We read with great interest the letter by Ji et al. 1 Obesity is a wellrecognized risk factor for the development of non-alcoholic fatty liver disease (NAFLD) or metabolic dysfunction-associated liver disease (MAFLD) and is associated with adverse outcomes in COVID-19 patients. 2,3 Qatar's population has a high prevalence of obesity 4 and also has one of the highest rates of COVID-19 cases per million population, with one of the lowest mortality rates. 5 We hypothesized that NAFLD is an independent risk factor for worse outcomes in hospitalized COVID-19 patients in our population.

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Introduction Vitamin B12 (VitB12) deficiency rarely manifests with visual symptoms. Optic nerve damage in VitB12 deficiency is thought to be via degeneration. However, optic neuritis, though infrequent, has been reported secondary to VitB12 deficiency. Material and methods We conducted a systematic review of all the reported cases of VitB12 deficiency with optic nerve involvement in Pubmed, Cochrane, and Google Scholar any date up to September 6, 2020. We have discussed the findings and compiled the available information on ophthalmological manifestations of VitB12 deficiency. We aim to provide a unified knowledge about the evidence related to types of optic neuropathies reported to date secondary to VitB12 deficiency. We also present a case of bilateral optic neuritis secondary to VitB12 deficiency. Presentation of case We present a 29-year-old previously healthy male with progressive, painful, bilateral, but asymmetric visual deterioration for forty-five days. A detailed history, examination, and laboratory workup were carried out. He was diagnosed as having optic neuritis secondary to VitB12 deficiency. He showed partial improvement with the replacement of VitB12. Conclusion We suggest promptly identifying and replacing VitB12 in patients with optic neuritis with proven VitB12 deficiency to prevent permanent damage to the optic nerve. Patients with VitB12 deficiency should have a baseline fundoscopic exam to rule out subclinical optic nerve damage. Moreover, patients who present with visual disturbances should be screened for VitB12 deficiency, especially the vegan population.

Rationale: BRASH syndrome is a relatively unknown medical entity in which there is a combination of bradycardia, renal injury, hypoperfusion, and hyperkalemia. It is clinically essential to take these manifestations as a syndrome rather than isolated findings because they are interrelated and have synergistic effects. Bradycardia can result in hypoperfusion, which can cause renal injury. The resultant renal injury causes hyperkalemia (which can also be the initial trigger), which potentiates the bradycardia. Deteriorating patients with the syndrome usually do not respond to regular Advanced Cardiac Life Support resuscitation protocols. Treatment focused on the timely replacement of fluids and electrolytes gives better outcomes. It is vital to keep BRASH syndrome in diagnostic possibilities while seeing patients with refractory bradycardia, hyperkalemia, and renal injury, especially when other diagnoses are ruled out. Patient concerns: In this report, we present a 64-years-old gentleman who came with generalized fatigue, non-bloody diarrhea, vomiting, and low oral intake for the past 5 days. Diagnoses: The patient was diagnosed with BRASH syndrome. Interventions: The patient received intravenous fluids, 2 doses of atropine 0.5 mg and received dextrose 50 percent with insulin regular 10 units, and salbutamol 5 mg for hyperkalemia. He was intubated due to a low Glasgow Coma Scale and received dialysis for resistant hyperkalemia. A transvenous pacemaker was inserted due to bradycardia. Outcomes: The patient had 2 cardiac arrests and could not survive the second. Lessons: BRASH is a life-threatening yet largely underdiagnosed condition. Physicians should keep a high index of suspicion for BRASH while seeing patients with resistant and self-potentiating bradycardia, hyperkalemia, and renal failure, as a timely diagnosis is crucial in the management. Variable clinical presentations and limited literature create a diagnostic challenge. Further studies are warranted to understand the pathophysiology and develop better and accurate management algorithms. Patients’ risk of developing BRASH syndrome should be considered while prescribing causative medications (Atrioventricular nodal blocking drugs such as beta-blockers) in hospitals and outpatient settings.