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Note: This article is based on research conducted by the Johns Hopkins University Evidence-based Practice Center under contract to AHRQ. Disclaimer: The authors of this article are responsible for its contents, including any clinical or treatment recommendations. Kohei Kaku Expert Opinion on Pharmacotherapy.
Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S adults.
Rationale for the use of insulin therapy alone as the pharmacological treatment of type 2 diabetes. A study of the effects of hypoglycemic agents on vascular complications in patients with adult-onset diabetes.
Evaluation of Guideline Recommendations on Oral Medications for Type 2 Diabetes Mellitus: A Systematic Review. No statement in this article should be construed as an official position of AHRQ or of the U.S. Bennett: The Johns Hopkins University School of Medicine, 2024 East Monument Street, Room 2-611, Baltimore, MD 21205.
Odelola: Department of Internal Medicine, Albert Einstein Medical Center, 5501 Old York Road, Philadelphia, PA 19141. Wilson: The Johns Hopkins University School of Medicine, 1830 East Monument Street, Baltimore, MD 21287. Selvaraj: The Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8066, Baltimore, MD 21287. Robinson: The Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8069, Baltimore, MD 21287. Bass: The Johns Hopkins University School of Medicine, 1830 East Monument Street, Room 8068, Baltimore, MD 21287.
Puhan: The Johns Hopkins University Bloomberg School of Public Health, 615 North Wolfe Street, Mail Room E6153, Baltimore, MD 21205. Demographic and epidemiologic transition in the developing world: Role of albuminuria in the early diagnosis and prevention of renal and cardiovascular disease. The rising global burden of diabetes and its complications: Estimates and projections to the year 2010.
Gender differences of regional abdominal fat distribution and their relationships with insulin sensitivity in healthy and glucose-intolerant Thais. Elevated levels of interleukin-6 are reduced in serum and subcutaneous adipose tissue of obese women after weight loss.
From the triumvirate to the ominous octet: A new paradigm for the treatment of type 2 diabetes mellitus. Understanding the pathogenesis of type 2 diabetes: Can we get off the metabolic merry-go-rounds? Ten-year follow up of subjects with impaired glucose tolerance: Prevention of diabetes with tolbutamide and diet regulation. The Indian Diabetes Prevention Programme shows that lifestyle modification and metformin prevent type 2 diabetes in Asian Indian subjects with impaired glucose tolerance (IDPP-1). The preventive effect of acarbose and metformin on the progression to diabetes mellitus in the IGT population: A 3-year multicenter prospective study.
Prevention of gestational diabetes mellitus by continuing metformin therapy throughout pregnancy in women with polycystic ovary syndrome.
Metformin therapy throughout pregnancy reduces the development of gestational diabetes in women with polycystic ovary syndrome. Is there a role for alpha-glucosidase inhibitors in the prevention of type 2 diabetes mellitus? Voglibose for prevention of type 2 diabetes mellitus: A randomised, double-blind trial in Japanese individuals with impaired glucose tolerance.
Peroxisome proliferator-activated receptor gene expression in human tissues-effects on obesity, weight loss, and regulation of by insulin and glucocorticoids. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Effect of pioglitazone on pancreatic beta-cell function and diabetes risk in Hispanic women with prior gestational diabetes.
Effect of Rosiglitazone on the frequency of diabetes inpatients with impaired glucose tolerance or impaired fasting glucose: A randomized controlled trial. Medical societies respond to the FDA′s safety announcement on the use of the diabetes medication actos.
Orlistat augments postprandial increases in glucagon-like peptide 1 in obese type 2 diabetic patients. Weight control and risk factor reduction in obese subjects treated for 2 years with orlistat: A randomized controlled trial.
Effects of weight loss with orlistat on glucose tolerance and progression to type 2 diabetes in obese adults.
XENical in the prevention of diabetes in obese subjects (XENDOS) study: A randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Effects of exenatide and lifestyle modification on body weight and glucose tolerance in obese subjects with and without pre-diabetes. Pravastatin and the development of diabetes mellitus: Evidence for a protective treatment effect in the West of Scotland Coronary Prevention Study. Secondary prevention of cardiovascular events with long-term pravastatin in patients with diabetes or impaired fasting glucose.
Prevention of coronary and stroke events with atorvastatin in hypertensive patients who have average or lower-than-average cholesterol concentrations, in the Anglo-Scandinavian Cardiac Outcomes Trial-Lipid Lowering Arm (ASCOT-LLA): A multicenter randomized controlled trial. Statins and risk of incident diabetes: A collaborative meta-analysis of randomised statin trials.
