Cardiac involvement in amyloidosis and sarcoidosis is poorly understood, and is associated with high morbidity and mortality. Atrial and ventricular arrhythmias, along with conduction defects, are frequent in cardiac amyloidosis and sarcoidosis. Atrial dysfunction in cardiac amyloidosis may result in atrial fibrillation and increases the risk of stroke, making anticoagulation significant and challenging. Ventricular arrhythmia and conduction defects are more common in AL amyloidosis and cardiac sarcoidosis. Premature ventricular contractions (PVCs) from Purkinje fibers trigger ventricular arrhythmias in cardiac amyloidosis, while the inflammation and scarring leading to the reentrant process is the cause in cardiac sarcoidosis. The typical treatment modalities include Class II and III antiarrhythmic drugs and ablation techniques, while corticosteroids and immunosuppressants are indicated in cardiac sarcoidosis to reduce the burden of the disease and arrhythmias. Sudden cardiac death can be a manifestation of both disorders that can be prevented by the Implantable cardioverterdefibrillator (ICD), although the predictive risk factors for primary prevention remain uncertain. In this review, we addressed the current understanding of the pathways involved in inducing arrhythmias in cardiac amyloidosis and sarcoidosis-also, the complications including sudden death and stroke associated with arrhythmia in both diseases. We have discussed other preventive steps needed to minimize arrhythmias to provide symptomatic relief and palliation to patients.

Atrial fibrillation (AF) is a common arrhythmia, and gastroesophageal reflux disease (GERD) is a common gastroenterology disease; both are highly encountered daily in clinical practice. Since both share common predisposing factors, we can conclude that there is a link between them. To date, the precise mechanism of reflux disease as a possible cause of atrial fibrillation remains uncertain. However, some possibilities can be postulated, such as the inflammation process, and sympathovagal imbalance represents the main factors for how GERD can initiate AF. Vigorous aerobic exercise in healthy people can bring about acidic esophageal reflux, which is a common risk factor for AF. Various inflammatory markers such as C-reaction protein (CRP) and interleukins have been a central role in initiating AF. A large hiatal hernia (HH) can cause direct compression on the left atrium that is possibly predisposing to atrial arrhythmogenesis. It has been sporadically reported that using a proton pump inhibitor to treat GERD in patients with coexisting AF has a noticeable effect on decreasing symptoms of AF and recurrence with less cost and side effects.

Fibromyalgia is a complex syndrome characterized by widespread chronic pain, without any obvious etiology, and it is often accompanied by a constellation of symptoms such as fatigue, sleep disturbances and cognitive dysfunction, to name a few. The syndrome may be associated with a variety of autoimmune and psychiatric conditions. Fibromyalgia can occur with other musculoskeletal pathologies and its symptoms can overlap with other chronic painful conditions such as chronic myofascial pain syndromes seen in cervical and lumbar spinal osteoarthritis and degenerative disc disease. Gene polymorphisms have been related to a decreased pain threshold and an increased susceptibility to disorders associated with chronic pain. Some of those genetic variants might trigger the onset of fibromyalgia. Researchers are looking into the possible factors that might contribute to its pathophysiology. It is important to study the connections between pro-inflammatory cytokines and genetic variants in painrelated genes and their roles in predisposition and development of fibromyalgia. The objective of this review article is to provide a brief overview of the pro-inflammatory cytokines commonly associated with fibromyalgia, as well as to look into the genes that have shown some level of involvement in the development of fibromyalgia and its symptomatology.

Posterior reversible encephalopathy syndrome (PRES) is an entity which is characterized by acute to subacute onset of neurological symptoms like altered mental status, seizures, headaches and other focal neurological deficits. It is diagnosed with the help of MRI findings which typically involve the subcortical white matter of parieto-occipital lobes. In this review, we will discuss the various etiologies and risk factors including some of the most common chemotherapeutic agents and immunosuppressant agents associated with this disorder. We will discuss the mechanism of actions and side effect profiles of a few drugs and their role in causation of PRES. This review article discusses if there is any difference in presentation and imaging findings of PRES caused by cytotoxic agents versus caused by other etiologies. It also highlights the difficulty in management of PRES caused by cytotoxic agents as the discontinuation of these drugs could be lifethreatening due to graft rejections or graft versus host disease.