Effect of injected heparin on platelet levels in man

Davey, Matthew G; Lander, Harry

doi:10.1136/jcp.21.1.55

Cited by 53 publications

(19 citation statements)

References 20 publications

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“…crease in plasma fibrinogen during heparinization in a patient with primary biliary cirrhosis suggests minimal functional alterations of the hepatocytes which may correspond to their inconspicuous changes on electron microscopy (45). Absence of obvious increase in circulating platelets during heparinization does not militate against the concept of intravascular coagulation because heparinization by itself tends to reduce the platelet level (46)(47)(48)(49)(50).…”

Section: Resultsmentioning

confidence: 99%

Metabolism of Fibrinogen in Cirrhosis of the Liver

Tytgat¹,

Collen²,

Verstraete³

1971

J. Clin. Invest.

128

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A B S T R A C T The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 ±+10 ml/kg; plasma fibrinogen concentration 250 ±102 mg/100 ml; total plasma fibrinogen pool 118 ±59 mg/kg, representing 0.73 +0.10 of the total body pool; fibrinogen half-life 2.99 +0.59 days; fractional catabolic rate 0.34 ±0.09 of the plasma pool per day; absolute catabolic rate 39 ±20 mg/kg per day; fractional transcapillary efflux rate 0.82 ±0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 ±7 ml/kg; plasma fibrinogen concentration 284 ±71 mg/100 ml; total plasma fibrinogen pool 119 ±40 mg/kg, representing 0.72 +0.07 of the total body pool; fibrinogen half-life 4.14 ±0.56 days; fractional catabolic rate 0.24 ±0.04 of the plasma pool per day; absolute catabolic rate 28 ±9 mg/kg per day; fractional transcapillary efflux rate 0.60 ±0.26 of the plasma pool per day.A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen halflife, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 ±0.69 to 4.59 ±0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects.These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.

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Section: Resultsmentioning

confidence: 99%

Metabolism of Fibrinogen in Cirrhosis of the Liver

Tytgat¹,

Collen²,

Verstraete³

1971

J. Clin. Invest.

128

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“…A number of years ago, several investiga tors reported that heparin resulted in an acute but transient drop in the platelet count in ani mals and sometimes in humans [7][8][9][10][11][12][13], The validity of this observation has been chal lenged, and one group suggested that it might be an artifact due to in vitro aggregation of the platelets caused by the heparin [13], In summary, heparin interacts with plate lets in vitro and this interaction depends pri marily upon characteristics of the heparin preparation.…”

Section: Non-idiosyncratic (Acute) Heparin-platelet Interactionsmentioning

confidence: 99%

Heparin-induced Thrombocytopenia

Kelton¹

1986

Pathophysiol Haemos Thromb

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Heparin-induced thrombocytopenia is the most frequent and the most important idiosyncratic haematological drug reaction. It is important for several reasons: first, because heparin is used so often, and the frequency of heparin-induced thrombocytopenia is high, the risk of a hospitalized patient developing heparin-induced thrombocytopenia is high. Second, heparin-induced thrombocytopenia poses a major therapeutic dilemma for the clinician -continue the heparin and risk a worsening of the thrombocytopenia, or stop the heparin and risk extension or embolism of the thrombus. Finally, a small subset of patients with heparin-induced thrombocytopenia develop the disastrous complication of heparin-induced thrombocytopenia plus arterial thrombosis. Some of these patients die. In this review, we will summarize some of the issues concerning heparin-induced thrombocytopenia, including its frequency, the various techniques used to diagnose the condition, its pathophysiology and approaches that can be used to manage patients with heparin-induced thrombocytopenia.

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“…The Type I or non-immune mediated HIT is a transient, benign, and self-limiting form of thrombocytopenia. In Type I HIT patients, a decrease in platelet count occurs in the first five days of the therapy due to the direct agglutinating impact of heparin on platelets 9,10 .…”

Section: Ijpsr (2017) Volume 8 Issue 8 (Review Article)mentioning

confidence: 99%

“…However, the development of thrombocytopenia in immune-mediated or Type II HIT appears within 5 th to 14 th day of the initiation of heparin therapy 9,11 . In the immunologically mediated HIT condition, the antibodies are directed to heparin/platelet factor 4 (PF4) complexes that are formed during the heparin treatment 3 .…”

Section: E-mail: Drsaldallal@outlookcommentioning

confidence: 99%

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2017

IJPSR

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Effect of injected heparin on platelet levels in man

Cited by 53 publications

References 20 publications

Metabolism of Fibrinogen in Cirrhosis of the Liver

Metabolism of Fibrinogen in Cirrhosis of the Liver

Heparin-induced Thrombocytopenia

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