Introduction
Acebutolol belongs to the class of beta-blockers called anti-hypertensive drugs. Medical researchers aver that antihypertensive medications such as beta-blockers and thiazide diuretics are causative agents of diabetes mellitus type 2 (Gress et al. 905). Additionally, numerous empirical studies have found a positive correlation between hypertension and incidence of diabetes mellitus with some professing that the two maladies overlap each other (Cheung and Li 161). Florea and Cohn state that heart failure stems from an imbalance between the sympathetic and parasympathetic nervous systems with beta-blockers making the disease progress due to the inhibition of the sympathetic system (1815). The determination of whether or not Acebutolol increases the chance of hypertensive patients developing diabetes mellitus 2 is central to the ultimate management of heart conditions.
Acebutolol: Mechanism of Action, Indications, and Uses
Acebutolol works by obstructing β I adrenergic receptors of neurons in the sympathetic nervous system that regulates high blood pressure. The sympathetic nervous system is one of the branches of the autonomic nervous system that regulates the unconscious activities of the body such as heartbeat (Dobre et al. 80). In particular, Acebutolol impairs the functions of epinephrine and norepinephrine, which are neurotransmitters that mediate the functioning of the heart and the sympathetic nervous system (Florea and Cohn 1816). The blockage of beta-adrenergic receptors in the heart by Acebutolol prevents the binding of epinephrine or norepinephrine. The attachment of these neurotransmitters initiates a signal transduction cascade that leads to the activation of the sympathetic nervous system, which controls the fight or flight mechanism in the body. Ultimately, Acebutolol reduces the rate of heartbeat, which in turn decreases the volume of blood it pumps and the amount of oxygen it requires.
The adverse reactions to Acebutolol are mild, and severity reduces with an increase in the chemotherapy period. These adverse effects include muscle aches, abdominal discomforts, dizziness, excessive fatigue, and diarrhea. However, experimental evidence shows that it also causes drug-induced lupus erythematosus (DILE) (Muta, Fukami, and Nakajima 659). DILE is an autoimmune disease, which leads to severe complications, and researchers have speculated it to be involved in the development of both type II and type I diabetes mellitus (Itariu and Stulnig 192). The administration of selective beta-blockers by some physicians to asthmatic individuals is still a subject of medical debate.
Doctors use Acebutolol in the treatment and management of hypertension, arrhythmia (anomalies in the heart rhythms), and chest pains emanating from angina. Arrhythmia is a severe disorder for it causes death to 50% of patients with cardiovascular disorders (Fu 291). As arrhythmia has a number of causative agents, doctors should determine them before prescribing beta-blockers.
Summary of the article
The study aimed at determining whether there is a link between the use of antihypertensive drugs and the development of diabetes mellitus 2. The study participants were 12,250 adults aged between 45-64 years who were randomly sampled from different geographical regions in the United States. The investigators grouped them into those suffering from hypertension and those who are not, and analyzed them using Chiang’s method for determining incidence. The researchers further divided those suffering from hypertension into those taking medications and those who are not, and analyzed them using proportional-hazard analysis. The results indicate that people who suffer from hypertension are 2.5 times more likely to get diabetes compared to those who do not. Amongst users of the antihypertensive drugs, users of beta-blockers are 28% more likely to develop diabetes compared to hypertensive sufferers who are not on medication. In conclusion, users of calcium-channel antagonists, thiazide diuretics, and angiotensin-converting enzyme inhibitors have a lower risk for diabetes than users of hypertensive drugs. However, users of beta-blocker are at risk of getting diabetes.
Analysis of the research study
Epidemiological data show that 1,146 new cases of diabetes have occurred over the past six years, which accounts for 16.6% of diabetic cases per 1,000 people. In the new cases, 569 people had hypertension while 577 did not have hypertension. In the multivariate assay to determine whether a correlation between the use of antihypertensive drugs and the development of diabetes mellitus type 2 existed, patients with hypertension taking β-blockers are 28% more likely to get diabetes compared to those not taking any drugs (Gress et al. 908). The users of angiotensin-converting enzyme inhibitors and calcium channel antagonists were not at risk of developing diabetes, which is the same as hypertensive sufferers who were not on any treatment. Furthermore, users of beta-blockers and thiazide diuretics were 1.34 and 0.88 times more likely to develop diabetes respectively. In the analysis to determine changes in treatment after three years, users of beta-blockers also had a higher propensity for developing diabetes at 33.6% when compared to users of thiazide diuretics and those who are not on medications at 27.5% and 26.3% respectively.
