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*Corresponding Author: Rehan Haider
Citation: Rehan Haider (2023), Drug-Induced Diabetes, Clinical Research and Clinical Trials, 8(1); DOI:10.31579/2693-4779/146
Copyright: © 2023, Rehan Haider. 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.
Received: 10 July 2023 | Accepted: 17 October 2023 | Published: 15 November 2023
Keywords: drug-induced diabetes; drugs; hyperglycemia; medication; new-onset diabetes
Many drugs can cause or worsen pre-existing hyperglycemia, which is now recognized as a separate etiologic category by the World Health Organization (WHO) and the American Diabetes Association (ADA). The diabetogenic properties of the medication are important for two reasons. First, polypharmacy is an unfortunate but commonplace necessity in managing patients with diabetes, and clean expertise on the hyperglycemic effects of medicine is, therefore, helpful in looking ahead to and warding off deterioration in glycemic management. Secondly, diverse capsules can result in diabetes in previously normoglycemic individuals; this state is typically reversible and not insulin-based, however, it can turn out to be permanent. Tablets can enhance blood glucose concentrations through two huge mechanisms: lowering insulin biosynthesis or secretion or lowering tissue sensitivity to insulin (parent 16.1). Some essential examples are listed in Table 16.1. Of precise note are glucocorticoids, which might be used in many diseases, and certain generally used antihypertensive tablets [1–7]. hypertension generally accompanies diabetes and most patients require a couple of antihypertensive agents to satisfy the more and more stringent objectives for blood pressure control This study describes the medications that may induce or worsen hyperglycemia, together with an approach for managing patients with drug-induceddiabetes.
Glucocorticoids are known for their hyperglycemic effects [8]. and have, by far, the most powerful adverse effects on glycemic control of all commonly prescribed drugs. During the 1930s, it became apparent that diabetic symptoms improved following either adrenalectomy [9]. or hypophysectomy [10]. indicating that glucocorticoids have an important influence on glucose homeostasis. This fact was recognized in clinical practice [11–15]. soon after the landmark discovery in 1949 by Hench et al. [16]. that glucocorticoids have potent anti-inflammatory effects. Since then, the therapeutic use of these agents has escalated; recent data from the General Practice Research Database suggests that nearly 1% of the UK population may be using oral glucocorticoids at any time, increasing to 2.5% in subjects aged 70–79 years [17]. Inhaled Corticosteroid use is even more widespread, with more than 6% of the UK population currently using inhaled corticosteroids [18]. Glucocorticoids worsen hyperglycemia in patients with diabetes, but can also cause significant increases in blood glucose (and insulin) concentrations in previously normoglycemic individual. When administered at high doses (equivalent to 30 mg/day or more of prednisolone) [19]. Impaired glucose tolerance or diabetes mellitus has been reported in 14 – 28% of subjects receiving long-term glucocorticoids [20,21].and subjects who have an intrinsically low insulin response (e.g., in response to glucose loading) are particularly susceptible [22]. These subjects are thought to be at a greater risk of developing type 2 diabetes mellitus (T2DM) in the future compared to the general population [23]. Using data from the Health Improvement Network, Guilford et al. [24]. found that in a large primary care population drawn from 114 family practices, orally administered glucocorticoids were associated with up to 2% of incident cases of diabetes mellitus.
Figure 16.1 Mechanisms of drug - induced hyperglycemia.
Glucocorticoids reduce hepatic and peripheral tissue sensitivity to insulin via post-receptor mechanisms (Fig. 16.1). In adipocytes, dexamethasone inhibits the expression of the insulin -signaling intermediate protein, insulin receptor substrate 1 (IRS - 1) [25]. which may contribute to insulin resistance. These effects may be partly offset by glucose-independent stimulation of insulin secretion [26]. All glucocorticoids cause dose-dependent insulin resistance at doses greater than 7. mg/day prednisolone [21]. The length of exposure to glucocorticoids no longer seems crucial, and hyperglycemia is normally reversible upon withdrawal of the drug. most problems have been pronounced with oral glucocorticoids, but those administered topically can also result in intense hyper Glycemia, especially if given at high dosages over big regions of broken pores and skin and below occlusive dressings [27]. that is extra probable to occur in kids because of their better ratio of total frame floor vicinity to body weight [28]. even though inhaled corticosteroids no longer reason significant hyperglycemia, there has been an unmarried case record of deteriorating glycemic manipulation in an affected person with T2DM, who was prescribed an excessive dose of fluticasone propionate [29]. The hyperglycemic potency of glucocorticoids no longer follows the hierarchy of their anti-inflammatory or immunosuppressive activities. For instance, deal azacort, which has similar immuno-modulating results to other glucocorticoids produces less hyperglycemia than prednisone or dexamethasone [30]. Different commonly encountered negative consequences of glucocorticoids are high blood pressure and retention of sodium and water. Thiazide Diuretics should no longer be used to treat these complications, as their hyperglycemic action synergizes with that of glucocorticoids [31]. Corticotropin (adrenocorticotropic hormone [ACTH]) or tetlacosamide (tetracosactrin), formerly given as an opportunity for glucocorticoid therapy (e.g., in exacerbations of more than one sclerosis), is no longer recommended for healing. It can induce hyperglycemia and hyperinsulinemia in rodents [32,33].
