A Case of Podostroma Cornu-Damae Intoxication Induced Pancytopenia and Skin Desquamation: Successful Treatment with Granulocyte Colony Stimulation Factor (G-CFS)

Podostroma cornu-damae is a rare species of fungus belonging to the Hyocreaceae family. Its fruit body is highly toxic, as it contains trichothecene mycotoxins. The morphology is similar to that of immature Ganoderma lucidum, making identification difficult for non-experts. We experienced such a case of a 56- year-old male who picked and consumed podostroma cornu-damae, and consumed. Later that day, he developed digestive system symptoms, including nausea, vomiting, and abdominal pain. He presented to the emergency room (ER), there were no abnormal physical findings, symptoms improved after gastric lavage, and the patient voluntarily discharged himself on the same day. The following day, as the symptoms gradually deteriorated, he was admitted via the ER. He was presented with severe pancytopenia, alopecia, desquamation of skin, and acute renal failure. He recovered without any complications after conservative care, antibiotics therapy, and granulocyte colony stimulating factor administration. The most commonly reported complications of podostroma cornu-damae intoxication were reported pancytopenia, infection, disseminated intravascular coagulation, acute renal failure, etc. since Prevention is especially important because its toxicity can be lethal and there is no particular treatment to date, prevention is especially important. Promotion and education for the public are needed.

A Case of Pleural Effusion and Pulmonary Edema Caused by Calcium Channel Blockers in a Patient of Systemic Hypertension

Calcium channel blockers (CCBs) are very popular drugs to lower blood pressure (BP) without significant side effects. A 72-year-old man admitted for uncontrolled hypertension. He had history of hypertension, atrial fibrillation with slow ventricular response, angina, abdominal aortic aneurysm, and stage 3 chronic kidney disease. He had taken several anti-hypertensives, such as amlodipine 5 mg, perindopril 8 mg, and indepamide 1.5 mg. To control BP, nifedipine 120 mg was added. Then pulmonary edema and pleural effusion was developed. Echocardiography showed preserved left ventricular ejection fraction and mild mitral regurgitation. Fluid restriction and high dose furosemide did not cease pleural fluid accumulation. Thus a total of 4 times of thoracentesis were done and all fluid analyses revealed transudate. We thought that pleural effusion and pulmonary edema was induced by CCBs and discontinued the drugs. He recovered quickly and finally discharged in a stable condition.