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October2013 Vol.50 Issue:      4 Table of Contents
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Plasma Gelsolin Level as a Predictive Factor for Ischemic Stroke Outcome

Sabah M. Lotfy1, Abdullah M. Sarhan1, Wafaa S. Mohamed1,

Hanaa H. El-Said2, Hoda A. Hagrass2

Departments of Neurology1, Clinical Pathology2, Zagazig University; Egypt



ABSTRACT

Background: Several biomarkers have been studied in ischemic stroke. Plasma gelsolin is a recent inflammatory stroke biomarker. Objective: The aim of this study was to determine whether plasma gelsolin level was altered in ischemic stroke patients and its ability to predict stroke outcome in these patients. Methods: This study was conducted on 50 patients with first-ever ischemic stroke and 30 healthy volunteers. Clinical and laboratory assessments were done to the patients and controls. After 3 months we divided our surviving patients into 2 groups according to modified Rankin Scale; group 1 included patients with good prognosis and group 2 included patients with bad prognosis and we compared between the 2 groups clinically, radiologically and as regarding baseline plasma gelsolin level. Results: We found that plasma gelsolin level was decreased significantly in the patients than controls. When we compared between good and bad prognosis groups we found that plasma gelsolin level was decreased significantly in the bad prognosis group and when we study the correlation of plasma gelsolin with other parameters we found that plasma gelsolin level was correlated significantly with National Institute of Health Stroke Scale and modified Rankin Scale and Barthel Index. Conclusion: This study suggested that plasma gelsolin level is a good marker for the severity of stroke and stroke outcome. [Egypt J Neurol Psychiat Neurosurg.  2013; 50(4): 419-424]

Key words: Ischemic stroke, Plasma gelsolin level, Stroke outcome.

Correspondence to Sabah M. Lotfy, Department of Neurology, Zagazig University, Egypt.Tel.: +201224819019       email: dr.sabahlotfy67@yahoo.com






INTRODUCTION

 

Ischemic stroke represents about 87% of all strokes.1 Currently, recombiant tissue plasmingen activator (rtPA) is the only FDA approved therapeutic agent for ischemic stroke, it is effective only if intravenously administered within 3 to 4.5 hours of stroke onset and can have adverse neurotic effects even with proper use.2 Therefore development of new agent for stroke is essential.3 The mechanisms involved in stroke injury and repair are extremely complex, involving excitotoxicity and necrotic cell death occurring within minutes of stroke.4 Also programmed cell death during post ischemic tissue inflammation (that can last days to weeks) has a detrimental effect. Therefore, therapeutic strategies that targeting delay or dampening inflammatory responses could inhibit the progression of the tissue damage and improve the overall outcome of stroke.5

Several stroke biomarkers have been studied in ischemic stroke and they are clearly have the potential to assist in both diagnosis and outcome prediction of stroke patients.6

Plasma gelsolin is a recent inflammatory stroke biomarker.7 Gelsolin was first identified as a cytoplasmic actin–regulatory protein essential for cell locomotion and phagocytosis.8

Plasma gelsolin level is an important and sensitive general prognostic biomarker for health and disease conditions in human, urging the need for gelsolin replacement therapy to improve  patient 's health status.9

There are two isoforms of gelsolin: isoform 1, a secretory (plasma) protein that is 51 amino acids longer than isoform 2, a cytosolic protein, at the N-terminus; the first 27 amino acids is a signal sequence. Both isoforms are coded by a single gene and differ as a result of alternative initiation site/splicing.10

Plasma gelsolin binds inflammatory mediators such as platelet-activating factor and lysophosphatidic acid suggests that its physiological function may be to localize inflammation and blunt its systemic effects and that extensive plasma gelsolin depletion due to actin exposure after injury allows inflammatory mediators to cause widespread tissue damage.11

Plasma gelsolin acts as debris cleaner limiting inflammation and possibly decrease blood clogging. Another possible mechanism of the neuroprotection effect of gelsolin is through anti-apoptotic activity, as it inhibit cytokine induced apoptosis.12

It is evidenced that gelsolin knockout mice have largely increased cerebral lesion volumes after brain ischemia.13

 

Aim of the Work

The aim of this study was to evaluate whether plasma gelsolin level was altered in ischemic stroke patients and its ability to predict acute ischemic stroke outcome and its relation with clinical and radiological findings in these patients.

