Hypoalbuminaemia and colonic polyps: a case of protein-losing enteropathy with cap polyposis?

Abstract

A 69-year-old woman was admitted in September 2005 dehydrated and unwell. She had a 6-month history of constipation, poor appetite and weight loss, and was hypoalbuminaemic (21 g/litre). She had initially been referred for colonoscopy in March to exclude colonic malignancy. Multiple pedunculated polyps up to the splenic flexure were seen, with histology felt to be consistent with hyperplastic polyps and mild inflammation. Her symptoms persisted, and by August she had lost 3 stone in weight. She started to experience loose stools, and repeat colonoscopy was planned. However, the bowel preparation made her feel unwell. She couldn't walk, and so presented to the acute medical take. The patient looked pale and dehydrated. Her chest was clear, with a diffusely tender abdomen. Bowel sounds were present, and there were no palpable masses. Bloods showed a corrected calcium of 1.58 mmol/litre. Fluid resuscitation and calcium replacement was started. A malignant process was queried. Liver function tests showed a low albumin of 21 g/litre but were otherwise unremarkable. A computed tomography scan of the abdomen and chest were normal. A gastroscopy showed mild oesophagitis with Candida in the mid and lower oesophagus, gastritis in the antrum of the stomach with heavy Helicobacter pylori growth, and a normal duodenum. Biopsies showed no evidence of coeliac disease or giardia. The patient's albumin fell to 8 g/litre. A 24-hour urine protein collection was 0.46 g, excluding nephrotic syndrome. Nasogastric feeding was commenced. Gut hormones showed a modestly elevated chromogranin A (164 pmol/litre) and gastrin (307 pmol/ litre) but were not diagnostic of a neuroendocrine tumour. Amyloid was queried and the original colonic biopsies re-examined. This was not found, but cap polyposis was suggested. The patient failed to improve and died 15 days after admission. Post mortem found the distal large bowel to contain multiple dark sessile polyps, looking like slugs, on exaggerated mucosal folds (Figure 1). The histological findings comprised elongated, tortorous and distended crypts, with evidence of inflammation and a 'cap' of granulation tissue, confirming cap polyposis. In addition the patient had a right haemothorax. This was caused by a dissection in the pulmonary artery, with evidence of atheroma identified. The right ventricle was hypertrophic, with the lungs showing multiple haemorrhagic infarcts. These changes suggested pulmonary hypertension. Whether this was related to the cap polyposis was unclear. A reasonable explanation is that the patient had showered off pulmonary emboli from a deep vein thrombosis (DVT) for some time, secondary to immobility associated with her poor state of health. This was supported by a right calf DVT identified at post mortem. The dissection of the pulmonary artery was probably secondary to the low protein state and pulmonary artery hypertension.