RESUMEN
Birt-Hogg-Dubé syndrome (BHD) is a rare genetic disorder caused by germline mutations in the tumor suppressor folliculin gene (FLCN). This condition is characterized by benign skin hamartomas, pulmonary cysts, spontaneous pneumothorax, and an increased risk for developing kidney tumors which range from benign oncocytomas to malignant renal cell carcinomas including chromophobe, clear cell, or papillary subtypes. We describe two cases of BHD with different initial presentations. Patients underwent genetic testing and an FLCN mutation was identified, confirming the diagnosis. Through this case series, we aim to highlight the importance of recognizing key manifestations of BHD whether alone or in combination, followed by genetic testing and counseling and the need for regular follow-ups with surveillance imaging tests to detect renal cancer early on.
RESUMEN
Amantadine, which is known for its antiviral activity, is presently used as therapy for Parkinson's disease. Adverse effects, such as cardiac arrhythmias, have been described in patients after ingestion of amantadine. Here, we present a patient who suffered a cardiac arrest following ingestion of a low dose of amantadine. A 71-year-old man was admitted to the emergency department for a witnessed cardiac arrest. He had developed an upper respiratory tract infection the preceding week and was prescribed 100 mg of amantadine. Within half an hour of taking the first dose, the patient collapsed. He was found to be in asystole by emergency medical services, and advanced cardiac life support protocols were initiated, including cardiopulmonary resuscitation and intubation for airway protection. However, he sustained multiple recurrences of cardiac arrest, and despite all resuscitation efforts, the patient expired.
RESUMEN
A 26-year-old male with a past medical history of intravenous opioid abuse was admitted with the diagnosis of double valve infective endocarditis and methicillin-resistant Staphylococcus aureus bacteremia. Imaging, excluding the head, was indicative of systemic arterial embolization, as abscesses had developed in the retroperitoneum and prostate. There was evidence of splenic infarct, and the presence of extensive pulmonary infiltrates indicative of showering septic foci from the heart. Antibiotic therapy was started and a transesophageal echocardiogram demonstrated mitral and tricuspid valve vegetations with a preserved ejection fraction. Fortunately, the valvular repair was successful and artificial valves were not needed. The patient had an uncomplicated postoperative course in the intensive care unit and was transferred back to the ward in stable condition. He remained on the ward for six weeks due to his unfunded status until his antibiotic course and physical rehabilitation were completed.
RESUMEN
Many drugs are known to potentially cause liver injury; however, only a few reports investigate the association between levofloxacin and acute liver failure (ALF). The case describes a 65-year-old man who was admitted with primary diagnoses of cerebrovascular accident (CVA) and acute coronary syndrome (ACS) who developed an upper respiratory tract infection for which he was started on levofloxacin. Following its administration, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) increased more than 100-fold above the upper limit of normal. Over the next 24 hours, AST peaked at 9334 U/L, ALT at 4525 U/L, prothrombin time to 24.6 seconds, international normalized ratio (INR) to 2.22, and serum ammonia to 157 µmol/L. The patient developed signs and symptoms of decompensated liver disease, namely hepatic encephalopathy (HE). Levofloxacin was discontinued immediately, and evidence-based treatment per society guidelines from The American Association for the Study of Liver Diseases consisting of IV n-acetylcysteine as well as lactulose and rifaximin was initiated. Such medical management resulted in clinical resolution of his ALF, but he had a poor overall prognosis and eventually succumbed to critical illness.