The Liver and Blood Coagulation: Physiology and Pathology

Roberts, Harold R.; Cederbaum, Andrew I.

doi:10.1016/s0016-5085(19)33318-9

Cited by 134 publications

(28 citation statements)

References 116 publications

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“…As factor VII has a short half-life of about three to 5j hours, plasma levels fall rapidly after hepatocellular damage (Roberts and Cederbaum, 1972). Also, plasma levels are less likely to be affected by intravascular coagulation, since factor VII is part of the extrinsic clotting system and is not destroyed by thrombin (Roberts and Cederbaum, 1972). Thus, of all the coagulation factors, factor VII is probably the most sensitive index of hepatic synthetic function.…”

Section: Discussionmentioning

confidence: 99%

Factor VII levels as a guide to prognosis in fulminant hepatic failure.

Gazzard¹,

Henderson²,

Williams³

1976

Gut

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SUMMARY Levels of clotting factors II, V, and VII were measured on admission and then daily in 12 patients with grade IV hepatic coma due to fulminant hepatic failure. Factor VII levels obtained within 36 hours of the development of grade IV coma were not of value in predicting which patients would subsequently recover consciousness. Four of the latter group had levels below 9 Y. at this time while the levels in three of the seven fatal cases were higher. Serial determinations were of more value and levels rose rapidly in those patients who ultimately made a complete recovery.The mortality in fulminant hepatic failure is closely related to the degree of encephalopathy which develops and is over 80% in those who deteriorate to deep coma-that is, grade IV encephalopathy- (Trey and Davidson, 1970). Within this fatal group there may well be cases with such extensive hepatic necrosis that recovery of the liver is impossible and the only conceivable treatment is liver transplantation. In others, recovery is a possibility provided that they can be brought through the acute phase of the illness by some means of temporary liver support. If these two groups of patients could be differentiated at an early stage, then this would clearly be of help in considering their possible management.Raised levels of oc foetoprotein indicate a good prognosis but these are found only later in the course of the illness (Karvountzis and Redeker, 1974). The galactose elimination test also appears to be of some value as a prognostic test but is relatively difficult to perform (Tygstrup et al., 1975). Recently, Dymock et al. (1975) have suggested that reductions in levels of clotting factor VII to less than 9% of normal carry a very poor prognosis. However, these results were obtained in a series of patients with hepatic encephalopathy of varying severity ranging from slight to severe, and it is well known that the prognosis is very much better in patients in whom the encephalopathy is relatively mild. The purpose of the present study therefore was to determine whether the measurement of factor VII levels would also be of value in patients with grade IV hepatic coma, in whom the problem of prediction is much more difficult.

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Section: Discussionmentioning

confidence: 99%

Factor VII levels as a guide to prognosis in fulminant hepatic failure.

Gazzard¹,

Henderson²,

Williams³

1976

Gut

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“…However, patients with severe acute liver disease or advanced chronic liver disease there often is a parenchymal defect in the synthesis of clotting factors not correctable with vitamin K. In these cases, measure ments of the prothrombin time after vitamin K repletion are useful clinically in the assessment of the severity and prognosis of the liver disease. Clotting factors may also be decreased because of increased utilization due to disseminated intravascular coagulation anq excessive fibrinolysis, which occur on occasion in various types of liver disease (139).…”

Section: Clotting Factorsmentioning

confidence: 99%

Liver Disease and Protein Needs

Mezey

1982

Annu. Rev. Nutr.

