As a worldwide aging population is on the rise, osteoporosis (OS) is becoming a global health burden. Therefore, many researchers and health authorities are looking into the potential prevention and treatment of OS. Although previously regarded as two separate pathological processes, diabetes (DM) and OS are now regarded as two conditions that can occur together. It is now believed that OS can develop as a complication of DM. This relationship is further evidenced through a reduction in bone mineral density in type-1 diabetes with a resulting increased risk of fracture. Although bone mineral density in type-2 diabetes mellitus is normal or increased, there is also increased fragility due to decreased bone quality. These abnormal bone qualities tend to occur through the production of reduced bone microvasculature and advanced glycation end product, AGE. Interestingly, one of the most common treatments for DM, metformin (MF), shows a promising result on the protection of diabetes and non-diabetes related bone turnover. It is believed that MF modulates its effect through the adenosine monophosphate-activated protein kinase (AMPK) pathway. Recent data regarded AMPK as a vital mediator of homeostasis. It is involved not only in glucose metabolism but also in osteogenesis. AMPK can directly influence the production of mature and good quality bone by decreasing osteoclasts, increasing osteoblast formation, and enhancing bone mineral deposition. As an activator of AMPK, MF also upregulates osteogenesis. Furthermore, MF can influence osteogenesis through a non-AMPK pathway, such as the fructose 1-6 phosphatase pathway, by reducing glucose levels. While already recognized as a safe and effective treatment for DM, this article discusses whether MF can be used for the prevention and treatment of OS.

Myasthenia gravis (MG) is a rare autoimmune neuromuscular junction disorder, and thyroid disorder is a disorder involving the thyroid receptor, of which Graves' disease (GD) is the most common autoimmune thyroid disorder, in which antibodies develop against thyroid receptors. Both may have similar clinical features. In myasthenia gravis, autoimmune antibodies develop against postsynaptic neuromuscular junction disrupting the neuromuscular transmission, resulting in fluctuating muscle weakness and fatigue. It is a disease of young women and older men. The two pathologies may coexist in a patient or can precede one another. Graves' disease (GD) among thyroid diseases is most often associated with MG. Similarities in clinical features lead to difficulty in distinguishing MG and GD. Despite the standard treatment of myasthenia gravis, including steroids, acetylcholinesterases, rituximab, immunosuppressants, and thymectomy, there is still an increased number of relapses and myasthenia crisis. Eculizumab and plasmapheresis are the two new treatment options for MG, with supporting evidence of marked improvement in recent studies. Myasthenia gravis and Graves' disease have a seesaw relationship. Treating one pathology may worsen the other, so physicians should always consider MG as a differential in patients of hyperthyroidism presenting with new symptoms of fatigue or respiratory failure or neuromuscular weakness. In this comprehensive review article, we tried to establish an association between myasthenia gravis and Graves' disease (GD) by exploring currently available literature from PubMed. However, more studies need to be done to establish an association between pathologies.

Takotsubo cardiomyopathy (TTC), also known as broken heart syndrome, stress cardiomyopathy (SCM), or apical ballooning syndrome, is a non-ischemic cardiac disease with an initial clinical presentation that is very similar to acute coronary syndrome (ACS). Ventricular arrhythmias (VAs) contribute significantly to an increase in the rates of death in patients with TTC, especially during the acute phase, in which patients with TTC are more susceptible to develop life-threatening arrhythmias (LTA) such as ventricular tachycardia (VT), ventricular fibrillation (VF), torsades de pointes (TdP), and sudden cardiac death (SCD). However, the pathophysiology of TTC and how VA occurs are still a mystery. We aim to review previous literature and discuss the possible mechanisms of VA in TTC patients. VA usually complicates the acute phase of the disease and worsens the long-term prognosis. Alterations of repolarization (negative T wave, prolonged QTc) indicate a high risk of arrhythmic events (TdP, VT, VF, and SCD). Catecholamine effect on myocardial cells and myocardial edema can create a substrate for the development of VA. Some of the most commonly proposed mechanisms for the development of VA in patients with TTC are coronary vasospasm, myocardial stunning due to catecholamines, re-entry, and triggered activity. Further prospective studies, including a more significant number of patients, are required to understand the disease's pathophysiology better and improve LTA management in patients with TTC.