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Plasma fibrinogen levels in stroke.
Correspondence Address:
Plasma fibrinogen levels were estimated in 56 patients of stroke, admitted in the hospital within 24 hours of symptoms. The levels were found to be raised significantly (531.73 +/- 74 mg%) compared to those of the age and sex matched control group (445.78 +/- 92.28 mg%). When the levels in stroke group with one risk factor were compared to those of individuals with comparable control group with same risk factor, a significant difference was observed in hypertensive, smokers, alcoholics and atherosclerotic stroke groups, which indicates that the observed rise is related to phenomenon of stroke rather than the associated risk factors. However, the rise observed in hypertensive stroke group (554.26 +/- 47.08 mg%) is significantly more (p. less than 0.01) than that occurring for nonhypertensive stroke group (497.82 +/- 93.12 mg%) indicating that the presence of hypertension does contribute to the rise.
In urban India, stroke accounts for 1% mortality in all hospital admissions, 4% in all medical cases and about 20% in all the disorders of central nervous systems[2]. The pathogenic factors in stroke viz. atherosclerosis and thrombosis are the same as for myocardial infarction. In the latter disease, significant increase in plasma fibrinogen level has been detected, which has a correlation with severity of myocardial damage[3]. It was therefore of interest to measure the plasma fibrinogen levels in patients with acute stroke and also to investigate whether these levels increase if the patient has additional risk factors viz. hypertension, diabetes, smoking or alcohol consumption.
Fifty-six patients of stroke (32 males, 24 females; age range 32-88 years, mean age 57.54 + 9.93 years) admitted within 24 hours of development of symptoms. Patients having evidence of renal failure (uremia), infection, inflammatory disease, active hepatic disease, severe dehydration and a history of myocardial infarction or surgery within the preceding 3 months were excluded from this study as all these factors are known to increase plasma fibrinogen levels[4],[6]. Of the 56 patients included in the study 34 were hypertensive, 14 were diabetic, 20 were smokers and 15 were alcoholic. No risk factor was detected in 9 patients except for the age. After admission, detailed history was obtained to find out any of -the abovementioned risk factors and thorough general and systemic examinations were carried out. In addition to routine biochemical investigations and diagnostic interventions (CSF examination, CT scanning) blood was collected from patients in fasting state to estimate plasma fibrinogen levels. Tyrosine method was used for estimation[8]. The levels of fibrinogen were compared with those obtained from a group of patients not suffering from stroke (control group). The control group comprised 40 patients (24 males, 16 females; age range 35-90 years, mean 56.48 + 11.26 yrs). This group matched with the study group with respect to age and sex. In this group 17 patients were hypertensive, 12 diabetic, 12 smokers and 15 alcoholics. In 8 patients, no risk factor was detected except for age.
The levels of plasma fibrinogen estimated in the control and stroke group are depicted in [Table - 1]. In the latter group significant elevation of plasma fibrinogen levels was observed. Nine patients (6 males, 3 females) from this group died during the hospital stay. However, plasma fibrinogen levels of these patients at the time of admission (559.56 + 79.75 mg%) were comparable to those of survivors. (526.36 + 71.65 mg%). [Table - 2] illustrates the plasma fibrinogen values in the control and stroke groups in presence of additional risk factor viz., hypertension, diabetes, smoking, alcohol, ageing. The plasma fibrinogen levels in patients with stroke, having hypertension as an additional risk factor were found to be significantly higher (p < 0.001) than those who had hypertension but no stroke (hypertensive control group). Within group comparison (between hypertensive-stroke and non-hypertensive stroke) revealed that the levels are higher in patients with hypertension. No significant difference in plasma fibrinogen levels was found when diabetic stroke group was compared with diabetic controls and non-diabetic stroke group. The mean plasma fibrinogen level in diabetic control (478.92 + 74.52 mg%) was higher than the normal range i.e. 200 - 400 mg% established in our laboratory. In stroke patients who were smokers, the levels of plasma fibrinogen were significantly higher (p < .05) compared to those of smokers from control group. However no significant difference was observed between smokers and non-smokers from control group. Similar results were obtained for alcoholic stroke patients, alcoholic control group and non-alcoholic stroke patients. When the patients with stroke who had no risk factor apart from age were compared with the matched controls, a significant rise in plasma fibrinogen level (510.56 + 86.75 mg%) was observed (p < 0.05).
Atheroselerosis is the basic pathogenic process in the development of stroke. By using immunofluorescent techniques Sadoshima and Tanaka[5] have shown deposition of fibrinogen in the intimas of cerebral arteries and have indicated its role in atherosclerotic process. In a long term follow up study (13.5 years’ duration), carried out to determine risk factors for cardiovascular disease and stroke Wilhelmsen et al[7] discovered that plasma fibrinogen is a significant predictor of stroke. However, this study does not give any information about the level of plasma fibrinogen at the time of stroke or in patients who have additional risk factors[1] responsible for atherosclerosis. These lacunae are overcome in the present study. A significant rise in plasma fibrinogen level was observed in all the patients with stroke compared to that in the control group who not respect to age and sex but also with respect to presence of risk factors for atherosclerosis. This acute rise in fibrinogen levels may be either a direct cause for stroke (which alters blood viscosity and promotes coagulation and thrombus formation) or an acute phase reaction secondary to ischaemia and/or necrosis of brain tissue. No significant difference was observed in the plasma fibrinogen levels of patients who died during hospital stay and those who survived, which means that estimation of this parameter will be of no prognostic value. When plasma fibrinogen levels in stroke group with one risk factor were compared with the control group with same risk factor, a significant difference in the levels was found (viz. in hypertensive, smokers, alcoholic and atherosclertoic groups). This indicates that the rise observed in patients with stroke is related to the phenomenon of stroke rather than the associated risk factors. However, diabetic control group did not differ from the stroke group with respect to fibrinogen values, suggesting that raised fibrinogen level may also be one of the features of diabetes. But both these groups did not differ from the non-diabetic stroke group, which also showed high fibrinogen values. The plasma fibrinogen levels in hypertensive patients of stroke were higher than observed in non-hypertensive population with stroke. This means that in this group hypertension also contributes to increase in plasma fibrinogen levels. Thus we conclude that plasma fibrinogen levels are abnormal in patients with acute stroke and this rise is more if the patients are hypertensives.
We wish to thank the Dean, Seth GS Medical College and KEM Hospital and the Head of Dept. of Medicine for permitting us to publish this paper.
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