Epicardial cysts: report of two rare cases

Epicardial cysts originating directly from the epicardium are seen very rarely. Complete surgical excision is recommended when these cysts are detected. If cysts compress surrounding vital structures, cardiopulmonary bypass (CPB) should also be considered. We report herein 2 cases of multiloculated epicardial cysts, both of which were successfully excised, 1 with CPB.     

The effect of non-steroidal anti-inflammatory drugs on the endothelial function of patients with osteoarthritis in short term

Objective: Our primary aim was to test whether non‐steroid anti‐inflammatory drug (NSAID) use may account for endothelial dysfunction (ED) in the acute period. Additionally, we also aimed to compare the effect of diclofenac and naproxen on endothelial function. Methods: Forty patients with osteoarthritis (OA) were included in the study. Subjects currently receiving NSAIDs were asked to discontinue their anti‐inflammatory medications (for at least 5 days) before the study. After the wash‐out period, all subjects underwent vascular ultrasound measurements. Following baseline vascular imaging, patients were randomly assigned in a 1 : 1 ratio to receive either diclofenac (75 mg twice daily, n = 20), or naproxen (500 mg twice daily, n = 20) for 7 days. Endothelial function was evaluated by using the flow‐mediated dilatation (FMD) method, at baseline, and after 1 week of NSAID treatment. Results: There were 40 OA patients (4 male, 36 female). The median age of the patients was 60 ± 14 years. There were equal numbers of subjects in each treatment group. Age, sex distribution, body mass index, serum lipids, erythrocyte sedimentation rate, C‐reactive protein and fasting glucose levels were similar between the diclofenac and naproxen groups (P > 0.05). The brachial artery diameter (BAD), endothelium‐dependent vasodilatation (FMD%) and nitroglycerin‐induced endothelium‐independent vasodilatation (NTG%) values were not different between pretreatment and on the seventh day in the NSAID treatment groups (P > 0.05). Subgroup analysis also showed similar values of BAD, FMD%, and NTG% between naproxen and diclofenac groups (P > 0.05). Conclusion: Our results suggest that nonselective cyclo‐oxygenase antagonists naproxen and diclofenac have no effect on endothelial function during short‐term use.     

A case of familial Mediterranean fever and polyarteritis nodosa complicated by spontaneous perirenal and subcapsular hepatic hemorrhage requiring multiple arterial embolizations

The association of familial Mediterranean fever (FMF) and polyarteritis nodosa (PAN) has been well established. These patients have been reported to have an overall better prognosis than other PAN patients. Herein we report a patient with FMF and PAN who died of sepsis following a severe course of recurrent bleeding episodes which required multiple embolization attempts. The 39-year-old Turkish male presented with abdominal pain of 1-month duration. He had been diagnosed with FMF at the age of 24. On admission, he had pallor with general ill appearance. Rebound tenderness was obtained in the right upper abdominal quadrant. He had mild anemia, leukocytosis, thrombocytosis, and hypoalbuminemia. On the 2nd day of his admission, he developed hypotension with a rapid decline in hemoglobin level. Abdominal angiography showed multiple aneurysms in the branches of renal arteries, superior mesenteric artery, and hepatic arterial system including left renal infarct, suggesting PAN. He was put on high-dose steroids and oral cyclophosphamide. Despite medical treatment, he developed intense abdominal pain, hypotension, tachycardia, and a rapid fall in hemoglobin on four occasions. Active bleeding sites were embolized in two different angiography sessions. Although the patient experienced no more recurrent bleeding, he died of multiorgan dysfunction syndrome resulting from sepsis 6 weeks after admission. Polyarteritis nodosa associated with FMF may follow a grave course despite immunosuppressive therapy. Arterial embolization should be considered in the presence of bleeding aneurysms in addition to immunosuppressive therapy.     

