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.

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.

Background: Bleomycin is chemotherapeutic agent that has been used for cancer treatment for several years. However, potentially life-threatening lung toxicity is a major concern limiting its use. Case report: This is a case of a 64-year-old male presenting sub acutely with gradual onset of exertional shortness of breath and cough after completing 4 cycles of ABVD regimen for Stage 2b Hodgkin’s lymphoma. CT scan showed extensive bibasilar reticular opacities with honey combing suggestive of pulmonary fibrosis with Usual interstitial pneumonia pattern. Based on temporal relations to bleomycin chemotherapy, a diagnosis of bleomycin induced lung fibrosis was made. Bleomycin was subsequently discontinued with some improvement of symptoms. Conclusion: Pulmonary toxicity with irreversible lung fibrosis is a life threatening and menacing adverse effects in patients receiving Bleomycin therapy. The probability of developing lung toxicity from Bleomycin is increased in older patients receiving multiple cycles of chemotherapy, with risk potentially outweighing benefits in select patients with early-stage lymphoma and favorable prognosis. and malignant pleural effusion [1]. It is produced by Streptomyces verticillus and was first isolated by Umezawa, et al. in 1966 [2]. Its mechanism of action involves breakdown of DNA double helix by the production of free radicals, which is dependent on oxygen and iron [2]. Although dermatological adverse effects are the most observed, Bleomycin induced lung toxicity crop up in up to 10% patients which can be life menacing if not diagnosed early with mortality rate of up to 20% [1,3]. Bleomycin induced lung injury encompasses several clinical syndromes including hypersensitivity, bronchiolitis obliterans with organizing pneumonia, hypersensitivity pneumonitis which may progress to pulmonary fibrosis [3]. Several factors including older age and cumulative drug dose have been shown to increase the risk of developing pulmonary toxicity from Bleomycin [4]. The following is a case of pulmonary fibrosis following chemotherapy with Bleomycin for Stage 2B Hodgkin’s Lymphoma (HL). This case emphasizes the need for careful selection of chemotherapy regimen in older patients with Hodgkin’s lymphoma who are risk for bleomycin pulmonary toxicity and the necessity for diligent surveillance in patients with increased baseline risks for toxicity. Introduction Bleomycin is an anti-tumor antibiotic indicated in the treatment of lymphomas, germ cell tumors ISSN: 2378-3656 DOI: 10.23937/2378-3656/1410390 Adetiloye et al. Clin Med Rev Case Rep 2022, 9:390 • Page 2 of 6 • residual mass or metabolic uptake in the neck and mediastinum (Figure 1). Initial evaluation, revealed blood pressure of 127/82 mmHg, heart rate of 104 beats per minute, respiratory rate of 22 breaths per minute, SpO2 90% on room air and Temperature was 97.8 F. He had inspiratory rales bilaterally and use of accessory muscles of respiration on examination. Pertinent negatives on examination were absence of ascites, leg swelling, distended neck veins, neck mass, rales, wheezes or stridor. Complete blood count, Basic metabolic panel, procalcitonin, Pro BNP and troponin T values were unremarkable. Chest x-ray shows bilateral interstitial disease prominent at the lung bases. Computed tomography angiography of the neck and chest showed moderate subpleural thickening bilaterally with some ground glass opacity and extensive honeycombing at the lung bases suggestive of usual interstitial pattern (UIP) (Figure 2). No pulmonary embolus, mass, mediastinal, hilar or axillary adenopathy were present on CT scan. Echocardiogram was unremarkable with normal Right and left ventricular function. Sputum culture and markers of connective tissue diseases and vasculitidies were negative. A diagnosis of Bleomycin induced pneumonitis and lung fibrosis was made based on CT findings and temporal relationship with Bleomycin chemotherapy and negative infectious work up. Patient was admitted to the medical floor and started on Prednisolone at 1 mg/kg per day for 4 weeks and subsequent taper. He also received Trimethoprimsulfamethoxazole for Pneumocystis Jirovei prophylaxis while on steroids. Shortness of breath improved with steroid treatment. However, he desaturates to low 80s on SpO2 during 6 minutes’ walk test. He was discharged home one week later with supplemental oxygen during exercise. Based on negative PET and CT findings for active Hodgkin’s lymphoma, patient was chemotherapy was discontinued. In addition, patient did not receive Case Report A 64-year-old male from Bangladesh presented to the emergency department with gradual onset of exertional shortness of breath of 1 week which has progressively worsened to shortness of breath at rest. He had a history of dry cough of 1 month but denied fever, chills, pleuritic chest pain, hemoptysis, orthopnea, paroxysmal nocturnal dyspnea or leg swelling. He was diagnosed with HL Stage 2B nodular sclerosis subtype 5 months earlier after presenting to the hematology and oncology department with weight loss, low grade fever and neck mass. At that time, CT neck and chest revealed large necrotic mass on the right side of the neck with multiple enhancing lymph node in the neck, adjacent to the trachea and carina and paraesophageal region; ESR was elevated at 120 mm/hr and diagnosis was confirmed with biopsy of neck mass. At that time, he was started on ABVD regimen for treatment which consists of Adriamycin (Doxorubicin) 42.25 mg (25 mg/ m2), Bleomycin 17 units (10 units/m2), Vinblastine 10 mg (6 mg/m2) and Dacarbazine 634 mg (375 mg/m2) all on Day 1 and day 15 per cycle every 4 weeks to complete 6 cycles of treatment, with pegfilgrastim on Day 2 and Day 16 per cycle. Patient had completed 4 cycles of chemotherapy prior to onset of exertional dyspnea. He has no significant medical history prior to being diagnosed with Hodgkin’s lymphoma and denies history of cigarette smoking. He had a baseline pulmonary function test before commencement of chemotherapy which showed normal lung volumes, FEV1 and FVC were 82% and 80% of predicted values respectively and mild reduction in diffusing capacity for carbon monoxide. PET scan done at onset of exertional dyspnea and one-week prior to presentation to the emergency department showed hypermetabolic activity in the lung periphery without Figure 1: PET scan showing increases hypermetabolic activity in the periphery of the lungs. ISSN: 2378-3656 DOI: 10.23937/2378-3656/1410390 Adetiloye et al. Clin Med Rev Case Rep 2022, 9:390 • Page 3 of 6 • United States. Nodular sclerosis Hodgkin lymphoma (NSHL) is the most common subtype of classical HL, accounting for 65% to 75% of cases [9]. Unfortunately, there is still conflicting data regarding how best to prevent complications extending from potentially fatal pneumonitis to irreversible and debilitating complication of pulmonary fibrosis in patients receiving Bleomycin containing chemotherapeutic regimen without compromising treatment efficacy. This is in part due to varying trial designs and treatment endpoints. Advances in chemotherapeutic agents and radiotherapy have improved patient outcomes; however, careful staging, risk stratification and consideration for potential treatment related adverse events are required in determining optimal standard of care. Prognostication and selection of treatment modalities is based on classification of Hodgkin’s lymphoma into early-stage favorable, early-stage unfavorable, and advanced stage. Early-stage Hodgkin lymphoma refers to Ann Arbor stage I or stage II disease. According to study groups (the European Organization for the Research and Treatment of Cancer (EORTC) and the German Hodgkin Study Group), earlystage Hodgkin lymphoma is stratified into a high risk (unfavorable) group defined by any of the following: a large mediastinal mass (one third of maximum thoracic diameter), any mass of ≥ 10 cm in the largest dimension, extra-nodal disease, 3 or more nodal areas, and an ESR of > 50 mm/hr in asymptomatic patients or > 30 mm/hr in patients with B symptoms, age greater than 50 years of age, intraabdominal disease [8]. consolidative radiation therapy due to extensive lung fibrosis. Unfortunately, patient continued to experience limitation of exercise due to exertional dyspnea with modified medical research Council Scale grade 3 at 5 months follow up. Repeat Pulmonary function test at that time showed restrictive lung pattern with FEV1 and FVC 40% and 34% of predicted values respectively (Table 1).

