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1.  Alcoholic ketoacidosis with multiple complications: a case report 
Emergency Medicine Journal : EMJ  2007;24(11):776-777.
Alcoholic ketoacidosis is a poorly diagnosed medical emergency usually identified in chronic alcohol misusers following an abrupt cessation or reduction of alcohol consumption. A high index of suspicion should be maintained by acute physicians as response to treatment is rapid with complete resolution of metabolic derangements. Complications are usually the result of not instituting the correct treatment or not addressing associated conditions. We describe a case of alcoholic ketoacidosis with multiple complications at presentation.
doi:10.1136/emj.2006.041822
PMCID: PMC2658323  PMID: 17954832
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.
doi:10.3748/wjg.v16.i28.3541
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.
doi:10.3748/wjg.v16.i17.2129
PMCID: PMC2864838  PMID: 20440853
Hepcidin; Hepcidin assay; Hepcidin in biological fluids; Hepcidin in ascitic fluid; Bile; Exudates; Antimicrobial peptides
4.  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.
doi:10.1159/000118035
PMCID: PMC3075166  PMID: 21490838
Hepcidin; Prohepcidin; Lead poisoning; Porphyrins; Abdominal pain; Sideroblastic anaemia

Results 1-4 (4)