Ventricular diastolic function of ankylosing spondylitis patients by using conventional pulsed wave Doppler, myocardial performance index and tissue Doppler imaging

OBJECTIVE: The aim of this study was to evaluate ventricular functions by using standard Doppler echocardiography (SDE), myocardial performance index (MPI), and pulsed wave tissue Doppler imaging (PW-TDI) in patients with ankylosing spondylitis (AS) and healthy controls. METHODS: Forty-nine AS patients (38 +/- 11 years, 25 M/24 F) and 33 controls (36 +/- 9 years, 17 M/16 F) were studied. Two-dimensional, M-Mode, SDE, PW-TDI echocardiography examinations were performed. Spinal mobility was assessed by the Bath ankylosing spondylitis metrology index (BASMI) measurement. Patients were also evaluated using the Bath ankylosing spondylitis functional index (BASFI) and the Bath ankylosing spondylitis disease activity index (BASDAI). RESULTS: Four control subjects and six AS patients met the left ventricular (LV) diastolic dysfunction (DD) criteria by using conventional Doppler echocardiography (p > 0.05). However, using PW-TDI method 22 patients in the AS group and six subjects in the control group were diagnosed to have LV DD (Em/Am < 1). Pseudonormalized pattern was present in 16 AS patients and two control subjects. Correlation analysis revealed significant moderate negative correlations between Em/Am and BASMI, age and body mass index (p < 0.05; r =-0.3, -0.6, and -0.4, respectively). No correlation was observed between Em/Am and disease duration, BASFI, BASDAI, CRP, and ESR. We could not detect any right ventricular function involvement either by conventional or by recently introduced echocardiography methods. The risk of developing LV DD was found to be 3.7 times higher in AS patients. CONCLUSION: When sensitive echocardiographic Doppler techniques such as MPI, TDI-derived MPI, and PW-TDI are utilized, DD can be detected in a significant proportion of patients with AS without cardiovascular (CV) disease which may contribute CV mortality in these patients.     

Increased secretion of insulin during oral glucose tolerance test can be a predictor of stent restenosis in nondiabetic patients.

Insulin is known to stimulate proliferation and migration of vascular smooth muscle cells. As the predominant mechanism of restenosis after stent implantation is neointimal tissue proliferation, one can expect a relationship between hyperinsulinemia and restenosis in these patients. The aim of this study was to determine whether hyperinsulinemia during oral glucose tolerance test is a predictor of the development of restenosis after stent implantation in nondiabetic patients. We prospectively studied 52 nondiabetic patients with effort angina who underwent elective stent implantation for single-vessel coronary artery disease. In order to increase the statistical power of the study, numerous exclusion criteria were applied. All patients were subjected to a 75 g oral glucose tolerance test a day before the stent implantation and underwent follow-up angiography 6 months later. Plasma insulin levels in fasting (6.77 +/- 1.57 vs. 5.36 +/- 1.35 micro U/ml; P = 0.005), at 30 min (102.48 +/- 10.6 vs. 47.74 +/- 12.75 micro U/ml; P = 0.001), 1 hr after (120.23 +/- 14.1 vs. 63.08 +/- 12.62 micro /ml; P = 0.001), 2 hr after (63.58 +/- 8.64 vs. 34.88 +/- 6.82 micro /ml; P = 0.001), and 3 hr after (25.71 +/- 5.65 vs. 23.02 +/- 4.61 micro /ml; P = 0.04) loading were significantly higher in patients with stent restenosis than in patients without stent restenosis. Insulin area and insulin area/glucose area were also significantly higher in patients with stent restenosis than in patients without (219.5 +/- 23.8 vs. 118.9 +/- 21.8, P = 0.001, and 0.62 +/- 0.09 vs. 0.33 +/- 0.06, P = 0.001, respectively). By multiple logistic regression analysis, insulin area during oral glucose tolerance test was found to be an independent predictor of stent restenosis (OR = 1.12; 95% CI = 1.01-1.25; P = 0.031). In conclusion, nondiabetic patients with hyperinsulinemia during oral glucose tolerance test have a high risk for restenosis after stent implantation, and performing this simple test before intervention may be useful for the prediction of stent restenosis.     

