{"id":858,"date":"2015-02-16T08:20:21","date_gmt":"2015-02-16T08:20:21","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=858"},"modified":"2017-01-05T07:08:05","modified_gmt":"2017-01-05T07:08:05","slug":"derangement-of-lipid-profile-in-stroke-patients","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol2no2\/derangement-of-lipid-profile-in-stroke-patients\/","title":{"rendered":"Derangement of Lipid Profile in Stroke Patients"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Stroke is a syndrome characterized by acute onset of neurologic deficit that persists for at least 24 hours, reflects focal involvement of the CNS.\u00a0 Amongst the leading neurologic disorder stroke is the 3rd<\/sup> most cause of death, disability, and health-care expenditure.7<\/sup><\/p>\n

Strong correlations between plasma lipids concentrations and the risk of stroke have never been clearly established.\u00a0 The present study attempts to associate this; specifically showing the derangement caused in the lipid profile patterns in the CVA patients and also the effect of stroke on this derangement (on the 1st<\/sup> day, i.e. of admission after an acute onset,\u00a0 and on 7th<\/sup> day of stroke).\u00a0 Hyperlipidemia is an independent risk factor for ischemic stroke (Gorelick & B etal (1997)).\u00a0 The present study establishes the role of lipids as a factor in stroke risk.<\/p>\n

Materials and Methods<\/strong><\/p>\n

Clinical material:\u00a0 The present work on,\u00a0 \u201cDerangement of Lipid Profile in Stroke Patients\u201d, was done in the Department of Medical Biochemistry, in association with the Department of Medicine, Gandhi Medical College, Hamidia Hospital, Bhopal, Madhya Pradesh.\u00a0 The present study comprised of 25 patients of CVA (20 males & 05 females), which were randomly selected from the emergency wards of medicine department, and 25 healthy subjects (15 males & 10 females), during the year 2004-05.\u00a0 All were in the age group 30-55 years and 56 & above years.<\/p>\n

Inclusion criteria:\u00a0 All types of stroke patients, particularly cerebrovascular accident (CVA), were included irrespective of etiology.<\/p>\n

Exclusion criteria:\u00a0 Patients suffering from diabetes, hypertension, myocardial infarction, and cases of unconsciousness, fever, & vomiting.<\/p>\n

Methods:\u00a0 Biochemical parameters included serum TC, HDL-c, TG, LDL-c, & VLDL-c which were estimated colorimetrically using appropriate wavelength filters. The 12-14 hr fasting samples (approximately 5 ml of whole blood) of patients were taken within 24 hrs of admission, i.e. on the 1st<\/sup> day and then again on the 7th<\/sup> day during the period of hospitalization.\u00a0 For invitro quantitative determination of activity of lipid fractions in serum following kit methods were implemented.\u00a0 Kits were manufactured by Sigma diagnostics (India) Pvt. Ltd., Baroda.\u00a0 The data were statistically analyzed using \u2018t-test\u2019.<\/p>\n\n\n\n\n\n\n\n\n
Lipid Parameter<\/td>\nMethod<\/td>\nWavelength<\/p>\n

(nms)<\/td>\n

Formula<\/td>\nNormal Value (mgs\/dL)<\/td>\n<\/tr>\n
TC<\/td>\nEnzymatic (CHE, CHO, & POD)<\/td>\n505 (green)<\/td>\nA (T)<\/u> * 200<\/sub><\/p>\n

A (S)<\/p>\n

 <\/td>\n

130 \u2013 250<\/td>\n<\/tr>\n
HDL-c<\/td>\nPTA Precipitation<\/p>\n

& Enzymatic Method<\/td>\n

505 (green)<\/td>\nA (T)<\/u> * 100<\/sub><\/p>\n

A (S)<\/p>\n

 <\/td>\n

30 \u2013 70<\/p>\n[Males =<\/p>\n

30 \u2013 63]\n[Females = 35 \u2013 75]<\/td>\n<\/tr>\n

TG<\/td>\nGPO-POD Enzymatic Method<\/td>\n520<\/td>\nA (T)<\/u> * 200<\/sub><\/p>\n

