A 64-Year-Old Man Hospitalized for COVID-19 Pneumonia and Treated with Tocilizumab Who Developed Chronic Cavitary Pulmonary Aspergillosis.

BACKGROUND The management of (Coronavirus disease 2019) COVID-19 pneumonia is ever-evolving. Tocilizumab, a monoclonal antibody against interleukin-6 (IL-6) receptor, have known mortality benefit in severe COVID-19 pneumonia, but data are limited regarding safety. Attributable to the immunomodulatory nature of this medication, patients may be at risk for opportunistic infections, including chronic cavitary pulmonary aspergillosis (CPPA), a slowly progressive disease characterized pulmonary infiltrates and often a newly-formed cavity. However, current guidelines do not emphasize post-treatment surveillance of patients for opportunistic infections, including CPPA. CASE REPORT We present a particular case of a 64-year-old man treated for COVID-19 pneumonia with Tocilizumab and dexamethasone who developed cavitary pulmonary aspergillosis. He presented to the emergency department with hemoptysis, associated with worsening productive cough, shortness of breath, and weight loss. Computed tomography (CT) of the chest showed areas of focal consolidation and a cavitary lung lesion within the left upper lobe. Sputum culture was positive for Aspergillus niger. The patient received a long course of oral triazole therapy for CPPA, with clinical improvement. CT scan of the chest at 9 months showed that the Itraconazole therapy was effective in resolving the extensive airspace disease and decreasing the size of the upper-lobe cavity and fungal ball. CONCLUSIONS This article illustrates the possibility of a serious infection such as CCPA as an adverse effect of Tocilizumab treatment, especially with concurrent immunosuppressive therapy. Furthermore, this case highlights the importance of regular monitoring of patients who have received Tocilizumab therapy to ensure that early signs of opportunistic infections such as CPPA are detected and treated promptly to prevent permanent lung damage.

Clozapine-Induced Myocarditis in a Young Man with Refractory Schizophrenia: Case Report of a Rare Adverse Event and Review of the Literature.

BACKGROUND Myocarditis is cardiac muscle inflammation caused by infectious or noninfectious agents. Rarely, clozapine, an atypical antipsychotic drug used to treat resistant schizophrenia, has been reported to cause myocarditis, as we report in this case. CASE REPORT A 29-year-old man, who was known to have schizophrenia and was on olanzapine therapy, presented in our Emergency Department with active psychosis, and was subsequently admitted to the psychiatric ward for refractory schizophrenia. He was started on clozapine, which was cross-titrated with olanzapine. On day 20 of being treated with clozapine, he developed a high-grade fever and chest pain. EKG demonstrated new-onset prolonged QT corrected for heart rate (QTc), premature ventricular contractions, ST-T wave changes with an increased ventricular rate, and ventricular bigeminy with elevated troponin and inflammatory markers. Echocardiography showed a reduced left ventricular ejection fraction. Coronary angiography showed normal coronary arteries, low cardiac output, and cardiac index consistent with cardiogenic shock was also observed. Other pertinent laboratory results included negative respiratory viral panel, including COVID-19 PCR, negative blood cultures, and negative stool screen for ova and parasite. Clozapine was discontinued and the patient received management for heart failure with reduced ejection fraction. He improved clinically with return of EKG to normal sinus rhythm and improved left ventricular ejection fraction on repeat echocardiogram. CONCLUSIONS Acute myocarditis can occur due to a myriad of causes, both infectious and noninfectious; thus, determining the lesser-known causes, such as drug-related etiology, is essential to provide appropriate treatment for patients.

Prediction of hemodynamically significant coronary artery disease using troponin I in hemodialysis patients presenting with chest pain: A case-control study.