The sample for the study considerably represents the target population since it comprises Americans who are genetically predisposed to developing diabetes mellitus. The sample size was adequate, despite the exclusion criteria of the study that omitted 1375 individuals. The research was not a double-blind study because the participants and the researchers knew each other, and the investigators did not terminate it at any point. In the future, researchers should probe shared risk factors ascertaining the association between the use of antihypertensive drugs and diabetes. The probe will provide evidence-based data to clinicians and help them deduce groups that are likely to develop diabetes.
Conclusion
In general, this is a robust study because it factored in confounding factors at baseline (presence of diabetes and hypertension) and had enough study participants, which formed an unbiased sample. The study also eliminated bias such as missing data at baseline and three and six years of study. However, researchers can only extrapolate the results to a section of society, the White Americans and the African Americans, since the exclusion criteria eliminated other races. The doses of the respective classes of antihypertensive drugs were not included. The missing data on the presence or absence of diabetes after three and six years is quite huge as they add up to 948. If the investigators could have captured these data, perhaps, it would have tilted the balance in terms of the disease outcome, following usage of the different classes of antihypertensive medications.
Acebutolol is not a safe drug because when compared with other antihypertensive drugs such as thiazide diuretics, calcium channel antagonists, and angiotensin-converting enzyme (ACE) inhibitors, it is a risk factor in the development of diabetes mellitus (Gress et al. 908). Empirical evidence indicates that the use of other classes of anti-high blood pressure drugs does predispose individuals to diabetes. Compared with patients who were not on any treatment for hypertension, beta-blockers had a 28% incidence of diabetes mellitus. In a different study of propranolol, a beta-blocker, the scientists found that it was 6.1 times more likely to cause diabetes in people who use it compared to those who do not. These data underscore why beta-blockers are not safe antihypertensive drugs.
The dangers that Acebutolol poses include the development of autoimmune disease due to DILE (Muta, Fukami, and Nakajima 659). In addition, according to Flore and Cohn, beta-blockers accelerate the cases of patients with heart failure by impeding the sympathetic nervous system (1815). There is an autonomic disparity between the sympathetic system (activation) and the parasympathetic (inhibition).
Works Cited
Cheung, Bernard, and Chao Li. “Diabetes and hypertension: Is there a common metabolic pathway?” Current Atherosclerosis Reports 14.2 (2012): 160–166. Print
Dobre, Daniela, Jeffrey Borer, Kim Fox, Karl Swedberg, Kirkwood Adams, John Cleland, Alain Cohen-Solal, Mihai Gheorghiade, Francois Gueyffier, Christopher O’Connor, Mona Fiuzat, Athul Patak, and Ileana Pina. “Heart rate: a prognostic factor and therapeutic target in chronic heart failure: The distinct roles of drugs with heart-rate-lowering properties.” European Journal of Heart Failure, 16.2 (2013): 76-85. Print.
Florea, Viorel, and Jay Cohn. “The autonomic nervous system and heart failure.” Circulation Research 114.11 (2014): 1815-1826. Print.
Fu, Du-Guang. Cardiac arrhythmias: Diagnosis, symptoms and Treatments. Cell Biochemistry and Biophysics 73.1 (2015): 291-296. Print.
Gress, Todd, Javier Nieto, Eyal Shahar, Marion Wofford, and Frederick Brancati. “Hypertension and Antihypertensive Therapy as Risk Factors for Type 2 Diabetes Mellitus.” The New England Journal of Medicine 342.13 (2000): 905-912. Print.
Itariu, Bianca and Thomas Stulnig. “Autoimmune Aspects of Type 2 Diabetes Mellitus: A Mini-Review.” Gerontology 60.3 (2014): 189-196. Print.
Muta, Kyotaka,Tatsuki Fukami, and Miki Nakajima. “A proposed mechanism for the adverse effects of Acebutolol: CES2 and CYP2C19-mediated metabolism and antinuclear antibody production.” Biochemical Pharmacology 98.4 (2015): 659-670. Print.