A (S)<\/p>\n

 <\/td>\n

70 \u2013 170<\/td>\n<\/tr>\n
LDL-c<\/td>\nFriedewald\u2019s Formula [Friedewald WT, etal (1972)] 4<\/sup><\/td>\n—<\/td>\nTC \u2013 HDL-c \u2013 TG\/5 (mg%)<\/td>\nUpto 110<\/td>\n<\/tr>\n
VLDL-c<\/td>\n—<\/td>\n—<\/td>\nTG\/5<\/td>\n< 40<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Results<\/strong><\/p>\n

Control Group \u2013Values of lipid profile in control group (table 1)<\/p>\n

Table 1: Mean values \u00b1 SD of lipid profile in control group.<\/strong><\/p>\n\n\n\n\n\n\n\n\n
Biochemical<\/p>\n

Parameter<\/td>\n

Range [Max-Min]\n

(mgs\/dL)<\/td>\n

Mean \u00b1 SD<\/td>\n<\/tr>\n
TC<\/td>\n195 \u2013 136<\/td>\n159.36 \u00b1 15.865<\/td>\n<\/tr>\n
HDL-c<\/td>\n74 \u2013 40<\/td>\n54.12 \u00b1 8.931<\/td>\n<\/tr>\n
TG<\/td>\n261 \u2013 55<\/td>\n110.8 \u00b1 51.873<\/td>\n<\/tr>\n
LDL-c<\/td>\n169 \u2013 61<\/td>\n86.29 \u00b1 22.678<\/td>\n<\/tr>\n
VLDL-c<\/td>\n52.2 \u2013 11<\/td>\n22.152 \u00b1 10.493<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Morbid Group \u2013<\/p>\n

Mean \u00b1 SD TC was reported to be 159.36 \u00b1 15.865 mgs\/dL while the other parameters included HDL-c, TG, LDL-c, & VLDL-c which were 54.12 \u00b1 8.93, 110.8 \u00b1 51.87, 86.29 \u00b1 22.7, & 22.152 \u00b1 10.5 mgs\/dL respectively.<\/p>\n

Morbid Group \u2013Mean Values \u00b1 SD in Morbid Group on the Day of Admission (table 2)<\/p>\n

Table 2: Mean values \u00b1 SD in morbid group on the day of admission.<\/span><\/strong><\/p>\n\n\n\n\n\n\n\n\n
Biochemical<\/p>\n

Parameter<\/td>\n

Range [Max-Min]\n

(mgs\/dL)<\/td>\n

Mean \u00b1 SD<\/td>\n<\/tr>\n
TC<\/td>\n398 \u2013 143<\/td>\n190.24 \u00b1 52.24*<\/td>\n<\/tr>\n
HDL-c<\/td>\n88 \u2013 25<\/td>\n38.68 \u00b1 11.8***<\/td>\n<\/tr>\n
TG<\/td>\n280 \u2013 110<\/td>\n147.32 \u00b1 46.81*<\/td>\n<\/tr>\n
LDL-c<\/td>\n254 \u2013 85<\/td>\n122.48 \u00b1 36.23***<\/td>\n<\/tr>\n
VLDL-c<\/td>\n56 \u2013 20<\/td>\n29.48 \u00b1 9.439**<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

* p < 0.01 (significant); ** p < 0.02 (significant); & *** p < 0.001 (highly significant) [on comparing control group values vs values of 1st<\/sup> day of admission of morbid group]; df = 48.<\/p>\n

 <\/p>\n

Mean \u00b1 SD values of TC, HDL-c, TG, LDL-c, & VLDL-c was reported to be 190.24 \u00b1 52.24, 38.68 \u00b1 11.8, 147.32 \u00b1 46.81, 122.48 \u00b1 36.23, 29.48 \u00b1 9.439, respectively.\u00a0 On statistical analysis of the above data versus the control group highly significant (p < 0.001) values were found for HDL-c & LDL-c whereas for TC (p < 0.01), TG (p < 0.01), & VLDL-c (p < 0.02) the t-value were found to be significant.<\/p>\n

Mean Values \u00b1 SD in Morbid Group on 7th<\/sup> Day of Admission (table 3)<\/strong><\/p>\n