Bilateral middle cerebral artery aneurysms: a comparative study of unilateral and bilateral approaches

The best surgical method for the treatment of patients with bilateral middle cerebral artery (bMCA) aneurysms has not been fully determined yet. The main purpose of this study is to compare the surgical results of unilateral and bilateral approaches to bMCA aneurysms including mean operation time, mean hospital stay, and mean cost, in the experience of the same neurosurgical team. Between January 2001 and June 2010, 22 patients with bMCA aneurysms were surgically treated in our institution. In 12 cases (54.5?%), ipsilateral and contralateral MCA aneurysms were successfully clipped via unilateral approach. In the remaining 10 cases, bilateral approach was necessary because of some technical difficulties. Although the surgical results were almost the same, mean operation time and mean hospital stay were, respectively, 46 and 37?% shorter and mean cost per person was 23?% lower for the patients in the unilateral group. In addition, the severity of brain edema, total length of the contralateral (A1+M1) segment, and the configuration of contralateral aneurysm were found to be the determinant parameters affecting the feasibility of the unilateral approach. To our knowledge, this is the first study in the literature that compares the clinical outcomes of unilateral and bilateral approaches to bMCA aneurysms. The results of surgery for both approaches are almost the same. However, the unilateral approach has certain advantages compared to the bilateral approach. Therefore, the unilateral approach may be a good alternative in surgical management of patients with bMCA aneurysms in selected cases and the abovementioned parameters can help the neurosurgeon in patient selection.     

The Clinical Significance of Serum Apoptotic Cytokeratin 18 Neoepitope M30 (CK-18 M30) and Matrix Metalloproteinase 2 (MMP-2) Levels in Chronic Hepatitis B Patients with Cirrhosis

Background

Serum apoptotic cytokeratine 18 neoepitope M30 (CK-18 M30) and matrix metalloproteinase 2 (MMP-2) have been popular markers for detecting liver fibrosis in recent years. CK-18 is a major intermediate filament protein in liver cells and one of the most prominent substrates of caspases during hepatocyte apoptosis. MMP-2 plays an important role in tissue remodeling and repairing processes during physiological and pathological states.

Objectives

The objective of this study was to investigate the significance of CK-18 M30 and MMP-2 levels for clinical use in patients with chronic hepatitis B (CHB), as well as their sensitivity in determining cirrhotic patients.

Patients and Methods

This study included 189 CHB patients and 51 healthy controls. A modified Knodell scoring system was used to determine the fibrosis level in chronic hepatitis B patients. CK-18 M30 levels were determined with an M30-Apoptosense ELISA assay. MMP-2 levels were determined with the ELISA assay.

Results

The study group consisted of 132 (69.8%) males and 57 (30.2%) females, and the control group consisted of 25 males (49.0%) and 26 females (51%). Patients’ CK-18 M30 levels were higher than values of the control group (308 [1–762] vs. 168 [67–287], P=0.001). Serum MMP-2 levels were found to be statistically higher in the patient group with respect to the controls (3.0 [1.1–6.8] vs. 2.0 [1.2–3.4], P=0.001). The highest serum CK-18 M30 and MMP-2 levels were measured in patients with cirrhosis. Serum apoptotic CK-18 M30 levels positively correlated with advanced age, fibrosis stage, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels (P= 0.001, 0.033, 0.001, and 0.001, respectively). Serum MMP-2 levels positively correlated with fibrosis stage, serum ALT, and AST levels (P= 0.001, 0.001, and 0.001, respectively).

Conclusions

Our study indicated that CK-18 M30 and MMP-2 levels were higher in CHB patients compared to healthy controls and they were in association with significant hepatic fibrosis, especially cirrhosis.     

Baseline sacroiliac joint magnetic resonance imaging abnormalities and male sex predict the development of radiographic sacroiliitis

We evaluated the relationship between the baseline sacroiliac joint (SIJ) magnetic resonance imaging (MRI) findings and the development of radiographic sacroiliitis and tested their prognostic significance in cases of ankylosing spondylitis. Patients who had undergone an SIJ MRI at the rheumatology department were identified. Individuals for whom pelvic X-rays were available after at least 1 year of MRI were included in the analysis. All radiographs and MRI examinations were scored by two independent readers. Medical records of the patients were reviewed to obtain potentially relevant demographic and clinical data. We identified 1,069 SIJ MRIs, and 328 fulfilled our inclusion criteria. Reliability analysis revealed moderate to good inter- and intra-observer agreement. On presentation data, 14 cases were excluded because they had unequivocal radiographic sacroiliitis at baseline. After a mean of 34.8 months of follow-up, 24 patients developed radiographic sacroiliitis. The presence of active sacroiliitis (odds ratio (OR) 15.1) and structural lesions on MRI (OR 8.3), male sex (OR 4.7), fulfillment of Calin’s inflammatory back pain criteria (P?=?0.001), and total MRI activity score (P?<?0.001) were found to be related to the development of radiographic sacroiliitis. By regression modeling, the presence of both active inflammatory and structural damage lesions on MRI and male sex were found to be predictive factors for the development of radiographic sacroiliitis. Our present results suggest that the occurrence of both active inflammatory and structural lesions in SIJs revealed by MRI is a significant risk factor for radiographic sacroiliitis, especially in male patients with early inflammatory back pain.     