 

SUBJECTS AND METHODS

 

This study was conducted on 50 patients with first ever-ischemic stroke who survived for 3 months and 30 healthy volunteers who were by sex and age matched to the patients and without vascular risk factors.

Our patients were selected from patients admitted to neurological intensive care unit, Zagazig university hospitals with a diagnosis of first-ever ischemic stroke in the period from May 2012 to March 2013. Ischemic stroke was defined according to World Health Organization (WHO) as acute focal neurological signs and/or symptoms thought to be of vascular origin that persisted for more than 24 hours, documented by brain-computed tomography (CT) or magnetic resonance imaging (MRI). We excluded patients with concurrent major trauma, recent infection, chronic inflammatory disease, renal or hepatic diseases, subarachnoid hemorrhage and cerebral hemorrhage. All patients or their relatives and controls gave their informed consent before the study.

Systematic routine procedures at admission included, clinical evaluation during which vital signs and blood pressure are registered. ECG was performed. The patients and their relatives were interviewed about the medical history of the patients, for detecting any risk factor for stroke such as hypertension, DM, atrial fibrillation and smoking. Quantitative assessment of neurological deficit was performed for all patients at admission, by using National Institutes of Health Stroke Scale (NIHSS)14, and on discharge, patients were assessed by the  use of Barthal index (BI).15

The patients were evaluated after three months by modified Rankin Scale (mRS) for assessment of the prognosis, considering 3 as good prognosis, 3-5 as bad prognosis.15 Then we divided our surviving patients into two groups: group 1 included patients with good prognosis, and group 2 included patients with bad prognosis and we compared between the two groups.

Venous blood samples were obtained immediately after admission for all patients and centrifuged at 2500g for 5 minutes, plasma was harvested and frozen at −80°C until analysis. Plasma gelsolin levels were measured using an enzyme-linked immunosorbent assay, in accordance with the manufacturer's instructions (Cusabio Biotech Co., Carlsbad, California, USA).

Beside plasma gelsolin estimation on admission, patients were investigated  by routine investigations: including, complete blood count, c-reactive protein (CRP),  blood glucose, liver and kidney functions,  lipid profile include: Triglycerides, Total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL).

All patients were subjected to brain CT and/or MRI for diagnosis of ischemic stroke and to determine the site and size of the infarction within 48 hours of stroke onset. The size of infraction was quantified into 3 categories.16 Small infraction, where lesion size less than 1 cm (including lacunar infraction), large infraction, when involving complete branch of cerebral arteries (middle, anterior or posterior cerebral artery), and finally, medium sized infraction when the size of infarction is between small and large ones.

 

Statistical Analysis

Data were checked, entered and analyzed using (SPSS version 15). Data were expressed as mean ± SD for quantitative variable, number and percentage for qualitative one. c2 or fisher exact, t-test and paired t-test were used when appropriate. The correlation coefficient(r) was used to test the association between two continuous variables. P-value <0.05 was considered significant and <0.001 as highly significant.

 

RESULTS

 

This study included 50 patients with ischemic stroke 28 had good prognosis (group 1) and 22 had bad prognosis (group 2) by using mRS at 3 months and 30 healthy volunteers.

The demographic and laboratory data of the studied patients and controls at base line were showed in Table (1).

From this table we found that no statistically significant differences were detected between patients and controls as regard age, sex and body mass index, CRP and HDL. While, level of gelsolin was significantly decreased in ischemic stroke patients compared to controls, levels of blood glucose, T.cholesterol, triglyceride and LDL were significantly increased in patients compared to control group.

Table (2) shows clinical and laboratory characteristics of good and bad prognosis groups.

There was no significant differences between good and bad prognosis groups as regard age, sex, BMI, smoking, side of lesion, heart disease, CRP and lipid profile while there were significant differences between two groups as regard diabetes, hypertension, size of lesion, NIHSS score, BI  and plasma gelsolin levels.

Correlation between gelsolin and some of clinical and laboratory parameters were illustrated in Table (3).

It showed that there were highly significant negative correlations between gelsolin level and CRP, T.cholesterol, LDL, NIHSS and mRS. while the correlation between gelsoline level and blood glucose and triglyceride levels was showing just a significant negative correlation. There was significant positive correlation between gelsolin and BI, HDL.

Cut-off point, sensitivity, specificity, accuracy, PPV, NPV, OR and CI 95% of NIHSS and gelsolin in prediction of prognosis were showed in Table (4).