Mean \u00b1 SD values of TC, HDL-c, TG, LDL-c, & VLDL-c, on 7th<\/sup> day of admission in morbid group, were found to be decreased to 158.16 \u00b1 33.65, 35.68 \u00b1 7.93, 128.88 \u00b1 38.505, 97.36 \u00b1 20.122, 25.64 \u00b1 7.739, respectively.\u00a0 On statistical analysis between 1st<\/sup> day values versus 7th<\/sup> day, significant relationship was obtained for TC (p < 0.02), TG (p < 0.05), & LDL-c (p < 0.01), whereas for HDL-c & VLDL-c p was insignificant (p > 0.05).<\/p>\n

Discussion<\/strong><\/p>\n[A] Control Group \u2013 Values of lipid profile in control group<\/p>\n

TC was reported at a value of (max \u2013 min) 195 \u2013 136 mgs\/dL [159.36 \u00b1 15.865] which was in accordance with average mean TC values of various studies conducted by Gardner (1929).5<\/sup> Other parameters included mean HDL-c, TG, LDL-c, & VLDL-c (54.12 \u00b1 8.93, 110.8 \u00b1 51.87, 86.29 \u00b1 22.7, & 22.152 \u00b1 10.5) respectively, which were in accordance with the study conducted by Kiran Hasija & Hardeep K Bagga (2005).6<\/sup><\/p>\n[B.]\u00a0 Morbid Group \u2013 Mean Values \u00b1 SD in Morbid Group on the Day of Admission<\/p>\n

Lindenstrom, etal (1994) showed that the association between plasma cholesterol and risk of non-hemorrhagic event is not log linear; only relatively high cholesterol concentrations are associated with significantly increased risk.3<\/sup>\u00a0 Some more studies found positive association with ischemic stroke {Quiziblash N, etal (1991)}10<\/sup> which was in accordance with the present study (p < 0.01) when compared with control group.\u00a0\u00a0 The predictive power of low HDL-c concentrations in serum for CAD, independently of other risk factors, has been well demonstrated in numerous epidemiological studies involving populations [Assmann & Schulte (1992)].1<\/sup>\u00a0 The present study demonstrated mean HDL-c value of 38.68 \u00b1 11.8 (ranged from 88 \u2013 25 mgs\/dl) on admission.\u00a0 A highly significant variation was found between HDL-c and stroke (p < 0.001).\u00a0\u00a0 Pasty BM (2004) reported only a marginally significant association between LDL-c and ischemic stroke, however in the present study it was reported to be highly significant (p < 0.001).9<\/sup>\u00a0 Shieh SM, etal (1985) reported significantly higher VLDL-c levels (p < 0.01) while in the present study the variation was significant with mean value of 29.48 \u00b1 9.439 mgs\/dL (max \u2013 min = 56 \u2013 20 mgs\/dL).13<\/sup>\u00a0 Accoding to Taggart H, etal (1979) HDL-c values were significantly lower in stroke subjects aged < 65 years.14<\/sup>\u00a0 Rossner S, etal (1978) demonstrated normal mean TC concentrations which was the result of slight increase in VLDL-c and a concomitant HDL-c reductions (age < 55).11<\/sup>\u00a0 According to Mendez I, etal (1987) both serum TC and TG levels are initially decreased in patients aged 50 \u2013 69 years with cerebral infarction, whereas only cholesterol is decreased in patients aged 60 \u2013 69 years with TIA (on comparing 1st<\/sup>, 7th<\/sup>, and after 3 months values).8<\/sup>\u00a0 Scherle CE, etal (1998) demonstrated no difference in levels of TC, HDL-c, LDL-c, & VLDL-c (between 3 weeks and 6 months after the initial stroke); average age being 64.5 years.12<\/sup> Forty five years or older for men and 55 years or older for women have been categorized as on the risk factors for CHD in addition to LDL-c.<\/p>\n

Mean Values \u00b1 SD in Morbid Group on 7th<\/sup> Day of Admission<\/strong><\/p>\n

All the values showed a considerable decrease on the 7th<\/sup> day of stoke.\u00a0 The values of HDL-c, & VLDL-c, though were found to be decreased on 7th<\/sup> day, but didn\u2019t show a very much compatible difference.\u00a0 Therefore it could be concluded that TC, TG, & LDL-c tends to fall on 7th<\/sup> day whereas no significant conclusion could be drawn out for values of HDL-c (p > 0.05) & VLDL-c (p > 0.05).\u00a0 Hence it can be said that stroke causes particular derangement in the values of lipid profile, which tends to decrease as the severity of stroke decreases.<\/p>\n