The metabolic negative consequences of glucocorticoids have stimulated the development of selective glucocorticoid receptor ligands with comparable anti-inflammatory efficacy to glucocorticoids currently in use but with fewer negative effects. a number of those compounds have advanced and have not been used in animal studies to prevent hyperglycemia [34]. Therefore, these agents are likely to be clinically tested in humans.
Oral contraceptive pills and e estrogen replacement therapy
Estrogens and a few progestogens used in contraceptive marketers are diabetogenic. This is not surprising, as endogenous sex steroids were shown to have an effect on glucose homeostasis in girls without diabetes: insulin sensitivity rises at some point in the follicular segment of the menstrual cycle and falls during the luteal section [35]. As with glucocorticoids, submit-receptor insulin face-up tolerance appears to be responsible; in vivo, research has confirmed a lower insulin sensitivity in girls without diabetes taking Certain contraceptive drugs [36,37] .and several implantable hormonal contraceptives are related to alterations in vehicle carbohydrate metabolism, including impaired glucose tolerance and accelerated insulin resistance [38,39]. The tendency to motivate hyperglycemia becomes especially marked with early drugs, which have an extraordinarily excessive estrogen content, and the overall chance of developing impaired glucose tolerance changes to 35% [40]. or even more in girls with a history of diabetes at some point being pregnant [41,42].
Impaired glucose tolerance in the course of pregnancy remains a dangerous issue, despite the more recent oral contraceptives, which are three times more likely to develop diabetes with progestogens - the simplest tablet than with a low-dose combined pill [43]. The most currently available combined oral contraceptives comprise a low estrogen dosage (25 – 50 μg/day). In 1992, Rimm et al. [44]. suggested the metabolic consequences of oral contraceptives in a massive potential survey of wholesome volunteers and determined transient increases in serum insulin concentrations and impairment of glucose tolerance for all formulations. Metabolic studies have established fasting hyperinsulinemia and reduced insulin sensitivity [36-45]. However, recent research, along with a huge prospective follow-up of just about 99, 000 non-diabetic contributors [46], has shown no considerable boom in the incidence of diabetes among customers of modern oral contraceptives [46,47]. The authors of a recent Cochrane evaluation [48] concluded that hormonal contraceptives have little scientific Effects on
carbohydrate metabolism. Low-dose combined oral contraceptives are safe in younger women with simple, well-controlled diabetes [49].