As regard NIHSS; we found that NIHSS score more than 14 predicted the bad prognosis of patients with   81.8% sensitivity and 78.6 % specificity (0.841; 95% CI (0.724-0.958) P = 0.000)

While  the base line plasma gelsolin level lower than 83.5 mg/L predicted the bad prognosis of patients with 86.4% sensitivity and 67.9% specificity (0.830; 95% CI (0.718-0.941); P=0.000) with positive predictive value 67.9% and negative predictive value 86.4%).

A multivariate analysis selected NIHSS score (odds ratio, 16.50; 95% CI (4.028-67.59); P = 0.000), diabetes mellitus (odds ratio, 4.330; 95% CI, (1.023-10.72); P = .003), and baseline plasma gelsolin level (odds ratio, 13.37; 95% CI, (3.126-57.180); P = 0.000) as the independent predictors for bad prognosis.


 

Table 1. Demographic and laboratory characteristics of both Patients and control groups.

 

P

Control

(n=30)

Patients

(n=50)

Variables

0.061

65.33 ±6.83

62.14±7.5

Age (year) ±SD

 

0.452

 

16 (53.3%)

14 (46.7%)

 

21 (42%)

29 (58%)

Sex n (%)

               Male

               Female

0.212

27.08± 1.6

27.53 ±1.5

BMI

<0.05*

159.46±22.59

77.28±25.59

Gelsolin (mg/L) ±SD

0.3

1.7±0.8

1.9±0.9

CRP (mg/L) ±SD

<0.001**

123±8.03

163.36±67.1

Blood glucose (mg/dl)  ±SD

<0.001**

210.76±45.2

242.38±57.14

T.cholesterol (mg/dl)  ±SD

0.006*

130.2±0.45

135±30.1

Triglyceride (mg/dl)  ±SD

0.07

36.26±5.8

33.2±9.12

HDL (mg/dl)  ±SD

<0.001**

142±25.0

179.81±56.75

LDL (mg/dl)  ±SD

BMI Body mass index, CRP c-Reactive Protein, HDL High density lipoprotein, LDL Low density lipoprotein

*Significant at p<0.05 ** Significant at p<0.01

 

Table 2. Clinical and laboratory characteristics  of good and bad prognosis groups.

 

P

Group 2

Bad prognosis (n=22)

Group 1

Good prognosis (n=28)

Variables

0.768

62.50 ±7.33

61.85±7.81

Age (years) ±SD

1.000

9 (40.9%)

13  (59.1%)

12 (42.9%)

6 (57.1%)

Male

Female

Sex n (%)

0.275

6 (27.3%)

13 (46.4%)

Smoking n (%)

0.282

27.79±1.53

27.32±1.5

BMI

0.046*

15 (68.2%)

10 (35.7%)

Diabetes n (%)

0.046*

15 (68.2%)

10 (35.7%)

Hypertension n (%)

1.000

8 (36.4%)

10 (35.7%)

Atrial fibration n (%)

0.776

10 (54.5%)

12 (45.5%)

15 (53.6%)

13 (46.4%)

Right

Left

Site of infarction

<0.001**

0 (0.0%)

8 (36.4%)

14 (63.6%)

17 (60.7%)

8 (28.6%)

3 (10.7%)

Small

Median

Large

Size of infarction

              

<0.001**

15.09±1.19

11.39±2.69

NIHSS  ±SD

0.007**

51±11.5

75±15.0

BI  ±SD

0.192

18 (81.8%)

17 (60.7%)

Hyperlipedemia n (%)

<0.001**

63.12±21.89

88.40±22.90

Gelsolin (mg/L)  ±SD

0. 006**

191.95±72.70

140.89±53.59

Blood glucose (mg/dl)  ±SD

0.128

2.1409±0.81

1.8036±0.71

CRP (mg/dl)  ±SD

BI Barthel index, BMI Body mass index, CRP C-Reactive protein, NIHSS National institute of health stroke scale

*Significant at p<0.05 ** Significant at p<0.01

 

Table 3. Correlation between gelsolin and some of clinical and laboratory parameters in the studied groups.