Effect of angiotensin-converting-enzyme inhibition compared with conventional therapy on cardiovascular morbidity and mortality in hypertension: The Captopril Prevention Project (CAPPP) randomised trial.
Cardiovascular morbidity and mortality in the Losartan Intervention for Endpoint reduction in hypertension study (LIFE): A randomised trial against atenolol.
Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).
The Study on Cognition and Prognosis in the Elderly (SCOPE): Principal results of a randomized double-blind intervention trial. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: The CHARM-Overall programme. Enalapril reduces the incidence of diabetes in patients with chronic heart failure: Insight from the Studies Of Left Ventricular Dysfunction (SOLVD). Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: The VALUE randomised trial.
Do nutrient-gut-microbiota interactions play a role in human obesity, insulin resistance and type 2 diabetes? This continues to pose a real challenge to physicians as the prevalence of this disease in the United States continues to rise.
The focus of this review will be the management of patients with type 2 diabetes using one or more of the five available classes of oral hypoglycemic agents: sulfonylureas, meglitinides, biguanides, thiazolidinediones and alphaglucosidase inhibitors (Table 1). Metformin (Glucophage) is currently the only agent in this antidiabetic class available in this country.
Food and Drug Administration (FDA) included troglitazone (Rezulin), rosiglitazone (Avandia) and pioglitazone (Actos). Alpha-glucosidase inhibitors act by inhibiting the enzyme alpha-glucosidase found in the brush border cells that line the small intestine, which cleaves more complex carbohydrates into sugars. Reasonable combinations of agents include a sulfonylurea plus metformin, a sulfonylurea plus an alpha-glucosidase inhibitor, a sulfonylurea plus a thiazolidinedione, metformin plus repaglinide, biguanide plus alpha-glucosidase inhibitor, and metformin plus a thiazolidinedione.
Randomised placebo-controlled trial of orlistat for weight loss and prevention of weight regain in obese patients.
Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. Type 2 diabetes is defined as a syndrome characterized by insulin deficiency, insulin resistance and increased hepatic glucose output. Metformin works by reducing hepatic glucose output and, to a lesser extent, enhancing insulin sensitivity in hepatic and peripheral tissues.
Subsequently, in March 2000, the FDA asked the manufacturer (Parke-Davis, Warner-Lambert) of troglitazone, the first agent in this class to receive labeling approval, to remove the product from the market. Because they inhibit the breakdown and subsequent absorption of carbohydrates (dextrins, maltose, sucrose and starch; no effect on glucose) from the gut following meals, the largest impact of these drugs is on postprandial hyperglycemia.


Type 2 diabetes mellitus and its associated chronic complications such as diabetic nephropathy, hypertension, and coronary heart disease are major contributors to the global burden of chronic diseases, leading to a rise in morbidity and mortality.
Medications used to treat type 2 diabetes are designed to correct one or more of these metabolic abnormalities. It is of particular concern with agents that are metabolized to an active metabolite with significant renal excretion. Currently, there are five distinct classes of hypoglycemic agents available, each class displaying unique pharmacologic properties. These agents include chlorpropamide (Diabinese) and glyburide, both of which should be avoided in the setting of impaired renal function and used with caution in elderly patients. Most of the related side effects (including metallic taste, gastrointestinal discomfort and nausea) are transient and commonly reported only during initiation of therapy. This changing trend is not restricted to isolated geographical areas, but is being seen across geographic distributions and boundaries. These classes are the sulfonylureas, meglitinides, biguanides, thiazolidinediones and alpha-glucosidase inhibitors. Unlike the commonly used sulfonylureas, the meglitinides have a very short onset of action and a short half-life. Therapy with acarbose has been linked to elevations in serum transaminase levels and the use of this agent is contraindicated in patients with liver cirrhosis. In patients for whom diet and exercise do not provide adequate glucose control, therapy with a single oral agent can be tried. All sulfonylureas have been associated with weight gain and thus, may not be the optimal first choice for obese patients.Unfortunately, not all patients treated with a sulfonylurea will have an adequate response.
