Hypertriglyceridemia (HTG) is the third most common cause of acute pancreatitis but it is relatively rare and requires a high level of clinic suspicion. We report a 30 years old male with no co-morbidities who is a non-alcoholic, non-smoker presented with epigastric pain associated with vomiting for two days. His vitals were stable and systemic examination was unremarkable. Serum lipase levels were elevated [7365 U/l (<40 U/l)]. Computed Tomography of the abdomen suggested acute pancreatitis with extensive peri-pancreatic inflammatory changes with no evidence of pancreatic necrosis. Serum triglycerides were found to be elevated (3450 mg/dl). A diagnosis of HTG induced acute pancreatitis was made. During evaluation he was found to be diabetic. He was treated with intravenous fluids, IV insulin infusion, and other supportive measures. He was started on statins, fenofibrate and omega 3 fatty acids. His condition improved and triglyceride levels after two days were in a declining trend and he was discharged on the same. He was currently under follow up and his serum amylase, serum lipase, serum triglycerides were normal. This case report provides insight into rare cause of acute pancreatitis-HTG which if diagnosed at the earliest can be treated promptly.

Sickle cell disease (SCD) is an inherited haemoglobinopathy that may present acutely as stroke, vaso-occlusive crisis or acute chest syndrome. Acute conditions require prompt diagnosis and intensive management to prevent morbidity and mortality. Here, we present a case of sickle cell anemia treated with therapeutic red cell exchange that manifested as acute chest syndrome. A 26 year old male who had history of high-grade intermittent fever and cough with expectoration was diagnosed as pneumonia and put on antibiotics. Peripheral smear showed sickle cells and HPLC showed HbS of 67%. we made a diagnosis of sickle cell anemia with acute chest syndrome. We treated the patient with therapeutic red cell exchange following which HbS reduced to 24% from the initial 67%. We observed significant clinical improvement suggesting red cell exchange as a useful therapeutic option for acute sickle cell anaemia.

Tumour lysis syndrome (TLS) is a serious life-threatening complication of cancer chemotherapy which is a constellation of metabolic disturbances that typically occurs during therapy of bulky, rapidly proliferative tumours. TLS is an oncological emergency that causes a significant release of phosphate, potassium, uric acid, and nucleic acids into the blood stream. Incidence of TLS in multiple myeloma is rare. Here we present a case of multiple myeloma who later developed tumour lysis syndrome in its due course which was rare. A 67-year-old male was diagnosed with Multiple myeloma on the basis of M spike, osteolytic lesions and bone marrow analysis. First cycle of chemotherapy with lenalidomide, bortezomib and denosumab was initiated. During the course of follow up he presented to our casualty with complaints of chills and rigor. Based on the biochemical abnormalities a diagnosis of tumour lysis syndrome was made. He received I.V fluids, anti-hyperkalemic measures, allopurinol. He had neutropenic sepsis and went into septic shock and died after multiple resuscitative efforts.

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