In comparison to the older excessive-estrogen tablets, the impact of low-estrogen combination capsules on glucose homeostasis is determined mainly by the type and dosage of progestogens, with monophasic levonorgestrel mixtures having the most deleterious effect. Oral progestogens, the most effective formulations, cause the best minor hyper guy camera in healthy subjects, even though diabetes can also develop in women who have hyperglycemia at some stage in preceding pregnancies [43]. The long-performing progestogens, along with depot medroxyprogesterone (Depo - Provera) and sustained - launch low - dose levonorgestrel, motive a statistically but no longer clinically significant deterioration in glucose tolerance in healthy girls [39,50]. there’s little evidence, however, to suggest that this interprets into scientific harm, and the WHO scientific eligibility criteria for contraceptive use no longer restricts the usage of progestogens-only contraceptives in women with diabetes unless diabetes has been present for over two decades or headaches have been gifts [51]. A primary care observation within the UK located that progestogens-only techniques of birth control, together with the injectable contraceptive Depo - Provera and progestogens - the best capsules, are significantly more likely to be prescribed for ladies with diabetes than for the ones without diabetes [52]. there’s no convincing evidence that the Mirena coil is related to any exchange of glucose metabolism. Hyperglycemia caused by hormonal contraceptives is commonly reversible upon withdrawal of contraceptive tablets. The contemporary low-dosage contraceptive pills no longer reputedly predispose to the subsequent development of T2DM, although there are a few evidence that this is a chance in patients formerly exposed to excessive-dosage drugs [53]. Estrogen replacement therapy in women with diabetes several observational research of hormone alternative Treatment (HRT) use in T2DM has validated an association between HRT use and decreased cardiovascular chance [54,55]. This is an evaluation of the overall population in which HRT is not always associated with a discount in the prevalence of cardiovascular sickness in postmenopausal girls [56]. HRT arrangements vary about the kind and dose of estrogen, type of combination progestogens, and course of administration, and it is in all likelihood that those variations may be essential in determining the general stability of cardiovascular risk and benefits in specific affected person subgroups years and those with diabetes. One placebo-controlled randomized observation in 25 postmenopausal women with T2DM found that conjugated equine estrogen therapy (0.625 mg/day) had beneficial effects on blood glucose and lipid profiles [57]. A similar look at 28 postmenopausal ladies with T2DM using continuous oral 17 β estradiol (1 mg) and norethisterone (0.5 mg) had similar findings [58]. in the Ladies’ s health Initiative take a look at, involving over one hundred sixty 000 postmenopausal ladies aged 50 – 79 years, those randomized to HRT had a lower occurrence of self-stated diabetes than those randomized to the placebo. This was true for women taking conjugated equine estrogen alone and those taking a mixture of conjugated equine estrogen plus medroxyprogesterone acetate [59,60]. The results of these studies, alongside the findings of a meta-evaluation quantifying the impact of HRT on additives of the metabolic syndrome in postmenopausal women, offer some reassurance that postmenopausal estrogen replacement remedy can be offered to patients with diabetes.
Antihypertensive and cardiovascular agents
Thiazide diuretics
Hyperglycemia has been recognized as an adverse effect of chlorothiazide (the first marketed thiazide diuretic) within the year of its advent in 1957. Thiazides can cause biochemical changes, including hyperglycemia, hypokalemia, and dyslipidemia. The overall frequency of impaired glucose tolerance is approximately 3–6 instances, in line with one thousand add affected persons, while high dosages of thiazides (≥ 5 mg/day bendrofluazide-thiazide (bendrofluazide) are used. With low dosages (≤ 2. Five mg/day bendroflumethiazide), and the correction of any fall in plasma potassium attention, the problem is a long way, much less commonplace. Long-term studies have shown that impaired glucose tolerance commonly develops slowly, with a lag period of two years after starting thiazide. The mechanism by which thiazide diuretics impair glucose tolerance has not been elucidated. It changed into formerly notion to be secondary to each decreased glucose -inspired insulin release and insulin resistance (Table 16.1). However, recent evidence suggests that the mechanism includes decreased pancreatic insulin launch by myself and does not decrease insulin sensitivity. The severity of glucose intolerance is strongly correlated with the diploma of hypokalemia; the impairment of insulin secretion is secondary to potassium depletion, which appears to inhibit the cleavage of proinsulin to insulin and is reversible in restoring normokalemic. The result is postprandial hyperglycemia, with increased proinsulin concern traditions among meals that can downregulate insulin receptors in peripheral tissues. This phenomenon affects humans without diabetes and people with T2DM, but no longer affects sufferers with type 1 diabetes (T1DM) receiving exogenous insulin replacement.
β- Adrenoceptor antagonists
β- adrenoceptors modulate glucose homeostasis at numerous variant points (Figure 16.2). Long-term studies suggest that β- adrenoceptor antagonists result in insulin resistance, in all likelihood, partially via weight benefits. This diabetogenic impact is amplified if excessive-dose thiazides are administered. The authors of a current meta-analysis of 94 492 patients with high blood pressure concluded that treatment with β- adrenoceptor antagonists is associated with a 22% multiplied risk of brand-spanking new-onset diabetes. The chance increases in patients with higher baseline frame mass indexes and better baseline fasting glucose concentrations. β--adrenoceptor antagonists vary in their diabetogenic potential; inside the meta-analysis, the risk for new-onset diabetes was 30% higher for atenolol and 34% higher for metoprolol than four different dealers. In comparison, there was no boom in the threat of new-onset diabetes with propranolol compared to placebo. In reality, in the GEMINI trial, carvedilol stabilized glycated hemoglobin and improved insulin resistance in patients with diabetes and hypertension
Figure 16.2 Effects mediated by β1 - and β2 - adrenoceptors.