Taking the drug with meals may also lessen the severity of the gastrointestinal side effects. Patients treated with pioglitazone have displayed mean decreases in triglyceride levels, mean increases in HDL cholesterol levels, and no consistent mean changes in LDL and total cholesterol levels.20,21Because these agents do not increase insulin secretion, hypoglycemia does not pose a risk when thiazolidinediones are taken as monotherapy. If these trends are not reversed, the physician, over the next couple of decades, will face the challenge of managing these complications in younger patients, in whom there is a limited understanding of the disease-course and the time-gap between the occurrence of complications; a scenario where they come across individuals in their late 20s or 30s presenting with coronary artery disease, or chronic kidney disease, or stroke. When choosing an agent, it is prudent to consider both patient- and drug-specific characteristics. Treatment failure with sulfonylurea therapy can be divided into two categories: primary and secondary.
If a meal is omitted throughout the day, patients should be instructed to skip the corresponding dose to prevent hypoglycemia.
Because metformin does not affect insulin secretion, it is not associated with hypoglycemia when used as monotherapy, but can potentiate hypoglycemia when used in combination with a sulfonylurea or insulin. Other contraindications include patients with inflammatory bowel disease or a history of bowel obstruction.32Therapy should be initiated with the lowest effective dose and titrated slowly over intervals of two to four weeks. If adequate blood glucose control is not attained using a single oral agent, a combination of agents with different mechanisms of action may have additive therapeutic effects and result in better glycemic control. Primary failure results when a patient exhibits an initial poor response to sulfonylurea therapy (a decrease in FPG levels of less than 20 mg per dL [1.1 mmol per L]). Likewise, if an extra meal is added throughout the day, the patient should add a dose to cover that meal. Repaglinide can be titrated to a dosage of 4 mg before each meal (maximum dosage of 16 mg per day).
The use of thiazolidinediones should be avoided in these patients.As referred to earlier, of greatest concern are the reports of an idiosyncratic drug reaction with troglitazone. Although hypoglycemia is not typically associated with monotherapy with the alpha-glucosidase inhibitors, it can occur in combination with other drugs. Most of the hypoglycemic effects of the sulfonylureas will be observed at one half of the maximum dose recommended for a specific agent. At least one week should be allowed between dosage adjustments to adequately assess blood glucose response. This reaction is initially characterized by increased serum transaminase levels, which in some cases progressed to hepatitis, hepatic failure and death. In patients undergoing contrast studies, metformin therapy should be withheld for approximately 48 hours following the procedure or until it has been determined that renal function has returned to baseline.
Preliminary attempts (before troglitazone was withdrawn from the market in March 2000) to prevent such incidents included a request by the FDA that Parke-Davis strengthen the drug's labeling and require stringent monitoring of transaminase levels in patients taking this agent. In March 1999, the FDA's Endocrine and Metabolic Drugs Advisory Committee reviewed the status of troglitazone and the potential toxicities and recommended continued availability in a select group of patients: those who are not well controlled with other antidiabetic agents.
Since then, it has been determined that patients requiring the use of an insulin sensitizer should be treated with one of the alternative agents.
Although results from pre-marketing trials revealed no evidence of hepatotoxicity with the newer agents (rosiglitazone and pioglitazone), two recent case reports demonstrated that rosiglitazone may be associated with hepatic failure following just 14 days of therapy, although a true cause-and-effect relationship has not been established.26,27The FDA recommends that serum transaminase levels be monitored every other month for the first year in all patients receiving a thiazolidinedione. Following one year of therapy with the newer agents, the incidence of serum transaminase elevations has been reported to be similar to placebo.The time to achieve a desired effect with the thiazolidinediones is somewhat longer than the other classes of hypoglycemic agents discussed thus far.
Intervals of at least three to four weeks should be allowed before increasing the dosage of these agents. Smaller dosages can be initiated if used as part of a combination regimen with a sulfonylurea or a sulfonylurea plus metformin. It should be highlighted that a majority of these expenses are made directly by the patient or the family, and when translated into overall costs for the entire population, they assume enormous proportions. It would therefore seem prudent to introduce pharmacological interventions to prevent type 2 diabetes in the 'at-risk' population. The history of pharmacological interventions for prevention goes a long way back to a small trial published in 1980, with 49 subjects, which demonstrated that the sulfonylurea tolbutamide was effective in blocking the progression of IGT to type 2 diabetes over a 10-year follow-up period, compared to a 29% incidence among control patients. Keeping in view the multimodal pathophysiological basis for type 2 diabetes, it is not necessary that these interventions be targeted at hyperglycemia alone.
Other agents that do not primarily target hyperglycemia may also reduce the risk of type 2 diabetes.
