Lean six sigma methodologies improve clinical laboratory efficiency and reduce turnaround times.

BACKGROUND: Organizing work flow is a major task of laboratory management. Recently, clinical laboratories have started to adopt methodologies such as Lean Six Sigma and some successful implementations have been reported. This study used Lean Six Sigma to simplify the laboratory work process and decrease the turnaround time by eliminating non-value-adding steps. METHODS: The five-stage Six Sigma system known as define, measure, analyze, improve, and control (DMAIC) is used to identify and solve problems. The laboratory turnaround time for individual tests, total delay time in the sample reception area, and percentage of steps involving risks of medical errors and biological hazards in the overall process are measured. RESULTS: The pre-analytical process in the reception area was improved by eliminating 3 h and 22.5 min of non-value-adding work. Turnaround time also improved for stat samples from 68 to 59 min after applying Lean. Steps prone to medical errors and posing potential biological hazards to receptionists were reduced from 30% to 3%. CONCLUSION: Successful implementation of Lean Six Sigma significantly improved all of the selected performance metrics. This quality-improvement methodology has the potential to significantly improve clinical laboratories.

Biological Variation and Reference Change Value Data for Serum Neuron-Specific Enolase in a Turkish Population.

BACKGROUND: Neuron-specific enolase (NSE) is a recognized biomarker for the assessment of cerebral injury in neurological disorders. This study aims to report a definitive assessment of the biological variation (BV) components of this biomarker, including within-subject BV (CVI), between-subject BV (CVG), index of individuality (II), and reference change value (RCV), in a cohort of Turkish participants using an experimental protocol. METHODS: Six blood specimens were collected from each of the 13 apparently healthy volunteers (seven women, six men; ranging in age from 23 to 36) on the same day, every 2 weeks for 2 months. Serum specimens were stored at -20°C until analysis. Neuron-specific enolase levels were evaluated in serum samples using an electrochemiluminescence (ECLIA) immunoassay kit with a Roche Cobas e 411 auto-analyser. ANOVA test was used to calculate the variations. RESULTS: The CVI and CVG for NSE were 21.5% and 28.8%, respectively. Analytical variation (CVA) was calculated as 10.2%. Additionally, II and RCV were calculated as 0.74 and 66% (95% confident interval, CI), respectively. CONCLUSION: As the performance index (PI) was found to be less than 2 (PI = 0.95), it is concluded that the NSE measurements have a desirable performance for analytical imprecision. Since the II was found to be less than 1 (II: 0.74), the reference values will be of little use. Thus, RCV would provide better information for deciding whether a significant change has occurred.

COVID-19 may enhance risk of thrombosis and hemolysis in the G6PD deficient patients.

COVID-19 has become a major public health problem since December, 2019 and no highly effective drug has been found until now. Numbers of infected people and deaths by COVID-19 are increasing every day worldwide, therefore self-isolation and protection are highly recommended to prevent the spread of the virus and especially to protect major risk groups such as the elderly population and people with comorbidities including diabetes, hypertension, cancer, cardiovascular diseases and metabolic syndrome. On the other hand, young people without any secondary disease have died by COVID-19 as well. In this study we compared two male patients infected by COVID-19 at the same age and one of them was diagnosed with G6PD deficiency. Both COVID-19 and G6PD deficiency enhance the risk of hemolysis and thrombosis. Serum biochemistry, hemogram and immunological parameters showed that risk of hemolysis and thrombosis may increase in the G6PD deficient patient infected by COVID-19.

Effects of selective Cox-2 inhibitor, rofecoxib, alone or combination with furosemide on renal functions and renal Cox-2 expression in rats.

