Türker Yardan

Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning

OBJECTIVE Carbon monoxide (CO) poisoning causes cerebral and generalized hypoxia. This study aimed to assess the possible use of serum glial marker S100B protein and neuron-specific enolase (NSE) as biochemical markers of hypoxic brain damage in acute CO poisoning. METHODS Patients with acute CO poisoning admitted to the ED of 2 training hospitals (Ankara, Turkey) were included in this cross-sectional study. Serum levels of S100B and NSE were measured on admission. The patients were divided into 2 groups (unconscious and conscious). Twenty healthy adults were included in the study to serve as controls. RESULTS A total of 70 patients poisoned by CO (mean age +/- SD, 36.6 +/- 16.3 years; 64.3% women) were enrolled. Although S100B concentrations were higher in patients than in the control group (P = .018), no significant difference was determined between patient and control groups with respect to NSE concentrations (P = .801). A positive correlation was noted between levels of S100B and NSE (r = 0.388; P = .001). The S100B and NSE values were higher in unconscious patients than in the control group (P = .002 and P = .013, respectively). Furthermore, S100B and NSE values were higher in unconscious vs unconscious patients (P = .047 and P = .005, respectively). CONCLUSION Elevated serum S100B and NSE levels were associated with loss of consciousness in CO poisoning in this series of patients. Serum S100B and NSE may be useful markers in the assessment of clinical status in CO poisoning.

Retrospective evaluation of emergency service patients with poisoning: A 3-year study

The purpose of this retrospective study was to evaluate the characteristics of cases of acute poisoning in adults who were admitted to emergency service over a 3-year period. Clinical charts were analyzed retrospectively for etiologic and demographic patient characteristics. A total of 810 adults were admitted to the emergency center with acute poisoning. The female-to-male ratio was 2:1. Mean ages of female and male patients were 28.8±12.9 years and 35.1 ±15.4 years, respectively, and many patients (46.9%) were between the ages of 16 and 25 years. Medicinal drugs were found to be the primary cause (60.5%) of poisoning, and tricyclic antide-pressants were the most frequent causative agents (36.3%). Seasonal distribution of poisoning cases suggested a peak in the summer months (35.4%). Overall, 68.6% of acute poisonings were suicide attempts, and of these patients, 84.9%, 14%, and 1.1% were attempting suicide for the first, second, and third times, respectively. Among 810 cases of acute poisoning, 15 were fatal. The following conclusions were reached by investigators: (1) in the test region, younger females, especially single females, were at greater risk for poisoning than other patient groups, (2) self-poisoning cases constituted the majority of all poisonings, and (3) the main agents of self-poisoning were medicinal drugs, with antidepressants used most frequently. It was also found that unintentional poisoning commonly resulted from intake of foods, especially mushrooms.

B‐type natriuretic peptide as an indicator of right ventricular dysfunction in acute pulmonary embolism*

Objective:  B‐type natriuretic peptide (BNP) is a neurohormone secreted from cardiac ventricles in response to ventricular strain. The aim of present study was to evaluate the role of BNP in the diagnosis of the right ventricular (RV) dysfunction in acute pulmonary embolism (PE).

Wild mushroom poisonings in the Middle Black Sea region in Turkey: analyses of 6 years.

Wild mushroom poisoning (MP) is an important medical emergency that may have serious clinical outcome. The aim of this study was to evaluate the demographic and clinical features of patients with wild MP. This study was designed retrospectively by examining files of the patients with wild MP who were admitted to Ondokuz Mayis University Emergency Department, between January 2002 and December 2007. Patients ≥16 years of age were included in the study. A total of 317 patients poisoned by wild mushrooms (mean age, 42.0 ± 16.3 years; 67.5% female) were studied. All poisonings were accidental, i.e. consumption of wild mushrooms collected from open fields and woodlands or purchased from local bazaars. The common symptoms and complaints on admission were nausea (86.8%) and vomiting (79.8%). The poisoning latent phase in most cases was <6 hours (86.8%). Most of the poisonings occurred in autumn (59.6%). Three patients died in the hospital due to acute liver failure and complications. The duration of hospitalization was a median 3 days (range: 1—12 days). The public should be informed about the probable hazards of wild mushroom ingestion.