The use of orlistat for use of orlistat for managing obesity, RAS blockade with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBS), and recently the use of vitamin D and bromocriptine are all different approaches toward the common goal.
Metformin Metformin has been found to be useful in the prevention of development of diabetes in many large, well-powered trials. It has been shown to lower fasting blood glucose in individuals at risk for type 2 diabetes, without causing hypoglycemia.
In addition, it has a favorable action on cardiovascular risk factors, which are often present in these individuals.
It helps in maintaining diet-induced weight loss and lowers fasting plasma insulin concentrations, total and low density lipoprotein-cholesterol, and free fatty acids. These effects make metformin a first-line agent for the prevention of type 2 diabetes as recommended by the ADA.
For participants in the lifestyle intervention group, the risk-reduction for type 2 diabetes was to the tune of 58%, while it was about 31% in the metformin group. The glycemic control deteriorated in the control group with elevations in both fasting and postprandial plasma glucose at the end of study period. In the diet and exercise groups, the fasting plasma glucose increased slightly and postprandial plasma glucose levels were reduced. At three years, there was an 8% risk reduction with acarbose and 37% with metformin, compared to placebo. In a study by Begum et al.,[27] the two main outcome measures in this trial were development of gestational diabetes and the fetal outcome. The occurrence of gestational diabetes was significantly lower in the metformin group with only one subject (3.44%) developing gestational diabetes.
On the other hand, nine of 30 pregnant (30%) subjects developed diabetes in the control group.
Of note was the observation that all the babies in the metformin group had an average birth weight, while four babies in the control group were large for date. One of the more important issues is whether the effect of metformin to reduce the incidence of diabetes during DPP is true prevention or simply a masking of diabetes, as the post-trial washout period is very short for testing that distinction. It is suggested that the very rapid effect of metformin to increase insulin sensitivity can similarly dissipate rapidly as well. These effects of metformin on insulin sensitivity may disappear two weeks after stopping metformin.
The available data does not provide direct measures of insulin sensitivity; it also remains uncertain whether the glucose levels are stabilized or still rise two weeks after discontinuing metformin. With the current understanding of the effects of metformin on carbohydrate metabolism, it is possible that only a part of the effects are due to beta-cell protection, while another part is simply a masking due to the acute glucose-lowering effects of metformin; it will probably be difficult to estimate the proportion of these two effects. Alpha-glucosidase inhibitorsThe alpha-glucosidase inhibitors acarbose, miglitol, and voglibose act by competitively inhibiting the alpha-glucosidase enzymes present in the intestines and are involved in carbohydrate digestion.


They decrease both postprandial hyperglycemia and hyperinsulinemia, and may improve insulin sensitivity and diminish the stress on pancreatic beta-cells. The Study TO Prevent Non-Insulin Dependent Diabetes Mellitus (STOP-NIDDM) was a multicenter, international, double-blind, placebo-controlled study to evaluate the effects of acarbose in delaying the progression of IGT to type 2 diabetes in 1418 subjects with IGT.
There was a 25% relative risk reduction of progression to type 2 diabetes in the acarbose group compared to the placebo group. Acarbose significantly increased the reversion of IGT to normal glucose tolerance.Voglibose has also been found to be useful in the prevention progression of IGT to type 2 diabetes. In a clinical trial by Ryuzo Kawamori et al.,[31] voglibose was seen to improve glycemic parameters in 1780 Japanese subjects with IGT. The patients treated with voglibose had a significantly lower risk of progression to type 2 diabetes compared to the placebo group. A significantly higher number of subjects in the voglibose group achieved normoglycemia than those in the placebo group. Voglibose was approved by the Japanese Ministry of Health, Labor, and Welfare, in the year 2009, for the prevention of new-onset type 2 diabetes, in patients with impaired glucose tolerance.Thiazolidinediones Pioglitazone, a PPAR-gamma agonist, is a member of the thiazolidinedione class (which also includes troglitazone and rosiglitazone).