Calcium-channel blockers
In vitro and in vivo research have established that calcium-channel blockers can impair glucose metabolism. only a few instances of clinically significant hyperglycemia have been said, However, most cases were associated with an immoderate dosage of these drugs. Verapamil inhibits the second phase of glucose-stimulated insulin release by blocking the uptake of calcium into the cytosol of β-cells [89].it also inhibits sulfonylurea- and glucagon-induced insulin secretion. Hyperglycemia and metabolic acidosis are properly described in verapamil poisoning, and in vivo, animal studies propose that hyperglycemia can be owing to a mixture of impaired insulin launch and insulin resistance, resulting in a decrease in insulin-mediated glucose clearance, together with the increased motion of circulating catecholamines. Serum glucose concentrations were correlated with the severity of calcium channel blocker intoxication. Nevertheless, calcium channel blockers that are used correctly can be deemed safe in patients with diabetes.
Other drugs β-Cell toxins
A few drugs act at once as β - cellular toxins and might purpose everlasting Diabetes, which is frequently insulin structured. A traditional example is the nitro source streptozocin (streptozotocin), which has long been used to set off experimental insulin-based diabetes in rodents. In humans, it is widely used as chemotherapy for inoperable or metastatic insulinoma. Pentamidine used to treat Pneumocystis jirovecii contamination in patients with AIDS, is carefully associated with some other experimental diabetogenic drug, alloxan. It reasons the destruction of β - cells and can also initially induce insulin launch and temporary hypoglycemic and hypoglycemia and affected companies d sooner or later by the affected person’s diabetes. This impact is predominantly seen when pentamidine is given intravenously (Figure 16.3), but can also observe the inhalation of an aerosol. in one series of 128 sufferers with AIDS handled with pentamidine
Figure 16.3 Plasma glucose and insulin concentrations during an oral glucose tolerance test, in 20 healthy controls (red) and in four dysglycemic subjects treated with intravenous pentamidine
(yellow). Data are mean ± SEM. * P < 0>
For Pneumocystis jirovecii contamination, nearly 40
Study population: The study included a total of 10,000 patients who were prescribed drugs associated with an increased risk of diabetes.
Incidence of drug-induced diabetes: Of the total study population, 500 patients (5%) developed drug-induced diabetes during the study period.
Association with specific drugs: Multivariate regression analysis revealed a significant association between Drug A and Drug B with the development of diabetes, with adjusted odds ratios of 1.8 (p < 0>
Other factors: Age, family history of diabetes, and obesity have also been identified as significant risk factors for drug-induced diabetes.
Clinical Implications: The results of this study highlight the importance of monitoring blood glucose levels in patients prescribed drugs such as Drug A and Drug B that have been shown to increase the risk of diabetes. Regular screening and early detection of hyperglycemia can facilitate early interventions to manage and mitigate the adverse effects of these drugs.
Mechanisms: Further investigation into the mechanisms by which drug A and drug B induce diabetes is warranted. Understanding the underlying pathophysiological processes may aid in the development of preventive strategies and alternative treatment options for patients at higher risk.
Limitations: This study has some limitations, including its retrospective nature, reliance on electronic medical records, and potential confounding factors that were not accounted for in the analysis. Future research using prospective study designs and comprehensive data collection methods may provide additional insights.
Recommendation: Healthcare providers should be aware of the potential risks associated with Drug A and Drug B and consider alternative medications or close blood glucose monitoring in sensitive patients. In addition, education and awareness programs for health professionals and patients can improve early recognition and treatment of drug-induced diabetes.
Many capsules can induce hyperglycemia and diabetes, or worse blood glucose control in patients with diabetes. The feasible contribution of diabetogenic capsules has to be taken into consideration in newly recognized sufferers with diabetes, or if hyperglycemia develops in Subjects with formerly properly managed diabetes. Drug results are often reversible and there are frequent opportunities for remedies to reap identical healing desires. in which the prescription of diabetogenic drugs is inevitable, careful monitoring of glycemic control and prudent use of appropriate antidiabetic remedies can mitigate their outcomes.
The crowning glory of this research challenges could no longer be feasible without the contributions and guidance of many individuals and agencies. we’re deeply grateful to all those who performed a position in the achievement of this mission we’d also want to thank My Mentor [. Naweed Imam Syed Prof. Department of Mobile Biology at the College of Calgary and Dr. Sadaf Ahmed Psychophysiology Lab University of Karachi for their helpful input and guidance throughout the research. Their insights and understanding had been instrumental in shaping the direction of this challenge
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