BACKGROUND: Nonsteroidal anti-inflammatory drugs act by inhibiting the rate-limiting enzymes cyclooxygenase-1 (Cox-1) and cyclooxygenase-2 (Cox-2), which are important in prostanoid formation. The aim of this experimental study was to examine the effects of selective Cox-2 inhibitor, rofecoxib, with or without furosemide, on urine and serum electrolytes, creatinine clearance, plasma renin activity (PRA), and Cox-2 expression in the renal cortex. METHODS: Forty male Wistar albino rats were randomized into four groups, group 1, group 2, group 3, and group 4, and were treated with placebo, furosemide (20 mg/kg), rofecoxib (10 mg/kg) plus furosemide (12 mg/kg), and rofecoxib (10 mg/kg), respectively, and followed for 7 days. Body weights were measured daily. Urine osmolality and volume, and serum and urinary creatinine, sodium (Na(+)), and potassium (K(+)) were measured. Renal cortical Cox-2 protein expression was examined by immunohistochemical method. RESULTS: Compared with groups 1 and 3, body weights were significantly reduced in groups 2 and 4 (16.2 and 19.8 g, respectively; P < 0.05 for all). Urine volume in group 2 increased significantly compared with groups 1, 3, and 4 (P < 0.001, P < 0.008, and P < 0.004, respectively). Urine osmolality in group 2 decreased significantly compared with groups 1 and 3 (P < 0.05 for all). Blood urea nitrogen, serum creatinine and sodium, creatinine clearance, and 24-h urine Na(+) and K(+) levels were similar in all groups. Serum K(+) level was lowest in group 2, and there was a statistically significant difference between groups 2 and 4 (P < 0.05). Plasma renin activity was similar in all groups (P > 0.05). Renal cortical Cox-2 protein expression was lowest in group 1 and was significantly different from the other groups (P < 0.01 for all). The relationship between Cox-2 expression and plasma renin activity was not significant in any group (P > 0.05, r(2):0.05). CONCLUSIONS: Rofecoxib neutralized the diuretic effect of furosemide in rats treated with a combination of furosemide and rofecoxib. Renal cortical Cox-2 protein expressions due to furosemide and rofecoxib with or without furosemide were similar and significantly increased compared with controls. Renal failure due to rofecoxib did not developed in any rat, but selective Cox-2 inhibitor, rofecoxib, might have similar renal effects as nonselective nonsteroidal drugs for blunting the diuretic effect of furosemide.

Validation of the Friedewald formula for the determination of low-density lipoprotein cholesterol in renal transplant recipients.

UNLABELLED: In large patient populations, it has been established that calculated (c) and measured (m) plasma levels of low-density lipoprotein cholesterol (LDL-C) were comparable, but this issue is not known to be tested in renal transplant recipients (RTRs). Herein we aimed to compare the plasma levels of LDL-C that was calculated by Friedewald formula (FF) and direct measurement in RTRs. METHODS: LDL-C was measured by direct method and by FF in 193 fasting venous blood samples obtained from 103 RTRs. Patients had triglyceride (TG) levels <400 mg/dL. Patients were treated with prednisolone, calcineurin inhibitors (CNIs), and/or sirolimus and everolimus. RESULTS: The mean plasma levels of LDL-C for calculated and direct measurement were 100.81 +/- 32.79 mg/dL and 107.82 +/- 33.23 mg/dL, respectively (p < 0.01). The differences between cLDL-C and mLDL-C were similar according to usage of angiotensin receptor blockers (ARB)/angiotensin-converting enzyme inhibitors (ACEI), CNI, or mammalian target of rapamycin inhibitor (mTOR), tacrolimus or cyclosporine, and serum creatinine levels. mLDL-C and cLDL (FF) were highly correlated (r = 0.977). The mLDL-C level was calculated by following formula: LDL-C = 8.018 + (0.99 x FF cLDL-C) and the mean difference was 0 for last formula. CONCLUSION: The LDL-C can be calculated by the following formula: LDL-C = 8.018 + (0.99 x FF LDL-C). The coefficient of determination correlation (r) for this regression was 0.977, which indicates that the calculated LDL-C levels can be used in RTRs with TG lower than 400 mg/dL. mLDL-C was significantly higher than cLDL-C. We observed that difference between cLDL-C and mLDL-C levels were not affected by serum creatinine levels and usage of CNIs, sirolimus, everolimus, ACEI, and ARB in RTRs.

Indirect reference intervals estimated from hospitalized population for thyrotropin and free thyroxine.

