Asthma, a chronic illness, is characterized by inflammation and airway constriction. Uncontrolled severe asthma is related to poor quality of life and increased utilization of health resources. Conventional treatments are associated with a significant amount of adverse effects. Recent years have seen the identification of various molecular effectors and signaling pathways as interesting targets for the biological therapy of severe asthma that is resistant to current therapies. Because they only target some downstream components of the inflammatory response in asthma, leaving other components unaffected, current biologic treatments only lower the exacerbation rate by 50%. If we focus on the upstream mediators of the inflammatory response in asthma, it might have a greater effect and be more efficient. Tezepelumab is a human monoclonal IgG2 antibody that specifically binds to thymic stromal lymphopoietin (TSLP) at the level of its TSLPR (thymic stromal lymphopoietin receptor) binding site, inhibiting the interaction between human TSLP and TSLPR. It is being used to treat the cytokines on the respiratory epithelial layer known as "alarmins." It is the only biologic drug available for treating severe uncontrolled asthma, despite limitations in biomarker and phenotype. In light of recent developments, the lack of knowledge on tezepelumab prompts us to publish a comprehensive systematic review. We discovered that regardless of blood eosinophil level and fractional exhaled nitric oxide levels, tezepelumab dramatically lowers asthma exacerbation in patients with severe uncontrolled asthma when compared to placebo. Tezepelumab also lessens patients' demand for healthcare resources while improving clinical indicators of lung function, health-related quality of life, and asthma management in patients. Tezepelumab plays a role in enhancing pre-bronchodilator FEV1 and lowering blood eosinophil count and fractional exhaled nitric oxide in patients with or without chronic allergies (FeNO). There have been no reports of fatalities or severe adverse events connected to tezepelumab.

A relatively new yet critical phenomenon of bradycardia, renal failure, atrioventricular (AV) blockade, shock, and hyperkalemia (BRASH) syndrome is hypothesized to happen in patients who take atrioventricular nodal blocking (AVNB) agents and have underlying renal insufficiency. In our case, a 67-year-old female with an extensive medical history presented to the emergency room with chief complaints of decreased appetite, nausea, vomiting, fatigue, and left-sided atypical chest pain for the past two weeks. The patient was taking losartan potassium 50 mg daily in addition to carvedilol 6.25 mg twice daily for her hypertension (HTN) and heart failure with reduced ejection fraction (HFrEF) with the addition of bumetanide 0.5 mg, which was added three weeks prior. On presentation, the patient had sinus bradycardia and hypotension along with the laboratory finding of acute kidney injury (AKI) in the setting of chronic kidney disease (CKD) and hyperkalemia. Cardiology and nephrology were consulted emergently; her clinical scenario raised suspicion of the BRASH syndrome. The patient was admitted to the intensive care unit (ICU), and all antihypertensive medications, including beta-blockers, were stopped. Intravenous (IV) fluid resuscitation and medical management of hyperkalemia were initiated, along with BiPAP for respiratory distress. She responded significantly, and her vitals remained stable. She was successfully discharged home with a cardiology and nephrology follow-up. We highlight the case to emphasize the consideration of BRASH in a patient on multiple cardiac medications who presented with deranged electrolytes and organ failure, and decompensated heart failure (HF) should not be fixed on as the principal diagnosis.