Atherothrombosis is the leading cause of acute coronary syndrome (ACS). Spontaneous coronary artery dissection (SCAD) refers to a nonatherosclerotic lesion involving the tearing and splitting of the coronary wall. The creation of a false lumen and blockage of the true lumen generates an oxygenation mismatch in the myocardial tissue. A middle-aged woman with unremarkable medical history developed chest pain. Uptrending cardiac enzymes and electrocardiogram changes prompted further testing. Coronary angiography showed a type 3 SCAD lesion in the left circumflex artery. SCAD lacks the average risk factors of ACS and its recognition can be delayed. On the other hand, it preserves the typical presentation of ACS.

Cryptococcosis is an invasive mycosis caused by Cryptococcus sp. Its presence is described closely with immunosuppressive states. Once it has reached the body, it has shown a predilection for two sites: the lungs and the central nervous system. Nonetheless, since it has hematogenous dissemination, it can colonize and yield disease at any organ. Hence, a patient will typically present with constitutional symptoms including fever, malaise, and weight loss, associated with cough, shortness of breath, chest pain, or associated headache, drowsiness, and meningeal irritation signs. We illustrate here one of the uncommon non-pulmonary non-cerebral forms of the disease of cryptococcosis, a newly diagnosed HIV/AIDS patient with a non-bleeding colon ulcer, who lacks respiratory or central nervous system (CNS)-related symptoms but endorses non-specific gastrointestinal complaints. The first evidence of the disease was the elevated cryptococcal antigen (CrAg). The direct visualization of the spores in the biopsy confirmed the infection.

Malignancy accounts for approximately 15-20% of moderate to large pericardial effusions. Pulmonary and colon are the most common primary causes. Large pleural effusions tend to present with a less dramatic clinical picture. It is because fluids tend to build up slowly, giving enough time to the pericardial sac to accommodate it until pressure reaches a critical value causing right heart chambers to collapse. In this report, we present the case of a 51-year-old male with cardiac tamponade as the first manifestation of esophageal adenocarcinoma. The patient presented with shortness of breath and pleuritic chest pain for one week, with no other associated symptoms. Early workup indicated a cardiac tamponade likely secondary to lung malignancy. Further workup demonstrated that the primary source was an esophageal malignancy. In this setting, pericardial effusions are usually related to radiation/chemotherapy, but in rare cases, cardiac tamponade can be the first manifestation of esophageal cancer.