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Lanthanum carbonate is a phosphate binder that is used to reduce serum phosphate levels in patients with end-stage renal disease (ESRD). Lanthanum forms insoluble lanthanum phosphate complexes that are supposed to pass through the gastrointestinal (GI) tract unabsorbed. Phosphate binders have been reported to deposit in the GI tract and can cause mucosal injury. There are few case reports of GI bleeding associated with phosphate binder deposits. This case report presents a patient with iron deficiency anaemia secondary to biopsy-proven lanthanum deposits in the upper GI tract. There were no overt signs of active GI bleeding. Patient’s anaemia improved with discontinuation of the phosphate binder. Lanthanum could be a hidden cause of resistant anaemia among patients with ESRD through asymptomatic GI blood loss.

Polycystic liver disease is the most common extrarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD). Hepatic cysts are typically incidental findings, with occasional complications including cyst haemorrhage, infection and rupture. In contrast to the typically benign course of polycystic liver disease, we present a rare case of fatal decompensated liver failure in a patient with ADPKD. This is a case of a 58-year-old man with end-stage renal disease on haemodialysis presenting with new-onset ascites and decompensated liver failure following bilateral nephrectomy. Cirrhosis in ADPKD is a late manifestation of the disease, but it should be considered in the perioperative risk of patients with ADPKD.

A 71-year-old woman with no chronic medical problems presented to the emergency room with a 24-month history of chronic non-productive cough, malaise, increasing fatigue and weight loss. On physical examination, she had significant cervical and axillary lymphadenopathy with no organomegaly. She was diagnosed with chronic lymphocytic leukaemia (CLL) due to her lymphocyte count of 1789.4×10(9)/L on admission. A few days after hospitalisation, she developed respiratory failure requiring intubation. A chest X-ray showed interstitial markings. The abnormally high number of mature lymphocytes could have caused leucostasis in the lungs of this patient with CLL.

Cholecystokinin (CCK) and gastrin stimulate growth of pancreatic cancer. Although down regulation of gastrin inhibits growth of pancreatic cancer, the contribution of endogenous CCK to tumor growth is unknown. The purpose of this study was to evaluate the role of endogenous CCK on autocrine growth of pancreatic cancer. Pancreatic cancer cell lines were analyzed for CCK mRNA and peptide expression by real time RT-PCR and radioimmunoassay, respectively. The effect of endogenous CCK on growth was evaluated by treating cancer cells with CCK neutralizing antibodies and by down regulating CCK mRNA by RNAi. Wild type pancreatic cancer cells expressed significantly lower CCK mRNA and peptide levels than gastrin. Neither treatment of pancreatic cancer cells with CCK antibodies nor the down regulation of CCK mRNA and peptide by shRNAs altered growth in vitro or in vivo. Conversely, when gastrin mRNA expression was down regulated, the same cells failed to produce tumors in spite of having sustained levels of endogenous CCK. Pancreatic cancer cells produce CCK and gastrin; however, the autocrine production of gastrin is more important for stimulating tumor growth.