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Protein deficiency is often associated with liver disease. The principal cause of protein deficiency is decreased dietary intake. Deficiencies in digestion and absorption that are common in alcoholics contribute to protein deficiency in alcoholic liver disease. The protein requirements in most patients with compensated chronic liver disease are not different from normal, but increase during episodes of hepatocellular deterioration. An increased demand for protein after liver injury drains nitrogen from other organs such as muscle. Aromatic amino acids released from muscle in increased amounts accumulate in the circulation of patients with chronic liver disease because of their decreased hepatic metabolism. By contrast branched chain amino acids decrease in the circulation because of their preferential uptake by extrahepatic tissues. Decreases in urea synthesis in liver disease result in the accumulation of ammonia. The causes of the decrease in urea synthesis include decreases in the enzymes and substrates of the urea cycle, alterations in portal blood flow, and a decrease in total hepatic mass. The resulting increase in ammonia in association with an increased accumulation and entry of aromatic amino acids into the brain are important factors in the pathogenesis of hepatic encephalopathy. Circulating proteins synthetized by the liver, such as albumin and clotting factors, are frequently decreased in chronic liver disease. Vitamin deficiencies that are common in liver disease contribute to abnormalities of protein metabolism. Hepatic regeneration following hepatic resection or injury is adversely affected by protein and vitamin deficiencies and by alcohol ingestion.

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“…The liver is the major site of synthesis of many clotting factors (Roberts and Cederbaum, 1972) and it is not unexpected that reduced levels of these have been reported in liver disease (Owren, 1949;Hallen and Nilsson, 1964;Donaldson et al, 1969). Biochemical tests of liver function have traditionally been used to assess and monitor the progress of patients with hepatic disorders.…”

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confidence: 99%

Factor VII as a marker of hepatocellular synthetic function in liver disease.

Green¹,

Poller²,

Thomson³

et al. 1976

J Clin Pathol

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SYNOPSIS Factor VII levels have been measured in 100 patients with liver disease following parenteral vitamin K1 therapy. There was good agreement between specific factor VII measurements and the one-stage prothrombin time apart from six patients with compensated cirrhosis in whom the prothrombin time was prolonged despite the presence of normal factor VII levels. A mean activity of 58 % was found in patients with cirrhosis. Cirrhotic patients with features of hepatic decompensation had a significantly lower mean level of activity (40 %) than the 'contrast' patients with surgical obstruction of the major bile ducts (93 %). Patients with chronic active liver disease had moderate depression of factor VII levels and those with non-cirrhotic alcoholic liver damage had mean activities similar to the contrast group.Factor VII levels could not be correlated with BSP retention but there was a correlation with serum albumin concentration.It is concluded that the prothrombin time using the Quick test with a standardized thromboplastin showing good sensitivity to factor VII, eg, the Manchester reagent (BCT), provides a reliable index of coagulability in chronic liver disease, and specific factor VII assays are not indicated.The liver is the major site of synthesis of many clotting factors (Roberts and Cederbaum, 1972) and it is not unexpected that reduced levels of these have been reported in liver disease (Owren, 1949;Hallen and Nilsson, 1964;Donaldson et al, 1969).Biochemical tests of liver function have traditionally been used to assess and monitor the progress of patients with hepatic disorders. More recently, both broad-spectrum tests of blood clotting, ie, onestage prothrombin time and partial thromboplastin time and specific clotting factor measurements, particularly factor VII assays (Dymock et al, 1975), have proved of additional value in the diagnosis and assessment of liver disease. When measuring factor VII levels most workers have had to rely on combined assays such as the P and P test and Normotest (Hillenbrand and Sherlock, 1973;Henning and Yano, 1973) which are affected by deficiencies of other clotting factors, eg, factors II and X as well as factor VII. However, the availability of a naturally occurring factor VII deficient plasma in beagle dogs (Poller et al, 1971) has provided a standardized specific clotting factor VII assay. Its importance in accurately reflecting the state of hepatic function in

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The Liver and Blood Coagulation: Physiology and Pathology

Cited by 134 publications

References 116 publications

Factor VII levels as a guide to prognosis in fulminant hepatic failure.

Factor VII levels as a guide to prognosis in fulminant hepatic failure.

Liver Disease and Protein Needs

Factor VII as a marker of hepatocellular synthetic function in liver disease.

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