The American journal of medicine
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Pulmonary hypertension (PH) is a disease that is generally first encountered by primary care physicians. Usually, patients present with dyspnea on exertion and a loss of exercise tolerance, although they can have symptoms of chest discomfort, syncope, or edema. Most patients are diagnosed with 2 dimensional doppler echocardiography although echo is not 100% sensitive nor specific in making this diagnosis. ⋯ This is best performed by those that specialize in management of this disease. It is important to diagnose patients who have pulmonary hypertension due to pulmonary artery hypertension and patients with chronic thromboembolic pulmonary hypertension as these patients require specialized treatment that is most effective if started early in the disease course. This review discusses issues related to diagnosis and appropriate referral of patients with pulmonary hypertension.
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Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) have become central in managing obesity and type 2 diabetes, primarily through appetite suppression and metabolic regulation. This review explores the mechanisms underlying GLP-1 RA-induced weight loss, focusing on central and peripheral pathways. Centrally, GLP-1 RAs modulate brain regions controlling appetite, influencing neurotransmitter and peptide release to regulate hunger and energy expenditure. ⋯ They also reduce triglycerides and low-density lipoprotein cholesterol, mitigate adipose tissue inflammation, and minimize ectopic fat deposition, promoting overall metabolic health. Emerging dual and triple co-agonists, targeting GLP-1 alongside glucose-dependent insulinotropic polypeptide, and glucagon pathways, may enhance weight loss and metabolic flexibility. Understanding these mechanisms is crucial as the therapeutic landscape evolves, offering clinicians and researchers insights to optimize the efficacy of current and future obesity treatments.
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Cardiologists and gastroenterologists often encounter the coexistence of symptoms and functional abnormalities, but determining causation is more difficult. In 1962 Smith and Papp first coined the term "linked angina". Their statement was preceded by the experiment whereby increase in bile duct pressure elicited the typical chest pain in patients with ischemic heart disease. It was demonstrated that dysphagia can be associated with ventricular arrhythmia suggestive of possible cardioesophageal reflex involvement. ⋯ It has been demonstrated that the patients suffering from prolonged gastro-esophageal acid reflux episodes and coronary spasm may be at higher risk for the development of linked-angina and acute myocardial infarction. We believe cardioesophageal reflex is a probable mediator of the linked angina. We recommend early treatment of gastroesophageal disorders in patients with symptomatic coronary arterial disease to alleviate the associated ischemic and arrhythmic burden.
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Review
Gut Microbiome Modulation in Allergy Treatment: The Role of Fecal Microbiota Transplantation.
The prevalence of allergic diseases has been rising, paralleling lifestyle changes and environmental exposures that have altered human microbiome composition. This review article examines the intricate relationship between the gut microbiome and allergic diseases, emphasizing the potential of fecal microbiota transplantation as a promising novel treatment approach. ⋯ The discussion also addresses immune homeostasis and its modulation by the gut microbiome, highlighting the shift from eubiosis to dysbiosis in allergic conditions. Furthermore, this article reviews existing studies and emerging research on the role of fecal microbiota transplantation in restoring microbial balance, providing insights into its mechanisms, efficacy, and safety.
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Persistence of COVID-19 symptoms may follow severe acute respiratory syndrome coronavirus 2 infection. The incidence of long COVID increases with the severity of acute disease, but even mild disease can be associated with sequelae. ⋯ Elevated levels of complement are present in acute COVID-19 patients and may persist at lower levels in long COVID. Evidence supports complement activation, with endotheliopathy-associated disease as the molecular mechanism causing both acute and long COVID.