Comparison of 1st<\/sup> Vs 7th<\/sup> day\u00a0 <\/strong><\/p>\n

The present study demonstrated a considerable decrease in values on 7th<\/sup> day as compared to 1st<\/sup> day.\u00a0 Mean TC value was 158.16 \u00b1 33.65 (278 \u2013 124), were lower on 7th<\/sup> day and were in accordance with the study by Mendez I, etal (1987).\u00a0 According to Mendez I, etal serum TC, LDL-c in cerebral infarction patients (50 \u2013 69 years) were lowest on 7th<\/sup> day; intermediate on 1st<\/sup> day, and highest at 3 months, whereas VLDL-c and HDL-c changed a little; however, the present study demonstrated HDL-c and VLDL-c to be insignificant.\u00a0 The 1st<\/sup> day mean fasting HDL-c of cerebral infarction patients was significantly lower in subjects aged 50 \u2013 59 years than in those aged 60 \u2013 69 years (23 \u00b1 3 Vs 42 \u00b1 5 mgs\/dl).\u00a0 Similarly, according to Aull S, etal (1996) TC and LDL-c levels of group B patients (levels determined within 49 \u2013 168 hours after an acute event) were significantly lower than group A levels (12 \u2013 48 hours).2<\/sup>\u00a0 The present study demonstrated significant association for both TC and LDL-c when 1st<\/sup> day was statistically analyzed versus 7th<\/sup> day.<\/p>\n

The present study demonstrated a significant variation for TG (p < 0.05) when 1st<\/sup> day values were statistically correlated with 7th<\/sup> day values.\u00a0 V Hachinski, etal (1996) demonstrated that elevated TG and LDL-c levels were significantly independent risk factors in patients with proven athero-thrombotic cerebrovascular disease manifesting as stroke or TIA.15<\/sup>\u00a0 Plasma TC was significantly higher among patients with thromboembotic strokes and TIAs than among control subjects.\u00a0 This is in accordance with the present study.\u00a0 Therefore, the study showed specific derangement in all lipid parameters (due to the effect of stoke) with all parameters found to be decreased on the 7th<\/sup> day, which is in accordance with the study by Aull S, etal (1996); Mendez I, etal (1987), which demonstrated that lipids tend to temporarily fall after an acute stroke.\u00a0 The phenomenon is probably not strictly related to inadequate nutrition that might result from the conservative early management of dysphagia because the same phenomenon has been seen in patients with many acute neurologic conditions.\u00a0 Thus to conclude, in the followup study a significant variation was seen for LDL-c, TC, and TG when compared with values on 1st<\/sup> day of admission.\u00a0 These variations could be the result of conservative treatment, the patients underwent for the proceeding seven days.\u00a0 However, no significant change was seen in the values of VLDL-c and HDL-c.<\/p>\n

Conclusions<\/strong><\/p>\n

All the values showed a considerable decrease on the 7th<\/sup> day as stroke severity decreased.<\/p>\n

Therefore, all the lipid parameters were found to be proportionally linked with stroke severity.\u00a0 These variations could be the result of conservative treatment, the patients underwent for the proceeding 7 days.\u00a0 Therefore, stroke was found to cause a significant derangement in all the lipid parameters while comparing the 1st<\/sup> day Vs 7th<\/sup> day values (which was shown to be increased on the 1st<\/sup> day with considerable decrease on 7th<\/sup> day).<\/p>\n

TC, TG, and LDL-c should be considered to be significant risk factors for stroke.\u00a0\u00a0 VLDL-c and HDL-c values couldn\u2019t draw out any significant conclusion.\u00a0 However a larger study with more population of similar clinical background is needed to be planned to establish the role of low HDL-c as a risk factor in stroke; also predicting the role of stroke in causing the derangement of lipid profile.<\/p>\n