Pioglitazone is primarily expressed in the adipose tissue and has a favorable influence on systemic insulin resistance. A 55% reduction in the incidence of diabetes was observed, with persistent protection from diabetes for eight months post the drug, and stable glucose and beta-cell function for 4.5 years, in women who did not get diabetes during the troglitazone treatment. The results were similar to the TRIPOD study, and a comparison of changes in beta-cell compensation for insulin resistance in both the studies showed that pioglitazone halted the decline in the beta-cell function that was seen with the placebo treatment in the TRIPOD study, and also maintained the stability of the beta-cell function that occurred in the TRIPOD with troglitazone treatment. Together, these two studies demonstrated that prevention of type 2 diabetes is possible with thiazolidinediones providing beta-cell rest.The Actos Now for the prevention of diabetes (ACT NOW) study, [35] was a randomized, double-blind, placebo-controlled trial conducted to examine the effectiveness of pioglitazone in the prevention of type 2 diabetes in 602 subjects with IGT.
The ramipril therapy had no effect on the incidence of diabetes or death, but was more effective than placebo in achieving normoglycemia (42.5 vs.
Importantly, rosiglitazone reduced the incidence of diabetes by 60% relative to the placebo and was effective in subjects with IFG and IGT.Although each of these drugs has been found to be useful in preventing the progression from prediabetic to the diabetic stage, these drugs have been mired by issues of safety. The United States Food and Drug Administration (USFDA) has restricted the use of Rosiglitazone, due to its increased risk for cardiac morbidity and mortality.
USFDA recently (June 2011) issued a safety announcement on the use of pioglitazone, stating that taking pioglitazone for more than one year may be associated with an increased risk of bladder cancer. Although the Endocrine Society, the American Association of Clinical Endocrinologists, and the American Diabetes Association have appealed to patients to continue taking their prescribed medications, unless instructed otherwise by their healthcare provider, one must address the issue of pioglitazone-use in the light of the fact that the highest risk of bladder cancer was noted among patients who had been on pioglitazone for the longest durations and had received higher doses. Orlistat also increases postprandial glucagon-like peptide 1 (GLP-1) levels, thereby enhancing the insulin secretory response to a meal and blunting the postprandial glucose surge in obese diabetics.
Seventy-two percent of the subjects on orlistat achieved fasting glucose values in the normal range, compared to 49%, in the placebo group.
The XENical in the prevention of Diabetes in Obese Subjects (XENDOS) study [42] led to the confirmation of results from previous studies.
Over four years of therapy, orlistat led to a risk reduction of 37.3% in the cumulative incidence of diabetes versus placebo.
Despite intensive lifestyle modifications in both the groups, weight loss was greater in the orlistat group versus the placebo group (- 6.9 vs. Incretin-mimeticsThe use of certain oral hypoglycemic agents has been known to cause weight gain and this constitutes an important risk factor for diabetes; there is an incremental risk of 9% for every kilogram increase in body weight. Exenatide acts through multiple mechanisms, the net result of which is improved glycemic control.
The effects have been categorized as immediate effects - glucose dependent insulin secretion, suppression of post-prandial high glucagon levels, and delayed gastric emptying and delayed effects - with weight loss and improvement in beta cell mass and function. As statins have variable and complex effects on glucose metabolism, the risk of diabetes remains an area of controversy.
In experimental studies statin lipophilicity as well as the potential to inhibit 3-hydroxy-3-methylglutaryl-coenzyme-A reductase are considered prognostic factors of an adverse impact of statin treatment on carbohydrate metabolism.
Other factors like hypotriglyceridemic capacity, increase in islet blood flow, anti-inflammatory properties, and the ability to alter circulating levels of several adipokines are known to affect glucose homeostasis. Among the various drugs in this class, pravastatin appears to possess beneficial effects on glucose metabolism and also reduces the risk of diabetes. In general, the hydrophilic statins pravastatin, rosuvastatin, and pitavastatin are preferable to the lipophilic agents atorvastatin and simvastatin. Having said this, it is also true that their benefits far outweigh any potential risk in populations where statin-use has proven benefits. RAS blockers help in maintaining a critical beta cell mass by blocking the effect of angiotensin II.
It has also been found that these drugs delay or prevent the development of insulin resistance through novel mechanisms. Table 5: Summary of clinical trials on the risk of new-onset type 2 diabetes with Renin Angiotensin System blocking drugsClick here to viewAll these trials taken together involved a large number of non-diabetic subjects and demonstrated that ACE inhibitors or ARBs produced a significant 25% reduction in the incidence of new-onset diabetes. Although these trials differed in their methods and only few had the development of diabetes as a pre-specified end point,[62] it could be inferred that the interplay of hypertension, hyperglycemia, and dyslipidemia worked as a cardiovascular risk factors and the RAS blockade had a positive effect on the metabolic milieu. Clinically, the inhibition of RAS improved insulin sensitivity and decreased the incidence of type 2 diabetes.Vitamin DVitamin D has been receiving attention for its potential role in preventing cardiovascular disease and type 2 diabetes mellitus. Epidemiological studies have suggested that individuals with low blood levels of vitamin D have increased risks of heart disease, stroke, hypertension, and diabetes.
