Introduction: Strongyloidiasis is endemic in the tropical and subtropical regions. Clinical manifestations of the dis-ease can range from asymptomatic eosinophilia in an immunocompetent host to a wide range of presentations in immunocompromised patients. Failure to consider the diagnosis of strongyloides infection, especially Strongyloides hyperinfection syndrome, is a major contributor of high mortality rate in such cases. Case Description: We report a case of 60 years old gentleman who was admitted to Sarawak General Hospital for a left subtrochanteric femur pathological fracture and the diagnosis of multiple myeloma was made in the same setting. He was started on treat-ment for multiple myeloma which includes high dose steroids. During his course of admission, he was diagnosed with hospital-acquired pneumonia was subsequently initiated with broad-spectrum antibiotics. Despite being exten-sively treated with multiple courses of broad-spectrum antibiotics, he deteriorated clinically, with eventual respirato-ry failure requiring ventilator support and ICU admission. A diagnosis of strongyloides hyperinfection syndrome was made after an incidental discovery of larvae in his sputum, which was later confirmed with stool sample. He was given a one-week course of albendazole 400mg twice daily and clinical improvement was observed. A repeated stool sample also demonstrated clearance of the parasites. Conclusion: This case highlights the need for clinical sus-picion of strongyloides hyperinfection syndrome in cases of unresolved pneumonia, especially for patients with risk factors of underlying immune-deficiency state. Preventive steps such early detection and eradication of strongyloides infection should be undertaken prior to initiation of immuno-suppressive therapy.
A 54-year-old Chinese man presented with ascites for 2 weeks. He had a preceding 2-year history of intermittent dysphagia, lethargy and general malaise. Blood investigations revealed leucocytosis with eosinophilia of 26.5%, whereas paracentesis showed turbid fluid with high protein content (45 g/L) and a high white blood cell count of 5580/µL, predominantly eosinophils (90%). An incidental assay of vitamin D showed a very low level of 13.5 ng/mL. No other cause of ascites was found. Gastroscopy was normal except for duodenitis. However, biopsies from lower oesophagus confirmed the presence of eosinophilic infiltration. Following vitamin D replacement, the patient experienced marked improvement in symptoms of dysphagia within 2 weeks and no recurrence of ascites after 3 months. The reason for the patient's vitamin D deficiency remains unclear. The marked improvement in the patient's health indicates a causative role of vitamin D deficiency in causing eosinophilic esophagogastroenteritis and associated eosinophilic ascites.