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© Borgis - New Medicine 4/2006, s. 90-96
*Charalambos Iliadis1, Dimitris J. Apostolopoulos2, Georgios Papadopoulos3, Fotis Tzortzidis1, Greta Wozniak4, Panagiotis Georgoulias4, Aleksandra Kunz5, Vasilis Panagiotopoulos1, Theodoros Maraziotis1, Pavlos J. Vassilakos2
Brain perfusion SPECT with 99mTc-ECD and serum neuron-specific enolase in patients with spontaneous subarachnoid haemorrhage and clinical vasospasm
Source of support:
Departmental Sources
1University of Patras, Medical School, Department of Neurosurgery, Patras, Greece
2University of Patras, Medical School, Department of Nuclear Medicine, Patras, Greece
3University of Thessaly, Department of Biochemical and Biotechnology, Larissa, Greece
4University of Thessaly, Medical School, Department of Nuclear Medicine, Larissa, Greece
5University of Harvard (Extension), Department of Evolutionary Anthropology, Boston, USA
Summary
Summary
Aim: To estimate the association between single photon emission computed tomography (SPECT) imaging and neuro-specific enolase (NSE) serum level measurement in patients with subarachnoid haemorrhage (SAH) and also to present our experience in using these data for patient evaluation.
Material and method: Thirty-five patients (18 female and 17 male, mean age 57.5 ± 11.9 y) with clinical findings of vasospasm after SAH underwent 99mTc-ECD SPECT imaging. In 23 out of the 35 patients, serum levels of NSE were assessed on admission. Brain perfusion was measured semi-quantitatively using symmetrical regions of interest, automatically drawn over cortical and subcortical structures on consecutive transverse slices. A summed perfusion defect score (SPDS) was used to quantify the brain perfusion. Statistical analysis was carried out using the Kruskal-Wallis test, Mann-Whitney U test and ROC analysis, as appropriate.
Results: Eighteen patients had abnormal SPECT studies. The patients were divided into three groups according to NSE levels. Group I comprised 13 patients with NSE values Ł 15 ng/ml, group II comprised 7 patients with 15 ng/ml ł 19 ng/ml. SPECT/SPDS data and NSE levels of groups II and I were positively linearly correlated (Spearman´s coeff = 0.71, p<0.05), while group III clearly defines a separate population. The linear correlation between SPECT/SPDS and NSE was statistically significant (p<0.05). Very high NSE values were noticed in three patients who eventually died.
Conclusion: Both SPECT abnormalities and high serum NSE concentration are potentially helpful in the evaluation of patients with SAH.
Introduction
Regional hypoperfusion is a very frequent complication of subarachnoid haemorrage (SAH), related to vasospasm. Single photon emission computed tomography (SPECT) provides three-dimensional data of brain tissue perfusion. Brain perfusion SPECT is a technique of functional neuroimaging that allows noninvasive study of physiology and physiopathology events in the human brain [1, 2]. The information that can be obtained using brain SPECT is complementary to the anatomical details provided by structural neuroimaging techniques such as CT and MRI. Furthermore, functional abnormalities can be detected by SPECT earlier and in more detail than structural neuroimaging techniques. Brain perfusion SPECT has a role in the diagnosis, therapeutic management and follow-up of patients after SAH.
Enolase is a dimeric, glycolytic enzyme with three subunit types and five isoenzymes (aa, bb, gg, ab, and ag). It is a glycolytic enzyme that catalyzes the interconversion of 2-phosphoglycerate and phosphoenolpyruvate. The three different isoforms of enolase (a, b, g) are found mainly as homodimers specific to different tissues: aa in the liver, bb in the muscle, and a subunit of enolase is prevalent in neurons and neuroendocrine cells as ag- and gg, [so-called neuro-specific enolase (NSE)] [1, 2, 3, 4]. It represents about 1.5% of total soluble brain proteins [5]. Thus, this protein appears as a major component of the cytosol of neurons. Increased serum levels of NSE are often measured after neuronal damage [6]. It has been proposed that after brain damage, specific neuronal proteins such as NSE are released from brain cells and appear in the systematic circulation possibly via direct passage through the disturbed blood-brain barrier. This characteristic of NSE is valuable for its use as a prognostic marker for patients after SAH [7, 8, 9].