Vitamin D receptors are present in most cells and tissues where they stimulate the nuclear transcription of various genes to alter cellular function. Vitamin D, appears to have an effect on numerous disease states and disorders, including osteoporosis, chronic musculoskeletal pain, diabetes (types 1 and 2), multiple sclerosis, cardiovascular disease, and various cancers. Many mechanisms are known, whereby, hypovitaminosis D may be involved in the causation of hyperglycemia, type 2 diabetes, and metabolic disorders like an increase in insulin resistance, reduction in insulin secretion, and an increase in damage to pancreatic islets.
In a recent trial of 12,719 non-diabetic participants, lower serum levels were associated with pre-diabetes after adjusting for a variety of factors such as age, sex, and race.[65]Pre-and-probioticsThis is another group of agents that has been recently postulated to be involved in the development of insulin resistance and a variety of other deleterious effects. It is being increasingly recognized that there is interplay between the gut flora, energy homeostasis, and inflammation, and that these have a role in the pathogenesis of obesity-related disorders. Several mechanisms have been considered to play a role in this interplay: increased energy from diet, altered fatty acid metabolism, and composition of the adipose tissue and liver are some of them. In summation, endotoxemia may play a key role in the pathogenesis of an obesity-associated inflammatory state and the type of food may affect the endotoxin levels.
Short-term clinical trials have shown the benefit of prebiotics and probiotics on insulin sensitivity, inflammatory markers, postprandial incretins, and glucose tolerance.The fascinating role of gut flora on metabolic disease opens new avenues in the treatment of obesity, insulin resistance, and type 2 diabetes. Concerns of safetyEven as the preventive aspect of diabetes may appear as a tremendous opportunity at all levels including those of the population, physician, and planners, in clinical practice, it is limited by the occurrence of a variety of therapy-related side effects, which limit the usefulness. Certain agents are also known to cause serious adverse effects during long-term use.Another problem area is of long-term adherence to these pharmacological interventions. While a majority of clinical trials demonstrate the benefits of appropriate therapy, they also highlight the issue of non-compliance. In the STOP-NIDDM [30] and XENical in the prevention of Diabetes in Obese Subjects (XENDOS) [42] trials, 30 and 48% of subjects, respectively, did not complete the active intervention. This is probably explained by the lack of tangible benefits for an asymptomatic subject with pre-diabetes, who has to constantly live with obvious adverse effects and the fear of developing frank diabetes.
Drugs causing hyperglycemiaEven when focusing on the preventive aspects of diabetes with the use of drugs one should not forget that there are certain drugs that can cause alter the glucose-insulin homeostasis through a variety of mechanisms, some of which are not fully understood. As hyperglycemia is one component of the metabolic changes, it is often seen that a patient already taking some medication for another component like hypertension or dyslipidemia is subsequently found to have an impaired glucose tolerance or frank diabetes. Diuretics and beta-blockers used for the treatment of hypertension, certain statins like rosuvastatin, and many other agents can cause hyperglycemia. Undoubtedly, the first step in diabetes prevention was, is, and will be lifestyle changes, including dietary modifications and increased physical activity. It is also known that a majority of patients have difficulty in sustaining lifestyle changes. Any other intervention, such as the use of pharmacological agents, will therefore follow logically. Although it is easy to add a pharmacological agent, the risks must be balanced by the benefits. The upside is the possibility of delaying or preventing the devastating consequences of diabetes, but at the same time metabolic disturbances beginning at an early age will increase the use of preventive therapy for much longer durations, with issues of long-term compliance and adverse effects, some of them serious.
Currently, the best approach is that the physician devotes enough time to motivate the patient to make suitable and effective lifestyle changes and utilize all the available resources to achieve these goals.
Pharmacological management may be indicated if the patient, despite adequate lifestyle changes, is still at a significant risk of developing diabetes and cardiovascular disease.



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Comments

  1. morello

    Known to have different types of side effects on the body and in case.

    17.05.2016

  2. GaLaTaSaRaY

    Develops when the pancreas cannot make enough insulin afford healthy meals.

    17.05.2016