Is there a relationship between the blood cholinesterase and QTc interval in the patients with acute organophosphate poisoning

Organophosphates cause poisoning as a result of the excessive accumulation of acetylcholine at the cholinergic synapses due to inhibition of acetylcholinesterase (ChE). In the literature, it has been reported that there have been electrocardiographic abnormalities, including QT‐interval prolongation in most patients with acute organophosphate poisoning (OPP), and a relation between blood ChE level and clinical severity in acute OPP. The aim of this study is to assess the relationship between blood ChE level and QTc interval in the patients with acute OPP. This retrospective study consists of 20 patients admitted to the emergency intensive care unit. A total of 93 QTc interval and blood ChE measures obtained on the same day from 20 cases were compared for their correlation. There were prolonged QTc intervals in 35.4% of the ECGs. There was a negative correlation between QTc interval and blood ChE measures. In following up the patients with acute OPP, QTc interval may be useful when blood ChE levels are low and may provide complementary information concerning the severity of poisoning. However, further prospective studies, supporting the present results, are needed.

Diagnostic value of ischaemia-modified albumin in pulmonary contusion in rats

BACKGROUND Patients with pulmonary contusion (PC) are at increased risk of development of complications and death after trauma. The early diagnosis and determination of severity of PC could improve clinical outcomes. The aim of the study was to determine the diagnostic value of ischaemia-modified albumin (IMA) in a PC model in rats. METHODS Thirty-two Sprague-Dawley rats were randomly allocated to four groups; the uninjured control Group I (n=7) and the uninjured control Group II (n=7) were euthanised at 2 and 6h, respectively, and PC groups III (n=9) and IV (n=9) were euthanised at 2 and 6h after trauma, respectively. The serum level of IMA, tissue and serum malondialdehyde (MDA) levels, and histopathological damage scores of the lung tissue were determined. RESULTS Serum IMA and lung tissue MDA levels in the PC groups were not significantly different to those of the control groups (p=0.555; p=0.086, respectively). Serum MDA levels were significantly higher in the PC groups than in the control groups (p=0.011). When histopathological changes in lung parenchyma were evaluated, there was a statistical difference between the injured and uninjured groups for inflammation and lung injury (p=0.017; p=0.001, respectively). However, there was no significant correlation between the histopathological score and biochemical parameters. CONCLUSION Our preliminary findings suggest that there is no significant change of serum IMA levels in the acute phase of PC induced by blunt chest trauma.

The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning

The main purpose of this study was to assess the role of S100B protein, neuron-specific enolase (NSE), and glial fibrillary acidic protein (GFAP) in the evaluation of hypoxic brain injury in acute carbon monoxide (CO)-poisoned patients. This cross-sectional study was conducted among the patients with acute CO poisoning who referred to the emergency department in a 1-year period. Serum levels of S100B protein, NSE, and GFAP were determined on admission. A total of 55 CO-poisoned patients (mean age ± standard deviation, 45 ± 20.3 years; 60% women) were included in the study. The control group consisted of 25 healthy adults. The patients were divided into two groups according to whether they were conscious or unconscious. The serum levels of S100B, NSE, and GFAP were higher in patients than that in the control group. There was no significant difference between unconscious and conscious patients with respect to these markers. There was a statistically significant difference between the conscious and unconscious patients and the control group in terms of S100B and NSE levels. There was also a statistically significant difference between the unconscious patients and the control group in terms of GFAP levels. Increased serum S100B, NSE, and GFAP levels are associated with acute CO poisoning. These biomarkers can be useful in assessing the clinical status of patients with CO poisoning.

