Carpal tunnel syndrome (CTS) is a common entrapment neuropathy characterized by pain, numbness, and impaired function of the hand due to compression of the median nerve at the level of the wrist. Although CTS can develop from repetitive strain, injury, or medical conditions, there are also congenital and genetic risk factors that can predispose individuals to the condition. With respect to anatomical factors, some individuals are born with a smaller carpal tunnel, which increases their susceptibility to median nerve compression. Variations in specific genes, such as those encoding proteins involved in extracellular matrix remodeling, inflammation, and nerve function, have also been linked to an increased risk for CTS. CTS is associated with a high cost of health care maintenance and loss of work productivity. Therefore, it is vital that primary care physicians fully understand the anatomy, epidemiology, pathophysiology, etiology, and risk factors of CTS, so they can be proactive in prevention, diagnosing, and guiding proper treatment. This integrated review also provides insights into how biological, genetic, environmental, and occupational factors interact with structural elements to determine who is most likely to acquire and suffer from CTS. Keeping health practitioners abreast of all the factors that could impact CTS should go a long way in decreasing the health care and socioeconomic burden of CTS.
Systemic hypertension (HTN) is the hallmark of cardiovascular disease and the forerunner of heart failure. These associations have been established over decades of research on essential HTN. Advancements in the treatment of patients diagnosed with HTN, consisting of alpha-or beta-adrenergic receptor blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, thiazide, or aldosterone receptor blockers known as anti-mineralocorticoids, in the presence or absence of low sodium salt diets, often fail to control blood pressure adequately to prevent morbidity and mortality. Low sodium diets have had limited success in controlling HTN because low sodium intake is associated with renin-angiotensin-aldosterone system upregulation. Therefore, upregulating aldosterone secretion, sodium, and water retention which, in turn, moves the blood pressure back toward the range of HTN dictated by the baroreceptor reset value, as a compensatory mechanism, especially in resistant HTN. These impediments to blood pressure control in HTN may have been effectively circumvented by the advent of a new class of drugs known as aldosterone synthase inhibitors, represented by baxdrostat. The mechanism of action of baxdrostat as an aldosterone synthase inhibitor demonstrates the inextricable linkage between sodium and blood pressure regulation. Theoretically, combining a low sodium diet with the activity of this aldosterone synthesis inhibitor should alleviate the adverse effect of renin-angiotensin-aldosterone system upregulation. Aldosterone synthesis inhibition should also decrease the oxidative stress and endothelial dysfunction associated with HTN, causing more endothelial nitric oxide synthesis, release, and vasorelaxation. To the best of our knowledge, this is the first systematic review to summarize evidence-based articles relevant to the use of a novel drug (aldosterone synthase inhibitor) in the treatment of HTN and cardiovascular disease. Making the current database of relevant information on baxdrostat and other aldosterone synthase inhibitors readily available will, no doubt, aid physicians and other medical practitioners in their decision-making about employing aldosterone synthase inhibitors in the treatment of patients.
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