References<\/strong><\/p>\n

    \n
  1. Assmann G, Schulte H.\u00a0 Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary artery disease (the PROCAM experience).\u00a0 Amm J Cardiol<\/em> 1992;70<\/strong>:733-737.<\/li>\n
  2. Aull S, Lalouschek W, Schnider P, Sinzinger H, Uhl F, Zeiler K.\u00a0 Dynamic changes of plasma lipids and lipoproteins in patients after transient ischemic attack or minor stroke.\u00a0 Am J Med<\/em> Sep 1996;101<\/strong>(3):291-8.<\/li>\n
  3. E Lindenstrom etal.\u00a0 Influence of total cholesterol, high density lipoprotein cholesterol, & triglycerides on risk of cerebrovascular disease:\u00a0 The Copenhagen City heart study.\u00a0 BMJ<\/em> 1994;309<\/strong>:11-15.<\/li>\n
  4. Friedewald WT, Levy RI, Fredrickson DS.\u00a0 Estimation of the concentration of LDL-c in plasma, without use of preparative ultracentrifuge.\u00a0 Clin Chem<\/em> 1972;18<\/strong>: 499-502.<\/li>\n
  5. Gardner JA & Gainsborough H.\u00a0 Studies on the cholesterol content of normal human plasma.\u00a0 Biochem Jr<\/em> 1929;21<\/strong>:130-140.<\/li>\n
  6. Kiran Hasija & Hardeep K Bagga.\u00a0 Alterations of serum cholesterol and serum lipoprotein in breast cancer of women.\u00a0 Ind J of Clin Biochem<\/em> 2005;20<\/strong>(1):62.<\/li>\n
  7. Li SC, Schoenberg BS, Wang C, et al. Cerebrovascular disease in the People\u2019s Republic of China: epidemiologic and clinical features. Neurology <\/em>1985;35<\/strong>:1708-13.<\/li>\n
  8. Mendez I, Hachinski V, and Wolf B.\u00a0 Serum lipids after stroke.\u00a0 Neurol<\/em> Mar 1987;37<\/strong>(3):507-11.<\/li>\n
  9. Pasty BM, Anderson M, Kronmal RA, Tracy RP, etal.\u00a0 The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality:\u00a0 The Cardiovascular Health Study.\u00a0 J Am Geriatr Soc<\/em>. Oct 2004;52<\/strong> (10):1639-47.<\/li>\n
  10. Quiziblash N, Josh L, Warlow C, Mann J.\u00a0 Fibrinogen and lipid concentrations as risk factors for transient ischemic attacks and minor ischemic strokes.\u00a0 BMJ <\/em>1991;303<\/strong>:605-9.<\/li>\n
  11. Rossner S, Kjellin KG, Mettinger KL, Siden A, Soderstrom CE.\u00a0 Normal serum cholesterol but low HDL-cholesterol concentrations in young patients with ischemic cerebrovascular disease.\u00a0 Lancet <\/em>1978;1<\/strong>:577-9.<\/li>\n
  12. Scherle CE, Nasiff A, Begueria RA, Perez-Nellar J, etal.\u00a0 Lipids and lipoproteins in a group of patients with ischemic cerebrovascular disease.\u00a0 Rev Neurol<\/em> Nov 1998;27<\/strong>(159):804-8.<\/li>\n
  13. Shieh SM, Shen MM, Tsai WJ, Shiuan LR, etal.\u00a0 Serum lipids and lipoprotein abnormalities in patients with thrombotic stroke \u2013 with exploring the protective role of HDL subfractions.\u00a0 Proc Natl Sci Counc Repub China B<\/em>. Oct 1985;9<\/strong>(4): 298-304.<\/li>\n
  14. Taggart H, Stout RW.\u00a0 Reduced high density lipoprotein in stroke:\u00a0 relationship with elevated Triglyceride and hypertension.\u00a0 Eur J Clin Invest<\/em> Jun 1979;9<\/strong>(3): 219-21.<\/li>\n
  15. V. Hachinski, C. Graffagnino, M. Beaudry, G. Bernier, C. Buck, A. Donner, J.D.\u00a0 Spence, G. Doig, and B.M. Wolfe.\u00a0 Lipid and stroke:\u00a0 a paradox resolved.\u00a0 Archives of Neurology<\/em> Apr 1996;53<\/strong>(4).<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction Stroke is a syndrome characterized by acute onset of […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[7],"tags":[],"class_list":["post-858","post","type-post","status-publish","format-standard","hentry","category-vol2no2"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/858","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=858"}],"version-history":[{"count":4,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/858\/revisions"}],"predecessor-version":[{"id":13164,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/858\/revisions\/13164"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=858"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=858"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=858"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}