Our investigation sought to determine the association between 99mTc-ECD SPECT imaging and serum NSE levels.
Material and Method
Population
Thirty-five patients (18 women, 17 men) with SAH who were admitted to the neurosurgery clinic of our hospitals between February 2001 and December 2003 were included in the study. Their age ranged from 17 to 80 years (mean age 57.5±11.9 years). All patients presented symptoms of subarachnoid haemorrhage, including headache, drowsiness, nuchal rigidity and confusion, and six of them also presented mild focal deficit. CT studies were performed during patients´ hospitalization.
Inclusion criteria were: a) SAH proven by CT examination to have occurred within the previous 24 hours from admission, b) 80 years=age=17 years, c) good clinical condition (Glasgow Coma Score=12, Hunt and Hess grade
Subjects with a history of previous stroke or with known cerebral infarcts, renal failure, cardiac failure, severe diabetes mellitus, Parkinson´s disease, Alzheimer´s dementia, epilepsy or other neurologic or psychiatric disorders were excluded.
Clinical and laboratory investigation
Patients had a routine laboratory work-up, which included repeated blood tests and CT examinations. The amount of blood in the subarachnoid space was graded according to the Fisher scale. The patients´ clinical condition on admission was graded according to the Hunt and Hess scale (H&H) and the Glasgow Coma Score (GCS). Neurological status was carefully assessed daily during hospitalization. Digital subtraction angiography (DSA) was performed within the first 2 days after admission in most of them, or later (after day 14) if the patient´s clinical condition did not permit it. If DSA failed to reveal an aneurysm, a second DSA was performed two weeks later. Whenever an aneurysm was demonstrated on the first or second DSA, surgery (clipping) was conducted. In 4 occasions endovascular treatment (coiling) was attempted. Vasospasm was assumed on a clinical basis if deterioration of consciousness, increase in body temperature or new neurological deficit developed at least 3 days after SAH, which could not be explained by electrolyte or metabolic disturbances, hydrocephalus or re-bleeding. When a new neurological deficit occurred after surgery, it was attributed to vasospasm only if it was detected 48 hours or more after craniotomy, and if it could not be explained otherwise.
Patients who developed severe hydrocephalus acutely after SAH or post-operatively were treated with ventricular-peritoneal shunting. The final outcome was assessed 6 months after SAH and was graded according to the Glasgow Outcome Scale (GOS) (Table I).
Table I. Demographic data and values of Hunt-Hess (H-H), single photon emission computed tomography/ summed perfusion defect score (SPECT/SPDS), neuro-specific enolase (NSE), Glasgow Coma Score (GCS) groups and Glasgow Outcome Score (GOS) on admission to hospital.
 Clinical status of patients on admission  
Patients SexAgeH-HNSESPECT/SPDSGCSGCS/GroupsGOS
1F64218.2161233
2M72212.1101425
3F712-101423
4F592-11515
5M512-51515
6M69218.4191031
7F741-141231
8F52110.371515
9M45229.0111421
10F6039.791324
11F651-191233
12M601-51515
13M532-151234
14M40316.6171323
15F52216.8171233
16F6029.271515
17M80336.8151131
18F601-201234
19F5526.211515
20F56213.5131235
21M5929.1221231
22M572-41515
23M17215.3121425
24F62211.0 31515
25M7029.8131515
26F38210.121515
27F532-141423
28M472-71515
29F462-41515
30F47214.511515
31M75311.971514
32M6927.751514
33M3229.3131515
34F69216.2171235
35M68216.0121514
SPECT perfusion imaging

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Adres do korespondencji:
*Charalambos Iliadis
Department of Neurosurgery,
Peripheral General University Hospital of Larissa, Greece
Tel. +302410-538531/Mobile phone +306944642526
e-mail: greta@med.uth.gr, ilia-oly@otenet.gr

New Medicine 4/2006
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