AIM: To establish indirect reference intervals from patient results obtained during routine laboratory work as an alternative to laborious and expensive producing of their own reference range values according to international instructions. METHODS: All results for thyrotropin (TSH) and free thyroxine (T4) that were stored in our laboratory information system between 2004 and 2008 were included in this study. After a logarithmic transformation of the raw data, outliers were excluded. Non-parametric reference intervals were estimated statistically after visual observation of the distribution using stem-and-leaf plots and histograms. A standard normal deviation test was performed to test the significance of differences between sub-groups. RESULTS: There was no significant difference in serum TSH or free T4 concentrations between male and female participants. Because no differences were found within the time span of the study, combined reference intervals were calculated. Indirect reference values were 0.43-3.93 mU/L for TSH and 11.98-21.33 pmol/L for free T4. CONCLUSION: Using patient laboratory data values is a relatively easy and cheap method of establishing laboratory-specific reference values if skewness and kurtosis of the distribution are not too large.

The effects of rosiglitazone on oxidative stress and lipid profile in left ventricular muscles of diabetic rats.

We investigated the effect of rosiglitazone (RSG), a high-affinity ligand for the peroxisome proliferator-activated receptor gamma which mediates insulin-sensitizing actions, on the lipid profile and oxidative status in streptozotocin (STZ)-induced Type 2 diabetes mellitus (DM) rats. Wistar albino male rats were randomly divided into an untreated control group (C), a C + RSG group which was treated with RSG (4 mg kg(-1)) two times a day by gavage, a diabetic group (D) that was treated with a single intraperitoneal injection of STZ (45 mgkg(-1)), D + RSG group which were treated with RSG two times a day by gavage, respectively. Lipid profiles, HbA(1c) and blood glucose levels in the circulation and malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels in left ventricular muscle were measured. Treatment of D rats with RSG resulted in a time-dependent decrease in blood glucose. We found that the lipid profile and HbA(1c) levels in D + RSG group reached the C rat values at the end of the treatment period. There was a statistically significant difference between the C + RSG and C groups in 3-NT levels. In group D, 3-NT and MDA levels were found to be increased when compared with C, C + RSG and D + RSG groups. In the D + RSG group, MDA levels were found to be decreased when compared with C and C + RSG. Our study suggests that the treatment of D rats with RSG for 8 weeks may decrease the oxidative/nitrosative stress in left ventricular tissue of rats. Thus in diabetes-related vascular diseases, RSG treatment may be cardioprotective.

Procollagen type I carboxy-terminal peptide shows left ventricular hypertrophy and diastolic dysfunction in hypertensive patients.

BACKGROUND: An excess of myocardial collagens in hypertension is a result of increased collagen synthesis and unchanged or decreased collagen degradation. Increased collagen content, which is shown by the procollagen type I carboxy-terminal peptide (PIP), promotes cardiac remodeling and function abnormalities. OBJECTIVES: The objectives of this study were to assess PIP levels as a marker of myocardial collagen synthesis and to investigate the relationship between PIP levels and left ventricular mass index (LVMI) as well as diastolic function in patients with mild-to-moderate essential hypertension. METHODS: The study subjects were divided into three groups: healthy subjects (Group I, n=30); hypertensive patients without left ventricular hypertrophy (Group II, n=30); and patients with left ventricular hypertrophy (Group III, n=30). Left ventricular diastolic function was assessed by standard echocardiography and tissue Doppler imaging. Serum PIP was measured by radioimmunoassay. RESULTS: The serum concentration of PIP was higher in Group III than in Groups I and II (P<.001). A positive correlation was found between serum PIP and LVMI in hypertensive patients (r=.57, P<.001). Patients with diastolic dysfunction (DD) had significantly higher PIP levels as compared with patients without DD (177.3+/-52.25 vs. 138.8+/-38.0 microg/L, P<.001). The cutoff values of PIP to predict left ventricular hypertrophy and DD were 155.0 microg/L (sensitivity, 84%; specificity, 73%) and 150.2 microg/L (sensitivity, 71%; specificity, 70%), respectively. CONCLUSION: An elevated serum concentration of PIP shows left ventricular hypertrophy and DD in the course of hypertension and may be used to follow up on the efficacy of the antihypertensive treatment used.

Cardiac troponin T as a prognostic marker in patients with heart failure : a 3-year outcome study.