Temporal relations among amyloid β-peptide-induced free-radical oxidative stress, neuronal toxicity, and neuronal defensive responses

Amyloid β-peptide (Aβ), the main constituent of senile plaques in Alzheimer’s disease (AD) brain, is hypothesized to be a key factor in the neurodegeneration seen in AD. Recently it has been shown that the neurotoxicity of Aβ occurs in conjunction with free-radical oxidative stress associated with the peptide. In the present study, we investigated the temporal relations among the formation of Aβ-associated free radicals, the oxidative damage to, and the activation of antioxidant defense mechanisms in rat embryonic hippocampal neuronal culture subjected to toxic Aβ(25–35). Temporal electron paramagnetic resonance (EPR) spectroscopy results show that synthetic Aβ(25–35) forms free radicals rapidly after solubilization with a high signal intensity at initial time points. At those time points, neuronal toxicity and oxidative stress gradually increase as assessed by reduction of 3-[4,5-dimethylthiazol-2-yl)-2,5-diphenyl] tetrazolium bromide, trypan blue exclusion, formation of reactive oxygen species, and detection of protein carbonyl levels. The latter occurs before neurotoxicity. When the EPR signal intensity of Aβ solution decreases at later time points, neuronal toxicity levels off and remains the same until the end of the experiment. The oxidative-sensitive enzyme creatine kinase (CK) (brain isoform) (CK-BB) content increases at initial points of the Aβ treatment in correlation with the EPR signal to keep the CK activity constant, presumably to overcome the Aβ-induced oxidative insult. CK-BB content returns to normal levels by the end of the experiment. CK activity normalized to CK content implies the presence of inactivated CK molecules during the treatment. Both Mn SOD and Cu/Zn superoxide dismutase (SOD) mRNA levels show robust increases initially, which later return to control level with decreasing oxidative insult. These results are consistent with the notion that Aβ(25–35) promotes a rapid free-radical oxidative stress to neurons, which respond by modulating various oxidative stress-handling genes.     

The use of chloride–sodium ratio in the evaluation of metabolic acidosis in critically ill neonates

Acid-base disturbances have been usually evaluated with the traditional Henderson-Hasselbach method and Stewart's physiochemical approach by quantifying anions of tissue acids (TA). It is hypothesized that an increase in tissue acids during metabolic acidosis would cause a compensatory decrease in the plasma chloride (Cl) relative to sodium (Cl-Na ratio) in order to preserve electroneutral balance. Therefore, we aimed to investigate the use of Cl-Na ratio as a bedside tool to evaluate the identifying raised TA in neonates as an alternative to complex calculations of Stewart's physiochemical approach. This retrospective study was conducted between January 2008 and December 2009. Infants were included in the study when blood gas analysis reveals a metabolic acidosis; pH?<7.25 and sHCO(3) concentration was <22?mEq/L. The Cl-Na ratio, sodium-chloride difference (Diff(NaCl)), anion gap (AG), albumin-corrected AG (AG(corr)), strong ion difference (SID), unmeasured anions (UMA), and TA were calculated at each episode of metabolic acidosis. A total of 105 metabolic acidosis episodes occurred in 59 infants during follow-up. Hypochloremic metabolic acidosis occurred in 17 (16%) of samples, and all had increased TA. The dominant component of TA was UMA rather than lactate. There was a negative correlation between the Cl-Na ratio and SID, AG(corr), UMA, and TA. Also, there was a positive correlation between Diff(NaCl) and SID, AG(corr), UMA, and TA. Base deficit and actual bicarbonate performed poorly in identifying the TA. In conclusion, our study suggested that Diff(NaCl) and Cl-Na ratio are simple and fast, and may be an alternative method to complex Stewart's physiochemical approach in identifying raised UMA and TA in critically ill neonates.