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During the ongoing pandemic, there have been varying presentations of coronavirus disease 2019 (COVID-19) infection, with the concern that patients who are immunosuppressed (due to underlying medical conditions and/or therapies) are at higher risk of severe disease. We report the case of an elderly renal transplant recipient working in a long-term health care facility who was being monitored by weekly surveillance testing and tested positive for COVID-19 by polymerase chain reaction (PCR) testing, despite having no clinical symptoms. He recovered with supportive care, despite being on multiple long-term immunosuppressant drugs and having multiple comorbidities. Additionally, it was found that he did not mount an antibody response, when he tested negative by serologic testing. Through this case, we wish to highlight the unique clinical scenario of asymptomatic patients who may have an underwhelming immune response to COVID-19, but may nevertheless be an important source of dissemination. We further discuss the probable mechanism of such asymptomatic presentations in immunosuppressed patients, while reinforcing the importance of self-isolation of COVID-19 patients (particularly in asymptomatic health care workers).

We present a case of a 48-year-old male who presented with worsening pleuritic chest pain for 2 h. He also complained of fever, malaise, headache and severe neck pain. Electrocardiogram (ECG) showed ST segment elevation in leads I, II, aVL and V5 with PR elevation and ST depression in aVR. On admission, troponin-I was 14.8 ng/mL. Based on ECG changes, elevated troponin and family history of early coronary artery disease, the patient was emergently taken to cardiac catheterization lab. Angiography showed non-obstructive coronaries, mild hypokinesis of mid inferior and anterolateral wall with ejection fraction (EF) of 40-45%. Based on above presentation and angiography findings, the diagnosis of acute myopericarditis was made. He was started on colchicine and ibuprofen. The other workup to determine etiology of myopericarditis was negative as shown below. Given the history of fever, headache and worsening neck pain, we also became suspicious of meningitis. Lumbar puncture was performed which was negative. On the day of admission, he was found to have blasts on complete blood count and peripheral smear. Bone marrow biopsy and flow cytometry confirmed the diagnosis of acute myeloid leukemia (AML). He received induction and salvage therapy. Repeat bone marrow confirmed complete remission and normal cytogenetics. Although pericardial or myocardial biopsies are unavailable for our patient, in the absence of other causes, it does appear that his acute myopericarditis was associated with AML.

A 70-year-old male presented with hematuria and bruising of arms and legs for the last three days. He also complained of urinary frequency and hesitancy and weight loss of 40 pounds over a span of four months. Initial blood tests showed prothrombin time (PT) of 25.1 seconds, international normalized ratio (INR) of 2.5, partial thromboplastin time (PTT) of 43.9 seconds, fibrinogen of 60 mg/dl, fibrin degradation products (FDP) of more than 20 μg/ml, and platelets of 88,000/μl. The impression was disseminated intravascular coagulation (DIC). A search was initiated to determine the underlying etiology precipitating DIC. Due to urinary symptoms and weight loss, prostate-specific antigen (PSA) was ordered. PSA was elevated at 942 μg/dl. Computed tomography (CT) of the abdomen and pelvis without contrast showed an enlarged prostate with mass effect on the bladder base, left-sided hydronephrosis, and numerous enlarged pelvic lymph nodes. A bone scan of the whole body showed increased sclerosis of the L3 vertebral body. There was a concern for metastatic prostate cancer precipitating DIC. On first admission, our patient’s DIC was stabilized with FFP and cryoprecipitate transfusions. He refused chemotherapy, and degarelix was not economically feasible. Accordingly, he was started on androgen deprivation therapy (ADT), bicalutamide, and leuprolide as an inpatient, pending the tissue biopsy. The patient refused a prostate biopsy. A bone marrow biopsy was performed which confirmed metastatic prostate adenocarcinoma. The patient was stable for discharge with a plan for outpatient chemotherapy. Subsequently, he was lost to follow-up with the oncology. Six months after the initial presentation, he was readmitted with hematuria. Repeat PSA worsened to 1,970 μg/dl. Blood work was consistent with acute DIC. He refused chemotherapy again. So, he was restarted on ADT. However, his hematuria and DIC panel were worsening. He was emergently started on docetaxel as an inpatient (after patient agreement). Within three days of starting chemotherapy, his hematuria resolved and DIC panel showed consistent improvement.