 

Parameter

Gelsolin

R

P

Age

-0.071

0.623

NIHSS

-0.532

<0.001**

mRS

-0.611

<0.001**

BI

0.46

0.01**

CRP

-0.566

<0.001**

Blood glucose

-0.355

0.011*

Total cholesterol

-0.516

<0.001**

Triglyceride

-0.464

0.001**

HDL

0.360

0.01**

LDL

-0.519

<0.001**

BI Barthel index, CRP C-Reactive protein, HDL High density lipoprotein, LDL Low density lipoprotein, NIHSS National institute of health stroke scale, mRS modified Rankin Scale

*Significant at p<0.05 ** Significant at p<0.01

 

Table 4. Cut-off point, sensitivity, specificity, accuracy, PPV, NPV, OR and CI 95% of NIHSS and Gasoline in prediction of prognosis.

 

CI 95%

OR

NPV%

PPV %

Specificity%

Sensitivity %

Cut off

 

4.02-67.59

16.5

84.6

75.0

78.6

81.8

14

NIHSS

3.1-57.2

13.4

86.4

67.9

67.9

86.4

83.5

Gasoline

NIHSS National institute of health stroke scale, NPV negative predictive value, OR Odds ratio, PPV positive predictive value

 


DISCUSSION

 

In recent decades, stroke, with characteristic high mortality and disability, has been the first leading cause of death and threatened health disease in middle-aged and elderly peoples.17

Gelsolin plays an important role in cell mobility, signal transduction of the cytoskeletal structure, dynamics rearrangement process, apoptotic regulation, tumorigenesis modulation, organism anti-damage and is a prognostic marker for injury.18,19

Our study was aiming to detect whether plasma gelsolin level was changed in acute ischemic stroke patients and its role in the prediction of stroke outcome. In this study when we compared between patients and controls we found that plasma gelsolin level was decreased significantly in patients than controls and our results were in accordance with Guo and colleagues.7 in their study of 172 ischemic stroke patients as they found that plasma gelsolin level was significantly lower in patients than controls.

When we evaluated our patients after three months by mRS for assessment of functional outcome, we found that 28 patients had good functional outcome (group 1) and 22 had poor outcome (group 2)

When we compared between the two groups we found that there was no significant difference regarding the mean age or gender distribution between the two groups although the bad prognosis group had higher mean age and this is in accordance with Carole and colleagues.20 in their review of 37 stoke outcome studies and they stated that stroke occurring in older age has been associated with poorer outcome.

Also in comparing between patients with good and bad prognosis, we found that there were a significant differences between the two groups as regards diabetes, hypertension and size of lesion in brain imaging. These results were in agreement with Hu and colleagues.21 as they found that, high blood pressure early after stoke is associated with poor outcome after stroke Also Megherbi and colleagues.22 examined the relationship between diabetes and outcome at 3 months controlling for risk factors, clinical presentation, they found that stroke in diabetic patients has a specific clinical pattern and a poor prognosis. And they reported that various mechanisms may account for this, including more comorbidity, more prestroke disability, more ischemic lacunes, more motor problems and diabetic neuropathy.

As regards the size of infarction in the two groups, we found that the bad prognosis group had a larger size of infarction and this results was in accordance with Wu and colleagues.23 who reported that the measurement of the size of infarction by MRI is a useful tool in assessing prognosis and will have a valuable role in assessing the new therapeutic agent, and the frequency of deterioration in acute ischemic stroke depends on infarct volume, topography and stroke subtype.

In our study assessment of stroke severity on admission by NIHSS and on discharge by Barthel index, demonstrated significant differences between the two groups with the bad prognosis group had a more sever stroke. In addition, there was a significant negative correlation between plasma gelsolin level and mRS and NIHSS and a significant positive correlation between gelsolin level and BI.

NIHSS score was found to be a good predictor of functional outcome in patients with ischemic stroke. Various factors were found to be significant for early prediction of stroke recovery and the NIHSS score was the strongest one.24

Our study showed that gelsolin was closely related to NIHSS score in the sensitivity (86.4%, 81.8% respectively) and specificity (67.9%, 78.6%, respectively), which in turn associated with clinical severity and outcome of ischemic stroke and this results was supported by Guo and colleagues.7 as they found that gelsolin was closely related to NIHSS score in multivariate regression model which in turn  associated with clinical severity and outcome of ischemic stroke, and also they reported that gelsolin was identified as a reliable and independent marker to predict 1 year mortality in patients with ischemic stroke and also gelsolin discriminative power was in the rang of NIHSS score and gelsolin improved the prognostic value of the NIHSS score for longterm mortality at 1year .In this context, gelsolin might be an interesting potential as a new prognostic biomarker.

