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The Sheila Sherlock Hepatobiliarypancreatic and Liver Transplantation Unit, Royal Free Hospital
December 7, 2007
Further evidence for hypercoagulability in Primary Biliary Cirrhosis
To the Editor:
It is with great interest that we read the description by Dr Lee and colleagues (1) of two sisters with primary biliary cirrhosis (PBC) whose liver function improved after anticoagulant treatment with warfarin.
Previously a study from our group reported the presence of marked hypercoagulability using thromboelastography (TEG) (a test that monitors haemostasis as a dynamic process, as compared to the static measurement provided by INR, aPTT, platelet and fibrinogen levels) in 13 of 47 patients with PBC (28 %) and 9 of 21 patients with primary sclerosing cholangitis (43 %) (2). Only 6 of these patients had lower than normal values of protein S, C, or antithrombin III, while differently to the two cases reported by Dr Lee and colleagues none of our patients had activated protein C resistance.
We recently confirmed the presence of hypercoagulability in patients with PBC and PSC on TEG by finding a statistically significant difference between 10 patients with PBC/PSC, 21 healthy volunteers and 20 patients with cirrhosis of non cholestatic origin (Unpublished data "“ revised manuscript submitted for publication). In particular, there was a markedly increased platelet aggregability in the PBC/PSC group as compared to the patients with non PBC/PSC cirrhosis (as shown by a ma value of 69.350Â±5.817 in the PBC/PSC group as compared to 55.415Â±9.465 in the non PBC/PSC group), pointing towards a possible role for platelets in the hypercoagulability in these patients. An increased platelet function together with a marked systemic inflammatory activity in this group of patients was also reported by another group (3). This hypercoagulability or other reasons may explain why patients with PBC tolerate variceal bleeding fairly well and have a much more favourable prognosis than patients with alcoholic cirrhosis (4;5).
The full implication and pathogenesis of the hypercoagulable state in patients with PBC and PSC still needs to be fully elucidated, but the interesting finding of a possible therapeutic implication by Dr Lee and colleagues encourages further study in this direction.
Ulrich Thalheimer, M.D. 1,2 Andrew K Burroughs, FRCP 1
1The Sheila Sherlock Hepatobiliarypancreatic and Liver Transplantation Unit Royal Free Hospital Pond Street NW3 2QG London - UK
2Dipartimento di Scienze Biomediche e Chirurgiche UniversitÃ¡ di Verona Policlinico G.B. Rossi Piazzale L.A. Scuro 37121 Verona, Italy
(1) Lee HM, Amin M, Kaplan MM, Herlihy EF. Reversible hepatic decompensation in primary biliary cirrhosis due to hypercoagulability. Ann Intern Med. 2007;147:675.
(2) Ben-Ari Z, Panagou M, Patch D, Bates S, Osman E, Pasi J et al. Hypercoagulability in patients with primary biliary cirrhosis and primary sclerosing cholangitis evaluated by thrombelastography. J Hepatol. 1997;26:554-59.
(3) Pihusch R, Rank A, Gohring P, Pihusch M, Hiller E, Beuers U. Platelet function rather than plasmatic coagulation explains hypercoagulable state in cholestatic liver disease. J Hepatol. 2002;37:548 -55.
(4) Biagini, M. R., Guardascione, M., McCormick, A. P., Raskino, C., McIntyre, N., and Burroughs, A. K. Bleeding varices in PBC and its prognostic significance. Gut 31, A1209. 1990.
(5) Gores GJ, Wiesner RH, Dickson ER, Zinsmeister AR, Jorgensen RA, Langworthy A. Prospective evaluation of esophageal varices in primary biliary cirrhosis: development, natural history, and influence on survival. Gastroenterology. 1989;96:1552-59.
Correction: Benzodiazepines and Hip Fractures. Ann Intern Med. 2007;147:675–676. doi: 10.7326/0003-4819-147-9-200711060-00025
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Published: Ann Intern Med. 2007;147(9):675-676.
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