Heart-type fatty acid-binding protein as a potential biomarker of acute carbon monoxide poisoning☆☆☆

BACKGROUND The aim of this study was to investigate the role of serum heart-type fatty acid-binding protein (H-FABP) in the evaluation of patients with carbon monoxide (CO) poisoning. METHODS Forty patients with acute CO poisoning admitted to the emergency department and 15 healthy adults as the control group were included in the study. Serum H-FABP levels of patients were studied on admission and at the 6th, 12th, and 18th hours. Patients were divided into 3 groups according to clinical severity as mild, moderate, and severe. Patients were also divided into 2 groups according to treatment with hyperbaric oxygen (HBO) or normobaric oxygen. RESULTS Serum H-FABP levels of the patients were higher than those of the control group. There was a negative correlation between H-FABP levels and Glasgow Coma Scale score on admission. Heart-type fatty acid-binding protein levels were significantly higher in patients in the severe compared with mild group. Heart-type fatty acid-binding protein levels in patients treated with HBO were significantly higher than in those treated with normobaric oxygen. The cutoff value of serum H-FABP as an indicator for HBO treatment was determined as 1.5 ng/mL or higher, with a sensitivity of 85.7% and specificity of 69.7%. Serial measurement revealed that H-FABP level peaked at the sixth hour and reduced over time but remained higher than in the control group at the 18th hour. CONCLUSION Heart-type fatty acid-binding protein may be a promising novel biomarker in the evaluation of clinical severity and in the selection of patients for HBO therapy in acute CO poisoning.

The role of heart-type fatty acid-binding protein in the evaluation of carbon monoxide poisoning in rats

Acute carbon monoxide (CO) poisoning can cause early and persistent damages in tissues sensitive to hypoxia. This study investigated serum heart-type fatty acid-binding protein (H-FABP) levels as a biomarker of acute CO poisoning in rats. The rats were exposed to a mixture of either 3000 (group A) or 5000 (group B) parts per million (ppm) CO in air, or to ambient air (group C, control group). Blood samples were taken just before, immediately after and 6 hours after the exposure, and serum H-FABP and troponin-I levels were measured. The consciousness level was evaluated just after the exposure. The survival rate was monitored for 7 days. Serum H-FABP levels increased just after the CO exposure in both groups A and B. Additionally, H-FABP level was higher in group B than in group A, immediately after the exposure. However, serum troponin-I levels only increased at 6 hours after the CO exposure in groups A and B. Consciousness and survival rates in group B were lower than that in group A. Our results suggest that H-FABP might have potential to be an early and quantitative parameter of clinical severity and prognosis in CO poisoning.

Time course of serum S100B protein and neuron-specific enolase levels of a single dose of chlorpyrifos in rats.

Organophosphate (OP) compounds are a large class of chemicals, many of which are used as pesticides. It is suggested that OPs specifically affect glia and neurons. Effects of acute exposure to chlorpyrifos (CPF), which is a common organophosphorus pesticide used worldwide, on neuron-specific enolase (NSE) and S100B levels in rat blood during 7 days were assessed. Rats were evaluated either before (0 hr) or 2, 12, 24, 48 and 168 hr (7 days) after injection of CPF (279 mg/kg, s.c.) or vehicle (peanut oil, 2 ml/kg, s.c.) for clinical signs of toxicity. Immediately after the evaluation of toxicity, blood samples were taken for biochemical assays. CPF administration produced decreases in body-weight and temperature, which were observed for first time at 12 hr after CPF administration and continued for 168 hr (p < 0.05-0.001). Serum S100B and NSE levels were acutely increased 2 hr after CPF administration and remained high at 12 hr (p < 0.01-0.001). NSE and S100B levels were not different in either CPF or vehicle groups at following time points. Serum butyrylcholinesterase (EC 3.1.1.8; BuChE) activity was dramatically reduced at 2 hr after CPF and remained low at each time points during 7 days (p < 0.01-0.001). Our results suggest that the usefulness of serum levels of these glia- and neuron-specific marker proteins in assessing OP toxicity, specifically CPF-induced toxicity.