The present study showed significant negative correlation between gelsolin level and acute phase protein and this result was explained by Guo and colleagues7, who said that the decrease of gelsolin is inversely related to the intensity of inflammation.

Inflammatory mediators are able to alter cellular metabolism by inducing oxidative stress and mitochondrial dysfunction, resulting in pathologic abnormalities.25 Abnormally high levels of cytokines in brain have been found to correlate with both morbidity and mortality in patients with extensive burn injury.7 Gelsolin treatment could significantly reduce expression and release of early as well as late proinflammatory cytokines.26

Le and colleagues3 in their experimental study on induced stroke in rates through middle cerebral artery occlusion, they injected gelsolin to a group of rates and they found that the infarct volume of gelsolin treated group was significantly reduced compared with the untreated rates at 72 hours, and also the sensory and motor deficit which arise after stroke were reduced in this group and they concluded that gelsolin could be a promising drug for protection against neurodegeneration following ischemic stroke.

 

Conclusion

This study showed that plasma gelosin was descrased after ischemic stroke and also plasma gelsolin level is a good marker for severity of stroke and stroke outcome.

 

Recommendations

Additional studies are needed to study the therapeutic effects, pharmacokinetic, dose response of gelsolin as a new therapeutic agent in ischemic stroke.

 

[Disclosure: Authors report no conflict of interest]

REFERENCES

 

1.        Roger VL, Go AS, Jones DM, Adams RJ, Berry JD, Braurn TM, et al. Heart disease and stroke statistics-2011 update: A report from the American Heart Association. Circulation. 2011; 123:e18-209.

2.        Hake W, Kast M, Pluhmki E, Brozman M, Davalos A, Guidetti D, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008; 359:1317-29.

3.        Le HT, Hirko AC, Theinschmidt JS, Grant M, Li Z, Peris H, Uing M. The protective effect of plasma gelsolin in stroke outcome in rats. ETSM. 2011; 3:13.

4.        Del Zappo GJ, Becker KJ, Hallenbeck JM. Inflammation after stroke: is it harmful? Arch Neurol. 2001; 58:669-72.

5.        Endres M, Englhardt B, Kaistinaho J, Lindvall O, Rearis S, Mohr JP, et al. Improving outcome after strokes: Cerebrovasc Dis. 2008; 25:268-78.

6.        Barone FC, Feuerstein GZ. Inflammatory mediators and stroke. J Cereb Blood Flow Metab. 1999; 19:819-34.

7.        Guo X, Luo B, Li X, Yang D, Zheng X, Zhang K. Plasma gelsolin levels and 1-year mortality after first-ever ischemic stroke. J Crit Care. 2011; 26:608-12.

8.        Kwiatkowski DJ, Mehl R, Lzumo S, Nadel G, Yin HL. Muscle is the major source of plasma gelsolin. J Biol Chem. 1988; 263:8239-43.

9.        DiNubil MJ. Plasma gelsolin as a biomarker of inflammation. Arthritis Res Ther. 2008; 10:124.

10.     Pottiez G, Havesland N, Ciborocuski P. Mass spectrometric characterization of gelsolin isoforms. Rapid Commun Mass Spectrom. 2010; 74:2620-4.

11.     Osborn TM, Dahlgerm C, Hartwig JH, Stossel TP. Modifications of cellular responses to lysophosphatidic acid and platelet-activating factor by plasma gelsolin. Am J Physiol Cell Physiol. 2007; 292:C1323-30.

12.     Oftsu M, Sakai N, Fujita H, Kashiwagi M, Gasa S, Shimizu S, et al. Inhibition of apoptosis by the actin-regulatory protein gelsolin. EMBO J. 1997; 16:4650-6.

13.     Enders M, Fink K, Zhu J, Stagliano W, Bondada V, Geddes J, et al. Neuroprotective effects of gelsolin during murine stroke. J Clin Invest. 1999; 103:347-51.

14.     Goldstein LB, Sansa GP. Reliability of the National Institutes of Health Stroke Scale. Extension to non-neurologists in the context of a clinical trial. Stroke. 1997; 28:307-10.

15.     Sulter G, Steen C, De Keyser J. Use of Barthel Index and modified Rankin scale in acute stroke trial. Stroke. 1999; 30:1538-41.

