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1.  Severe Refractory Coeliac Disease with Response Only to Parenteral Nutrition 
Case Reports in Gastroenterology  2014;8(2):297-303.
Refractory coeliac disease (RCD) is characterised by recurrent or persistent malabsorptive symptoms and villous atrophy, despite strict adherence to a gluten-free diet for at least 6 months and where other causes of malabsorption including malignancy have been excluded. There is limited evidence and guidance on the effective management of these patients. We describe a case of severe RCD in our hospital, with symptoms controlled effectively only by total parenteral nutrition (TPN). This 68-year-old woman initially presented to the clinic with persistent non-bloody diarrhoea and vomiting. A diagnosis of coeliac disease was confirmed with a positive tissue transglutaminase assay and histology. A strict gluten-free diet was ineffective and she represented 6 months later with 13 kg weight loss (16.7%), ongoing abdominal pain and diarrhoea, with bowels opening 16 times a day. She was oedematous, had an albumin of 12 g/l and required hospital admission. She was treated for pancreatic insufficiency and presumptively for small bowel bacterial overgrowth with no resolution of symptoms. We ruled out infectious causes and investigated for small bowel malignancy; all results were negative. Small bowel enteroscopy showed ulcerative jejunitis. She was given 5 days of TPN, following which her symptoms improved and albumin normalised. This was sustained with symptom resolution and weight gain seen at follow-up. TPN successfully and rapidly induced remission in this case. Thus, a short period of TPN should be considered as a potential component of management in patients with severe RCD.
PMCID: PMC4241638  PMID: 25473387
Refractory; Coeliac disease; Parenteral nutrition
2.  Hepcidin levels in hereditary hyperferritinemia: Insights into the iron-sensing mechanism in hepatocytes 
AIM: To study the role of hepcidin in hereditary hyperferritinemia cataract syndrome (HHCS).
METHODS: Six patients from two families with HHCS, confirmed by genetic analysis showing A to G mutation at position +40 in the L-ferritin gene, were recruited to undergo serum hepcidin and prohepcidin measurements using radioimmunoassay and enzyme linked immunoassay, respectively, and measurements were compared with levels in serum from 25 healthy volunteers (14 females), mean age 36 ± 11.9 years.
RESULTS: The serum hepcidin and prohepcidin levels in patients with HHCS were 19.1 ± 18.6 and 187 ± 120.9 ng/mL, respectively. Serum ferritin was 1716.3 ± 376 μg/L. Liver biopsy in one patient did not show any evidence of iron overload. Serum hepcidin and prohepcidin values in healthy controls (HCs) were 15.30 ± 15.71 and 236.88 ± 83.68 ng/mL, respectively, while serum ferritin was 110 ± 128.08 μg/L. There was no statistical difference in serum hepcidin level between the two cohorts (19.1 ± 18.6 ng/mL vs 15.30 ± 15.71 ng/mL, P = 0.612) using two-tailed t-test.
CONCLUSION: Serum hepcidin levels in HHCS patients is similar to that in HCs. Our study suggests that circulating ferritin is not a factor influencing hepcidin synthesis and does not have a role in the iron-sensing mechanism in hepatocytes.
PMCID: PMC2909553  PMID: 20653062
Hereditary hyperferritinemia; Hereditary hyperferritinemia cataract syndrome; Hepcidin; Hepcidin assay; Iron-sensing mechanism; Iron responsive element; Ferritin
3.  Presence of hepcidin-25 in biological fluids: Bile, ascitic and pleural fluids 
AIM: To examine body fluids such as ascitic fluid (AF), saliva, bile and pleural effusions for the presence of hepcidin using a novel radioimmunoassay (RIA).
METHODS: Serum samples were collected from 25 healthy volunteers (mean age: 36 ± 11.9 years, 11 males, 14 females). In addition bile was obtained from 12 patients undergoing endoscopic retrograde cholangiopancreatography (mean age: 66.9 ± 16.7 years, M:F = 5:7). Saliva was collected from 17 healthy volunteers (mean age: 35 ± 9.9 years, M:F = 8:9). Pleural and AF were collected from 11 and 16 patients [(mean age: 72 ± 20.5 years, M:F = 7:4) and (mean age: 67.32 ± 15.2 years, M:F = 12:4)], respectively. All biological fluid samples (serum, exudative and transudative fluids) were tested for the presence of hepcidin-25 molecule using RIA.
RESULTS: Hepcidin-25 was detected in all biological fluids tested. The mean ± SD hepcidin-25 in serum was 15.68 ± 15.7 ng/mL, bile 7.37 ± 7.4 ng/mL, saliva 3.4 ± 2.8 ng/mL, exudative fluid 65.64 ± 96.82 ng/mL and transudative fluid 14.1 ± 17.8 ng/mL.
CONCLUSION: We provide clear evidence that hepcidin-25 is present in bile, saliva, pleural and ascitic fluids. Hepcidin is likely to play a role here in innate immunity.
PMCID: PMC2864838  PMID: 20440853
Hepcidin; Hepcidin assay; Hepcidin in biological fluids; Hepcidin in ascitic fluid; Bile; Exudates; Antimicrobial peptides
4.  Acute Appendagitis Presenting with Features of Appendicitis: Value of Abdominal CT Evaluation 
Case Reports in Gastroenterology  2008;2(2):191-195.
We report a case of acute appendagitis in a patient who presented initially with typical features of acute appendicitis. The diagnosis of acute appendagitis was made on pathognomonic signs on computed tomography (CT) scan. Abdominal pain is a common surgical emergency. CT is not always done if there are clear features of acute appendicitis. The rare but important differential diagnosis of acute appendagitis must be borne in mind when dealing with patients with suspected acute appendicitis. A CT scan of the abdomen may avoid unnecessary surgery in these patients.
PMCID: PMC3075141  PMID: 21505556
Appendagitis; Appendicitis; CT scan
5.  Prohepcidin Levels in Refractory Anaemia Caused by Lead Poisoning 
Recent research evidence suggests a central role for hepcidin in iron homeostasis. Hepcidin is a hormone synthesized in the liver. Hepcidin is also thought to play a vital role in the pathogenic mechanism of anaemia in patients with inflammation or chronic disease. A 38-year-old female who presented with recurrent abdominal pain was found to have raised urinary porphyrins and a blood lead level of 779 μg/l. Her haemoglobin level was 8.3 g/dl. Her MCV was normal. Serum ferritin, B12 and folate were normal. Her serum prohepcidin level was 2,489 ng/ml (normal <450 ng/ml). To our knowledge, this is the first report of raised prohepcidin levels in a patient with anaemia of chronic disease resulting from lead poisoning.
PMCID: PMC3075166  PMID: 21490838
Hepcidin; Prohepcidin; Lead poisoning; Porphyrins; Abdominal pain; Sideroblastic anaemia

Results 1-5 (5)