Cardiac troponin T (cTnT), a highly sensitive and specific indicator of myocardial cell death, may be elevated in congestive heart failure (CHF). The aims of this study were to test the hypothesis that decompensated CHF may be associated with an increase in cTnT release and to correlate between cTnT levels and patient outcomes. The authors studied 55 patients aged between 38 and 86 years (30 women and 25 men) who were hospitalized for CHF. Left ventricular ejection fraction (EF) was calculated by using modified Simpson's rule by echocardiography. cTnT levels were assessed. Troponin T >or=0.1 ng/mL was considered as positive. All patients were contacted by phone annually during the next 3 years, and their history of subsequent hospital admissions and current health status were recorded. cTnT was negative in 44 (80%) and positive in 11 (20%) patients. EF was significantly lower and NYHA was higher in cTnT-positive patients. During the 3-year follow-up period, 25 patients died from CHF. The mortality rate was 8/11 (72.7%) among cTnT-positive patients, whereas the mortality rate was 17/44 (38.6%) among cTnT-negative patients. There were significant relationships among positivity of cTnT, NYHA, EF, and mortality rate. Multivariate regression analysis yielded an independent relationship between positivity of cTnT, NYHA classification, and mortality rate. The percent of hospital admissions due to CHF was also higher in patients with cTnT positive (63.6% versus, 27.3%, p <0.05). In conclusion, this study shows that cTnT positivity is an independent risk factor in predicting the long-term mortality and morbidity rate in patients with CHF. Patients with worsening CHF may possibly be identified early on the basis of their elevated serum cTnT levels.

eNOS gene intron 4 a/b VNTR polymorphism is a risk factor for coronary artery disease in Southern Turkey.

BACKGROUND: Nitric oxide (NO) plays a major role in the regulation of vascular tone Associations between NO genotypes, coronary artery disease (CAD) and other risk factors have been described by many authors. The aim of this study was to investigate the role of endothelial nitric oxide synthase (eNOS) gene intron 4 a/b variable number of tandem repeats (VNTR) polymorphism and other risk factors in the development of CAD in subjects living in Southern Turkey. METHODS: Two-hundred and sixty-six patients (154 males and 112 females, aged between 30 and 80 years, mean 52.4+/-10.3) whose coronary arteries were evaluated by means of coronary angiography were enrolled in the study. Of the total, 133 had CAD (Group I) and the remaining had normal coronary arteries (Group II). The eNOS gene intron 4 a/b VNTR polymorphism was analyzed by polymerase chain reaction. The plasma lipid levels and other risk factors were also determined in all subjects. RESULTS: The a allele frequencies and genotypes carrying a allele were significantly higher in Group I. Plasma lipids, except HDL-C, were also increased in this group. We found that hypertension (HT), diabetes mellitus (DM), male gender, age and smoking were the independent predictors of CAD. CONCLUSION: a allele of eNOS intron 4 a/b VNTR polymorphism is not an independent predictor of CAD. eNOS intron 4 a/b polymorphism (presence of a allele) is a risk factor in addition to HT, DM, male gender, age and smoking for the development of CAD in Southern Turkey.

Protective effect of L-arginine intake on the impaired renal vascular responses in the gentamicin-treated rats.

The purpose of this study was to investigate the effect of gentamicin (100 mg/kg/day, i.p.) treatment on endothelium-dependent and -independent vasodilation in isolated perfused rat kidney, and the effect of amino acid L-arginine (in the drinking water, 2.25 g/l) on renal dysfunction induced by gentamicin. When gentamicin-treated groups were compared with the control group, it was observed that BUN and creatinine levels increased significantly. Also, the relaxant responses induced by acetylcholine, sodium nitroprusside and pinacidil decreased. Histopathological examination indicated acute tubular necrosis in this group. In animals treated with gentamicin together with L-arginine, there was a significant amelioration in the BUN and creatinine levels. The vasodilator responses were similar to those of the control group. Histopathological examination indicated only hydropic degeneration in tubular epithelium of kidney. Co-administration of L-NG-nitroarginine methyl ester (L-NAME) (112.5 mg/l), an inhibitor of nitric oxide synthase, and L-arginine to rats treated with gentamicin did not change the protective effect of L-arginine. In rats receiving L-NAME alone, the level of BUN and creatinine and vasodilation to acetylcholine were not significantly different when compared to those of the control group, while relaxant responses to sodium nitroprusside and pinacidil were increased. These results suggest that gentamicin leads to an impairment in vascular smooth muscle relaxation in addition to acute tubular necrosis in the rat kidney. Supplementation of L-arginine has an important protective effect on gentamicin-induced nephropathy.