16.     Kiers L, Davis SM, Larkins R, Hopper J, Tress B, Rossiter SC, et al. Stroke topgraphy and outcome in relation to hyperglycemia and diabetes. J Neurol Neurosurg Psychiatry. 1992; 55:263-70.

17.     Lloyd-Jones D, Adams R, Carnethon M, DeSimone G, Ferguson TB, Flegal K, et al. Heart disease and stroke statistics-2009 update: Circulation. 2009; 19:e21-181.

18.     Mcgough AM, Staiger CJ, Min JK, Simometti KD. The gelsolin family of actin regulatory proteins: modular structures, versatile function. FEBS Lett. 2003; 552:75-81.

19.     Marrocco C, Rinalducci S, Mohamadkhabi A, D'Amici GM, Zalla L. Plasma gelsolin protein a candidate biomarker for hepatitis B-associated liver cirrhosis by proteomic approach. Blood Transfus. 2010; 8:105-12.

20.     Carole L, David J, Smith DV. Comparison  of risk factors for stroke incidence and stroke mortality in 20 years of follow up. Stroke. 31:1893-940.

21.     Hu G, Sarti C, Jouysilaahti P, Peltonen M, Qiao Q, Antikainen R, et al. The impact of history of hypertension and type 2 diabetes at baseline on the incidence of stroke and stroke mortality. Stroke. 2005; 36:2538-53.

22.     Megherbi SE, Milan C, Minier C, Couvreur G, Osseby GV, Tilling K, et al. Association between diabetes and stroke subtype on survival and functional outcome 3 months after stroke: data from the European BIOMED Stroke Project. Stroke. 2003; 34:688-94.

23.     Wu B, Lin S, Hao Z, Yang J, Xu Y, Wu L, et al. Proportion, Risk Factors and Outcome of Lacunar Infarction: A Hospital-Based Study in a Chinese Population. Cerebrovasc Dis. 2010; 29 (2):181-7.

24.     Ahmed R, Zuberi BF, Afsar S. Stroke scale score and early prediction of outcome after stroke. J Coll Physicians Surg Park. 2004; 14(5):267-79.

25.     Sharshar T, Gray F, Lorin D, Hopkinson NS, Ross E, Donandeu A, et al. Apoptosis of neurons in cardiovascular autonomic centers triggerd by inducible nitric oxide synthase after death from septic shock. Lancet. 2003; 362:1299-305.

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الملخص العربى

 

معدل الجيلسولين فى البلازما كعامل للتنبؤ بمصير السكتة الدماغية الاحتشائية

 

أن السكتة الدماغية الوعائية الاحتشائية تمثل 87% من اجمالى السكتات الدماغية وهناك دراسات عديدة لقياس دلالات كيميائية لهذه السكتات ومن الدلالات الحديثة قياس معدل الجيلسولين فى الدم والغرض من هذا البحث هو تحديد ما اذا كان معدل الجيلسولين فى الدم يتغير بحدوث السكتة الدماغية الاحتشائية ومدى تأثير هذا التغير فى تطور المرض وتوقع ناتج المرض.

ولقد أجريت هذه الدراسة على خمسون مريضا بالسكتة الوعائية الاحتشائية بوحدة العناية المركزية قسم المخ والأعصاب جامعة الزقازيق وبالإضافة إلى ثلاثون شخصا من الأصحاء.

ولقد تم فحص المرضى إكلينيكيا ومعمليا وأيضا بعمل الأشعة المقطعية وثم تقسيم المرضى إلى مجموعتين بعد ثلاثة أشهر من المرض المجموعة الأولى تضم المرضى الذين كانوا معدل التحسن فيهم كبير والمجموعة الثانية وكانت تضم المرضى الذين كان معدل التحسن فيهم قليل.

وكانت النتائج كالآتى:

1-   كان معدل الجيلسولين فى الدم فى المرضى اقل من المجموعة الضابطة.

2-   عند مقارنة المجموعة الأولى ذات التحسن الكبير والمجموعة الثانية ذات التحسن القليل وجد أن معدل الجلسولين كان أقل فى المجموعة الثانية بدرجة كبيرة.

3-   وجد أن معدل الجيلسولين فى الدم استطاع توقع حدوث التحسن بالمرضى مقارنة بالعوامل الأخرى التى تتوقع التحسن.

 

 



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