Furosemide-induced haemolytic anaemia in an extreme elderly patient.

Furosemide, a loop diuretic, is commonly used to treat fluid overload symptoms and heart failure. Drug-induced immune haemolytic anaemia is an unusual drug-adverse event. Furosemide-induced haemolysis is even rarer. This case report presents a 91-year-old male who developed acute haemolytic anaemia 3 days after initiating furosemide to treat myocardial infarction complicated with acute decompensated heart failure. He had increased lactate dehydrogenase and unconjugated bilirubin with undetectable haptoglobin, which indicated the destruction of red blood cells. Other causes for haemolytic anaemia, including hereditary, microangiopathic haemolytic anaemia, and paroxysmal nocturnal haemoglobinuria, were also excluded. He improved with drug cessation and a short course of glucocorticoids. This report aims to raise awareness of this rare complication caused by commonly prescribed drugs. Despite a negative result of a direct antiglobulin test, physicians must remain suspicious of drug-induced immune haemolytic anaemia in unclear cases of haemolysis.

Sunitinib-Induced Congestive Heart Failure in a Patient with Gastrointestinal Stromal Tumor.

Common cardiovascular toxicities of sunitinib mainly include hypertension, QT prolongation, left ventricular dysfunction (LVD) and less frequently, congestive heart failure (CHF). Here, we report the case of a 67-year-old woman who developed heart failure after 24 months of sunitinib. Our case highlights the importance of strict and regular cardiovascular monitoring during sunitinib. It also shows that the reintroduction of sunitinib with maintaining heart failure treatment can be safe. The exact mechanisms of this cardiotoxicity have not been understood. There is no protective therapy available. Therefore, further investigations are needed in these areas. Medical specialists who prescribe and treat patients with sunitinib should be aware of the possible occurrence of these conditions and perform regular checkup of sunitinib-treated patients.

It is time to drop hydroxychloroquine from our COVID-19 armamentarium.

Chloroquine (CQ) and hydroxychloroquine (HCQ) were among the first drugs repurposed for the treatment of SARS-CoV-2 infection. A few in vitro studies confirmed that both drugs exhibited dose dependent anti-SARS-CoV-2 activities. These observations and the encouraging results from early poorly conducted observational studies created a major hype about the therapeutic potential of these drugs in the treatment of COVID-19 disease. This was further catalyzed by media and political influences leading to a widespread use of these agents. Subsequent randomized trials revealed lack of efficacy of these agents in improving the outcomes of COVID-19 or in preventing infection in post-exposure prophylaxis studies. Nevertheless, many ongoing trials continue to actively recruit tens of thousands of patients to receive HCQ worldwide. In this perspective, we address the possible mechanisms behind the lack of efficacy and the increased risk of cardiac toxicity of HCQ in COVID-19 disease. For the lack of efficacy, we discuss the fundamental differences of treatment initiation between in vitro and in vivo studies, the pitfalls of the pharmacological calculations of effective blood drug concentrations and related dosing regimens, and the possible negative effect of HCQ on the antiviral type-I interferon response. Although it has been repeatedly claimed that HCQ has a longstanding safety track record for many decades in use, we present counterarguments for this contention due to disease-drug and drug-drug interactions. We discuss the molecular mechanisms and the cumulative epidemiological evidence of HCQ cardiac toxicity.