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Cirrhosis phosphate





High serum glyceraldehyde-3-phosphate dehydrogenase levels in

10/22/2014
04:32 | Author: Caitlin White

Phosphate transport
High serum glyceraldehyde-3-phosphate dehydrogenase levels in

High serum glyceraldehyde-3-phosphate dehydrogenase levels in patients with liver cirrhosis. Shibuya A, Ikewaki N. We have developed a mouse monoclonal.

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We have developed a mouse monoclonal antibody against glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and established a form of semi-quantitative latex particle aggregation as a first-screening technique for determining serum levels of GAPDH. Focusing on chronic liver diseases, we measured serum GAPDH in 213 patients to clarify its clinical significance. However, the levels were significantly increased in patients with cirrhosis (P<0.001). Elevated serum GAPDH was also confirmed in a patient with cirrhosis associated with hepatocellular carcinoma using Western blotting analysis. The mechanism(s) of serum GAPDH elevation remains unclear, but one possible source is increased leakage of the GAPDH molecule into the serum from damaged cirrhotic hepatocytes underlying hepatocarcinogenesis or chronic inflammation. Logistic regression analysis indicated that the presence of hepatocellular carcinoma and a high gamma-globulin level were closely associated with high GAPDH levels (P=0.006 and 0.011, respectively). Serum GAPDH levels were similar in healthy control subjects, patients who were hepatitis B or C virus carriers, or with chronic hepatitis.

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Reduced renal phosphate threshold concentration in alcoholic

12/21/2014
02:04 | Author: Evan Martin

Sodium phosphate chemical formula
Reduced renal phosphate threshold concentration in alcoholic

Reduced renal phosphate threshold concentration in alcoholic cirrhosis. Adler AJ, Gudis S, Berlyne GM. Hypophosphatemia is frequently found in patients with.

We conclude that hypophosphatemia in alcoholic cirrhosis is associated with a low Tm/GFR and that this may be related to hypomagnesemia. The median serum Mg was 2.0 mg/dl. Simultaneous mid-morning serum and urine samples were obtained and analyzed for creatinine, Ca, PO4, and Mg. Median serum PO4 was 2.75 mg/dl, including 8 patients who were hypophosphatemic (serum PO4 less than 2.5 mg/dl). 24 patients with alcoholic cirrhosis were studied. The median Tm/GFR was 2.3 mg/dl; 13 of the patients had values below 2.5 mg/dl. All had normal renal function. Serum magnesium was significantly correlated with Tm/GFR (p less than 0.05). Of these, the first two would be expected to be associated with a high threshold concentration (Tm/GFR) and the last with a low Tm/GFR. Hypophosphatemia is frequently found in patients with alcoholic cirrhosis, and its postulated causes include inadequate phosphorus (PO4) intake, reduced gastrointestinal absorption, and inappropriate PO4 loss in the urine. There was a significant correlation between serum PO4 and Tm/GFR (p less than 0.001). The median serum Ca was 8.5 mg/dl and did not correlate with Tm/GFR.

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High serum glyceraldehyde-3-phosphate - ResearchGate

10/20/2014
12:44 | Author: Devin Garcia

Phosphate transport
High serum glyceraldehyde-3-phosphate - ResearchGate

Publication » High serum glyceraldehyde-3-phosphate dehydrogenase levels in patients with liver cirrhosis.

Logistic regression analysis indicated that the presence of hepatocellular carcinoma and a high gamma-globulin level were closely associated with high GAPDH levels (P=0.006 and 0.011, respectively). The mechanism(s) of serum GAPDH elevation remains unclear, but one possible source is increased leakage of the GAPDH molecule into the serum from damaged cirrhotic hepatocytes underlying hepatocarcinogenesis or chronic inflammation. Focusing on chronic liver diseases, we measured serum GAPDH in 213 patients to clarify its clinical significance. However, the levels were significantly increased in patients with cirrhosis (P<0.001). Serum GAPDH levels were similar in healthy control subjects, patients who were hepatitis B or C virus carriers, or with chronic hepatitis. ABSTRACT We have developed a mouse monoclonal antibody against glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and established a form of semi-quantitative latex particle aggregation as a first-screening technique for determining serum levels of GAPDH. Elevated serum GAPDH was also confirmed in a patient with cirrhosis associated with hepatocellular carcinoma using Western blotting analysis.