OBJECTIVES: Controversy exists regarding utility of cardiac troponin I (cTnI) in predicting significant coronary artery disease (CAD) in hemodialysis (HD) patients with chest pain and no acute ischemia on electrocardiogram (non-ST segment elevation myocardial infarction, non-STEMI). We sought to determine if cTnI elevation predicts significant CAD (>70% stenosis) in these patients. METHODS: Ninety patients with non-STEMI referred for cardiac catheterization were included, divided equally into HD and non-HD groups. RESULTS: Mean age and baseline characteristics were not significantly different between groups, except for left ventricular hypertrophy which was higher in HD patients (56 vs. 27%, p = 0.012). Initial cTnI correlated with obstructive CAD and was stratified into <0.3 and >0.3 ng/ml. By logistic regression, cTnI >0.3 ng/ml was not predictive of CAD in HD patients [odds ratio = 0.87 (95% CI 0.19-4.0), p = 0.8], while non-HD patients had an increased risk of CAD if first cTnI was >0.3 ng/ml [odds ratio = 1.461 (95% CI 1.01-2.11), p = 0.04] as expected. Sensitivity, specificity, negative and positive predictive values of cTnI in predicting obstructive CAD were better in non-HD patients. CONCLUSION: cTnI in these patients had no predictive value for obstructive CAD. This contrasts with the general population, suggesting a higher index of suspicion for high-grade CAD irrespective of cTnI levels in HD patients.

Frequency of swing-segment stenosis in referred dialysis patients with angiographically documented lesions.

BACKGROUND: The segment of the vein mobilized for arterial anastomosis in the creation of an arteriovenous fistula (AVF) is the swing segment. This segment may experience turbulent flow and altered shear mechanical stress that result in stenosis. We sought to determine the frequency of stenotic lesions in the swing segment. STUDY DESIGN: Case series. SETTINGS & PARTICIPANTS: From January 31, 2003, to June 30, 2005, records of all patients referred to an outpatient hemodialysis vascular access center for AVF dysfunction were reviewed (n = 484). Of these, 278 patients had angiographically documented stenosis (any degree of luminal narrowing) on their first visit. OUTCOMES & MEASUREMENTS: Distribution of stenoses in different segments of the AVF. Swing-segment stenoses were classified as proximal (outflow into axillary vein system), distal or juxta-anastomotic (adjacent to the anastomosis), and the cephalic arch. RESULTS: Overall prevalence of angiographically documented swing segment stenosis (proximal, distal or juxta-anastomotic, and cephalic arch) was 45.7% (127 of 278 patients), whereas the remaining stenoses (151 of 278 patients) were distributed among the puncture zone, arterial, arterial anastomosis, and central veins. The most frequent location of the swing-segment stenosis was juxta-anatomosis (63%; 80 of 127 patients), followed by cephalic arch (19%; 24 of 127 patients) and proximal swing segment (18%; 23 of 127 patients). The distribution of swing-segment stenosis (n = 127) was equivalent among the various fistulas (brachial-cephalic, 35.4%; radial-cephalic, 33.9%; and brachial-basilic, 30.7%). Eighty-three percent of swing-segment stenoses were significant (>50% luminal narrowing) and underwent percutaneous transluminal angioplasty, with a 93% success rate. LIMITATIONS: Retrospective nature of the study and potential selection bias. CONCLUSION: In our population, swing-segment stenosis is the most common lesion in dysfunctional AVFs; juxta-anastomotic stenosis is the predominant lesion independent of fistula type. Whether the occurrence of swing-segment stenosis is caused by mobilization of the vein during surgery is not clear.

Challenges in the diagnosis and management of renal artery stenosis.

Renal artery stenosis (RAS) is a common cause of secondary hypertension, with the activation of the renin-angiotensin-aldosterone system being the pathophysiologic hallmark of the disease. Renovascular hypertension, ischemic nephropathy, proteinuria, and flash pulmonary edema are the main clinical syndromes associated with RAS. The prevalence of RAS is on the rise, owing to an increasing prevalence of diabetes and atherosclerotic disease among our aging population. This rise in RAS prevalence poses major challenges for clinicians making diagnostic and treatment decisions. Although renal angioplasty is of proven benefit in fibromuscular dysplasia, randomized trials in atherosclerotic RAS have not shown any advantage for revascularization over medical therapy in terms of blood pressure control or renal function preservation. Angioplasty and surgical interventions should be reserved for patients with preserved kidney size and hemodynamically significant stenosis.