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Question answered:11/09/07 Warning! this question is over two years old.

The literature suggests there may be a link between hepatitis or liver cirrhosis and brain haemorrhage.

 

In a case-control study, Karibe et al examined hepatitis C virus (HCV) as a risk factor for intracerebral haemorrhage. They report:

 

“Hepatitis C Virus (HCV) infection was investigated as a risk factor for intracerebral hemorrhage (ICH) by HCV antibody screening in 462 patients with ICH and 462 control patients with cerebral infarction matched by age and sex… HCV infection was significantly more frequent in patients with ICH than controls (8.7% vs 3.5%, P< 0.01). ICH patients with HCV infection had significantly higher L-alanine:2-oxoglutarate aminotransferase level (P< 0.001), lower cholesterol level (P< 0.05), lower platelet count (P< 0.05), and longer prothrombin time (P< 0.01) than ICH patients without HCV infection, although most of these values were within the normal range.”

 

They add:

 

“These results demonstrate that HCV infection is a risk factor for spontaneous ICH. Subclinical clotting disorder and/or vessel wall friability resulting from hypocholesteremia may be associated with ICH in patients with HCV infection.” [1]

 

Aiba et al report on their study examined the prevalence of HCV in cases of spontaneous intracerebral haemorrhage:

 

“Patients under 30 and over 79 years of age were omitted from this study, and those with complicating malignancies and undergoing anti-coagulation or antiplatelet therapy were also excluded. The prevalence of HCV was significantly higher among the ICH group as a whole (19 out of 139 cases, p < 0.05) especially in the non-hypertensive group (7 out of 29 cases, p < 0.01), compared to the control group (7 out of 140 cases without ICH). The non-hypertensive HCV-positive group (7 cases) had significantly higher GOT and GPT levels, prolonged PT and a-PTT values, and lower platelet counts, compared to the hypertensive HCV-negative group (74 cases). The HCV antibody titers did not differ among the HCV-positive groups. The results suggest that chronic hepatitis due to HCV infection is a major risk factor for spontaneous intracerebral hemorrhage, especially in non-hypertensive patients.” [2]

 

A second Japanese study investigated liver function and ICH. The Medline abstract of this study reads:

 

“The purpose of this study was to investigate the relationship between mild degrees of liver dysfunction and spontaneous intracerebral hemorrhage (ICH) from the hemostatic standpoint. A detailed study of hemostatic systems was made in 462 patients with ICH. To compare ICH with the other cerebrovascular diseases, data from 120 patients with subarachnoid hemorrhage and 114 others with cerebral infarction were reviewed …

 

The incidence of liver dysfunction and alcohol consumption in patients with ICH was significantly (P < 0.05) higher than in patients with subarachnoid hemorrhage and in those with cerebral infarction. Hematoma volume, mortality rate, and past alcohol consumption in patients with ICH significantly increased with worsening severity of liver dysfunction. Although almost all hemostatic parameters became worse with increasing severity of liver dysfunction, they changed within the normal limits. Platelet aggregability and alpha 2-antiplasmin activity in patients with liver dysfunction were remarkably deteriorated beyond normal limits.

 

 In conclusion, liver dysfunction associated with alcohol consumption appears to be an important factor in the deterioration of the clinical status of patients with ICH and may be one of the causative factors in the development of ICH. Although mildly impaired hemostatic systems may be partially responsible for these adverse effects of liver dysfunction on ICH, it seems probable that nonhemostatic mechanisms are attributed to the effects.” [3]

 

 Finally, a study dating from 1979 presented data from 500 cases of adult ICH:

 

“The systematic pathological study of 500 patients with intracranial hemorrhages (ICH) [341 (68 P. 100) CEREBRAL HEMORRHAGES (C.H.); 119 (24 p. 100) meningeal hemorrhages (M.H.); 39 (7,8 p. 100) subdural hematomas (S.H.) and, at last, one extradural hematoma] has been practiced. ..High blood pressure is the main etiological factor in C.H. This is confirmed by the statistical comparison between the incidence of this factor in our material and in the whole French population. However, nearly 50 p. 100 of ICH occuring in normotensive patients are C.H. The incidence of cirrhosis is much higher in our study than in other reports from the literature. The frequently associated high blood pressure does not seem to enhance the incidence of CH in patients with liver cirrhosis. Although this last factor can be found alone, its real etiological importance in CH cannot be assessed on account of the lack of data concerning the incidence of liver cirrhosis in the French population…” [4]

References
1. Karibe H, Niizuma H, Ohyama H et al. . Hepatitis C virus (HCV) infection as a risk factor for spontaneous intracerebral hemorrhage: hospital based case-control study. : J Clin Neurosci. 2001 Sep;8(5):423-5. (http://www.hubmed.org/display.cgi?uids=11535009)
2. Aiba T, Watanabe T, Koike T et al. [C-type hepatitis in spontaneous intracerebral hemorrhage]. No To Shinkei. 1996 Dec;48(12):1116-9. (http://www.hubmed.org/display.cgi?uids=8990478)
3. Fujii Y, Takeuchi S, Tanaka R et al. Liver dysfunction in spontaneous intracerebral hemorrhage. Neurosurgery. 1994 Oct;35(4):592-6. (http://www.hubmed.org/display.cgi?uids=7808601)
4.  Boudouresques G, Hauw JJ, Meininger V et al. [Neuropathological study of adult intracranial hemorrhage. General data in 500 cases]. Rev Neurol (Paris). 1979 Mar;135(3):197-210. (http://www.hubmed.org/display.cgi?uids=493782).

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