Unmasking the Unusual: Cryptococcal Pericarditis in a Patient with Liver Failure - a Rare Occurrence.

BACKGROUND Cryptococcosis is an invasive fungal infection caused by Cryptococcus species complex. C. neoformans is one of the pathogenic species within the genus. C. neoformans infections often present as an opportunistic infection in severely immunocompromised individuals. Infection of the pericardium in the setting of liver failure is uncommon. We present a case of cryptococcal pericarditis in a patient with liver failure. CASE REPORT A 47-year-old man with a past medical history of psoriatic arthritis, and alcohol use disorder presented to the emergency department with a 2-week history of progressively worsening generalized weakness, malaise, and yellowish skin changes. Physical examination revealed scleral icterus, jaundiced skin, and ascites. Initial laboratory workup revealed thrombocytopenia, transaminitis (aspartate transaminase (AST) level of 502 IU/L, alanine transaminase (ALT) level of 82 IU/L), hyperbilirubinemia (total bilirubin of 15.7 mg/dL), International Nationalized Ratio (INR) of 3.6, and lactic acidosis (lactic acid of 11.7 mmol/L). The patient developed encephalopathy and acute hypoxic respiratory failure requiring intubation. A bedside point-of-care cardiac ultrasound, performed following intubation, revealed a pericardial effusion without signs of tamponade. This finding was later confirmed by a formal transthoracic echocardiogram. Percutaneous pericardiocentesis was performed, and the pericardial fluid culture revealed the presence of C. neoformans. Human immunodeficiency virus (HIV) tests were negative. The patient received antifungal therapy. Due to his poor prognosis, he was transitioned to comfort care and eventually died. CONCLUSIONS This case report describes an unusual presentation of acute liver failure complicated by cryptococcal pericarditis, emphasizing the importance of considering atypical fungal infections in such patients.

The First Occurrence of Angioedema After Discontinuation of Angiotensin-Converting Enzyme Inhibitor.

Angioedema is one of the dreaded side effects of angiotensin-converting enzyme (ACE) inhibitors. It has been well established in the literature and the timing of onset is variable from months to years after initiation of therapy. Patients remain at risk of recurrence of angioedema even after discontinuation of the drug if they developed it once while on the drug. While only recurrences of ACE inhibitor-induced angioedema are described in the literature, our patient did not develop angioedema while being on the drug and had the first occurrence of angioedema one month after the medication was discontinued. We argue that since our patient did report an ACE inhibitor-related dry cough, this case emphasizes the strength of the relation between the two common side effects of the ACE inhibitors. This favors that among the risk factors that predispose individuals to develop angioedema, ACE inhibitor-associated cough is a major one. Although the mechanism of ACE inhibitor-related cough is poorly understood, bradykinin seems to be the common culprit mediator for these two side effects. Hence, clinicians need to be aware of this potential threat and be cautioned when they witness an ACE inhibitor-related cough.