was reported. Increased tumor size was developed by about 2.2%-3.2% of acromegalic patients treated with PEG, without differences to that described for other modalities of treatment. Only one third of cases corresponded with true growth after initiation of PEG treatment. Involved mechanism is currently unknown. New modalities of treatments by the combined use of PEG with somatostatin analog or cabergoline have been developed with promising results. Recently, two clinical guidelines written to optimize the use of these treatment modalities and to monitor possible adverse events have been published.
The ability of heat shock protein 90 (Hsp90) to modulate many growth and signal- ing pathways simultaneously makes it an attractive target in the field of cancer therapeutics and provided the initial impetus for significant efforts over the past decade to identify Hsp90 inhibitors, several of which are now showing promise in the clinic for cancer treatment. The four known human Hsp90 members are compartmentalized: Hsp90α and β in the cytoplasm, GRP94 in the endoplasmic reticulum, and TRAP1 in the mitochondrial matrix. While these isoforms share a similar N-terminal domain adenosine triphosphate-binding pocket, structural variations allow unique interactions for inhibitors targeting this binding site, providing an avenue for the development of paralog-selective drugs with different biological effects applicable therapeuti- cally to a wide range of diseases. At the same time, the conformational flexibility of the Hsp90 molecular chaperone has unveiled multiple small-molecule target sites within all subdomains of the protein, greatly expanding opportunities for viable drug development. This review summa- rizes the function, expression, and clinical significance of the Hsp90 isoforms and elaborates on the inhibitors and modulators that impact Hsp90 chaperone activity. Finally, the review focuses on the therapeutic utility of a range of Hsp90-modulating agents in the treatment of specific diseases associated with the endocrine system.
Exogenous testosterone was introduced nearly 80 years ago as a pharmaceutical agent to treat male hypogonadism. Researchers continue to enhance the pharmacokinetic profile of testosterone to improve various benefits, including mood and sexual function, among other potential benefits. The modalities that are currently available include implants, intramuscular injections, oral formulations, transdermal delivery systems (ie, patches, gels, and a solution), transbuccal delivery systems, and most recently, intranasal testosterone. Each of these products differs by the delivery system, half-life, and ability to mimic physiological levels of testosterone. While we recognize the unique characteristics and benefits of existing agents, we must address unmet needs, including how best to mimic physiological levels of testosterone and how to administer it through a more effective, safe, and convenient mechanism. In our overview of current and emerging testosterone therapies, we will examine these topics and address the controversy of prostate cancer and cardiovascular risk.
Background: It has been demonstrated that statins can reduce major cardiovascular complications throughout a broad range of patients with dyslipidemia and multiple cardiovascular risk. Despite the impact of statin therapy on cardiovascular morbidity and mortality, a residual cardiovascular risk remains following lowering of low-density lipoprotein cholesterol. In many patients, optimization of the lipid profile cannot be achieved with statin therapy. Therefore, pharmacologic interventions with non-statin therapy can be used.Aims: The objective of this review was to analyze current clinical evidence of the effects of simvastatin/fenofibrate combination therapy.Methods: We searched and analyzed the evidence up to June 2014, regarding the effects of statin/fibrate combination therapy for reducing cardiovascular complications.Results: Forty-nine studies reporting the efficacy and safety of statin/fibrate combination therapy were analyzed. Of the forty-nine, 19 analyzed the simvastatin/fenofibrate combination therapy. This therapy was demonstrated to be safe and superior to the statin monotherapy in modifying atherogenic dyslipidemia, including lipoprotein subclasses. Nevertheless, in randomized clinical trials cardiovascular endpoints were not significantly different when fenofibrate was added to a standard low-density lipoprotein cholesterol reducing therapy. Of note, in the subgroup analysis, positive results were observed in patients with high triglycerides and low high-density lipoproteins. The inclusion of heterogeneous populations in these studies may explain the mixed results of cardiovascular outcomes seen in randomized clinical trials.Conclusion: Future clinical studies that rigorously address the effects of simvastatin/fenofibrate in patients with triglycerides >2.25 mmol/L and high density lipoprotein cholesterol <0.90 mmol/L, will provide a more accurate conclusion regarding the use of simvastatin/fenofibrate combination therapy. For now, emphasis must be put on non-pharmacological interventions that effectively induce weight loss and strict glycemic control in diabetics. The initiation of simvastatin/fenofibrate combination therapy among patients with residual cardiovascular risk should be employed at the physician's discretion, as this strategy lacks hard cardiovascular end points.
Diabetes mellitus (DM) is a disorder of abnormal glucose metabolism resulting primarily from insulin resistance and relative insulin deficiency and characterized by hyperglycemia causing significant short-and long-term complications. Type 2 diabetes mellitus (T2DM) contributes to more than 90% of cases of diabetes. Obesity, sedentary lifestyles, and consumption of very high-caloric meals are thought to be the primary triggering factors causing T2DM in genetically predisposed individuals. Although treatment of hyperglycemia plays a key role in the management, therapies directed at other comorbid conditions, such as dyslipidemia, hypertension, hypercoagulability, obesity, and insulin resistance, have also been a major focus of research and therapy. DM is rising to an epidemic proportion globally, and it is, indeed, one of the most challenging public health problems in the 21st century. According to 2011 statistics, there were approximately 366 million diabetes cases worldwide, and this figure would probably increase to 552 million by 2030. Long-term complications from high blood sugar include coronary artery disease, cerebrovascular events, peripheral arterial diseases leading to amputation, retinopathy, nephropathy leading to end-stage renal disease requiring hemodialysis and transplantation, and neuropathy. The acute complication of T2DM includes drug-induced hypoglycemia, hyperosmolar hyperglycemic state, and although uncommon, ketoacidosis. Diabetes care requires a comprehensive and multidisciplinary approach to delay the progression to acute as well as chronic and debilitating long-term complications. This approach requires the thorough understanding of the pathophysiology of hyperglycemia and impact of various risk factors and comorbidities, careful selection of antihyperglycemic agents, active and frequent participation of diabetes educator, and involvement of multidisciplinary team. The objective of this review is to highlight recent trends in hormonal treatment and to explore new and innovative therapeutic modalities in the management of T2DM.