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Cirrhosis Associated with Pyridoxal 5-Phosphate Treatment of

8/19/2014
02:12 | Author: Evan Martin

Sodium phosphate chemical formula
Cirrhosis Associated with Pyridoxal 5-Phosphate Treatment of

We report the case of an 8-year-old boy with pyridoxamine 5′-phosphate oxidase (PNPO) deficiency. He developed seizures at 24 h of age.

We report the case of an 8-year-old boy with pyridoxamine 5′-phosphate oxidase (PNPO) deficiency. However, at 8 years of age, there is persistent evidence of hepatic fibrosis and early portal hypertension. Routine blood tests at this time showed significantly deranged liver function tests (LFTs). The PLP dose was weaned to 50 mg/kg/day before episodes of encephalopathy recurred. Concurrent with the reduction of his PLP dose, LFTs showed improvement. A wedge liver biopsy showed early cirrhosis with marked elevation of pyridoxal and pyridoxic acid levels in the liver sample. We hypothesise that hepatic toxicity due to PLP or its degradation products is the cause of cirrhosis in this boy. Genetic testing identified compound heterozygous mutations in the PNPO gene. He developed seizures at 24 h of age that were refractory to standard anticonvulsant therapy and a trial of pyridoxine but responded to pyridoxal phosphate (PLP) at 28 days of life. Until further evidence becomes available, we would suggest that people with PNPO deficiency are treated with the minimum dose of PLP required to prevent episodes of encephalopathy. Management of encephalopathic episodes required escalation of PLP dose to 100 mg/kg/day by 2 years of age. Despite extensive investigation, no cause other than PLP therapy could be identified for the cirrhosis.

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Primary biliary cirrhosis (PBC) - Geeky Medics

6/18/2014
04:00 | Author: Caitlin White

Sodium phosphate chemical formula
Primary biliary cirrhosis (PBC) - Geeky Medics

Primary Biliary Cirrhosis (PBC) is characterised by damage to interlobular diagnosed after incidental finding of increased alkaline phosphate.

Primary Biliary Cirrhosis (PBC) is characterised by damage to interlobular bile ducts by chronic inflammation, which results in progressive cholestasis, cirrhosis & portal hypertension. It is different from Primary Sclerosing Cholangitis(PSC) in that it only affects intra-hepatic bile ducts, unlike PSC which affects intra & extra-hepatic ducts.

Ursodeoxycholic acid - improves cholestasis & LFT’s – no effect on outcome.

Lewis Potter Doctor. Internet Junkie. Gadget Fanatic.

Prevalence is <4 in a 100,000.

Often asymptomatic & diagnosed after incidental finding of increased alkaline phosphate Pruritis Lethargy Jaundice Hyper-pigmentation of skin Xanthelasma Xanthomata Splenomegaly Osteoporosis.

Used to stage the disease.

ERCP - not used as often anymore as antibodies+ liver function tests are diagnostic.

Free medical revision notes crafted for medical students including OSCE guides, clinical skills videos, quizzes and more!

Codeine Phosphate – diarrhoea Osteoporosis prevention.

Granulomas around bile ducts progressing to cirrhosis Colestyramine – pruritis.

Recurrence of disease with graft is 17% at 5 years.

End stage disease – Bilirubin >100 Intractable pruritis.

↑ AST & ALT - mildly raised Late disease ↑ Bilirubin ↓ Albumin ↑ Prothrombin time.

The peak age for presentation is 50 years old Thyroid disease Rheumatoid arthritis Sjogrens syndrome Systemic sclerosis Membranous glomerulonephritis.

Osteomalacia - softened bones – malabsortion of fat soluble vitamins (A,D & K).

Hypergammaglobulinemia - especially IgM.

USS - exclude extra-hepatic cholestasis.

Published on October 18th, 2010| by Lewis Potter.

Graft failure is rare.

Tags: Autoimmunity, Hepatology.

Fat soluble vitamin prophylaxis – Vitamin A,D & K.

Complications of Cirrhosis & Portal Hypertension: - Ascites - Variceal haemorrhage - Hepatic encephalopathy ↑ Alkaline Phosphatase ↑ Gamma GT.

Female to male ratio is approximay 9:1.

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