Iodine status in Turkish populations and exposure to iodide uptake inhibitors.

Perchlorate, nitrate, and thiocyanate are competitive inhibitors of the sodium iodide symporter of the thyroid membrane. These inhibitors can decrease iodine uptake by the symporter into the thyroid gland and may disrupt thyroid function. This study assesses iodine status and exposure to iodide uptake inhibitors of non-pregnant and non-lactating adult women living in three different cities in Turkey (Istanbul, Isparta and Kayseri). We measured iodine and iodide uptake inhibitors in 24-hr urines collected from study participants (N = 255). All three study populations were mildly iodine deficient, with median urinary iodine (UI) levels of 77.5 µg/L in Istanbul, 58.8 µg/L in Isparta, and 69.8 µg/L in Kayseri. Perchlorate doses were higher in the study population (median 0.13 µg/kg/day), compared with a reference population (median 0.059 µg/kg/day), but lower than the U.S. EPA reference dose (0.7 µg/kg/day). Urinary thiocyanate levels increased with increasing exposure to tobacco smoke, with non-smokers (268 µg/L) significantly lower than light smokers (1110 µg/L), who were significantly lower than heavy smokers (2410 µg/L). This pilot study provides novel data indicating that study participants were moderately iodine deficient and had higher intakes of the iodide uptake inhibitor perchlorate compared with a reference population. Further investigation is needed to characterize the thyroid impact resulting from iodine deficiency coupled with exposure to iodide uptake inhibitors such as perchlorate, thiocyanate and nitrate.

Reference interval of pregnancy-associated plasma protein-a in healthy men and non-pregnant women.

OBJECTIVE: The serum pregnancy-associated plasma protein-A (PAPP-A) concentration is a predictor of ischemic cardiac events and renal impairment. However, the reference interval of PAPP-A has not been determined. This study determined the reference interval of PAPP-A in men and non-pregnant women. METHODS: The study enrolled 126 apparently healthy individuals (52 males and 74 females). The mean age of the men and women was 34.7 (range 20-66) years and 34.6 (range 18-65) years, respectively. Serum PAPP-A concentrations were determined using an ultrasensitive enzyme-linked immunoassay kit. Reference intervals were calculated using the bootstrap method. RESULTS: The results for three subjects were outliers, so the reference interval of PAPP-A was calculated using the data for 123 subjects. PAPP-A was undetectable in 26 subjects. The reference interval of PAPP-A for men and women (with the 90% confidence interval) was <22.9 ng/mL (19.7-23.3) and <33.6 ng/mL (25.2-36.7), respectively. In male subjects, serum PAPP-A levels of smokers [3.10 (UD, 7.30)ng/mL] were significantly lower than that of non-smokers [11.00 (UD, 24.4)ng/mL] (p<0.001) and there was a positive correlation between serum PAPP-A levels and subjects' age (r=0.439; p<0.001). CONCLUSIONS: The reference interval of PAPP-A differed for men and non-pregnant women. In clinical practice, <22.9 ng/mL for men and <33.6 ng/mL for non-pregnant women may be used as reference intervals for PAPP-A.

Macrophage depletion delays progression of neuropathic pain in diabetic animals.

Despite the fact that it is a frequent diabetic complication, the mechanisms underlying the manifestation of diabetic neuropathic pain remain poorly understood. In this study, we hypothesized that the depletion of peripheral macrophages with liposome-encapsulated clodronate (LEC) can prevent, at least delay, the progression of diabetes-induced neuropathic pain. Therefore, the aim of this study was to evaluate the effects of macrophage depletion on mechanical allodynia and thermal hyperalgesia in the streptozotocin (STZ)-induced rat model of diabetic neuropathy. LEC was intravenously administrated to rats three times with 5-day intervals. A single intravenous injection of STZ caused an increase in the average blood glucose levels and a decrease in body weight. Although LEC treatment did not affect the body weight gain, the blood glucose level was lower and serum insulin level higher in LEC-treated diabetic rats than in that of diabetic rats. In addition, LEC treatment alleviated the excessive damage in beta cells in diabetic rats. Diabetic animals displayed marked mechanical allodynia and thermal hyperalgesia. While the treatment of diabetic rats with LEC did not significantly change the thermal withdrawal latency, diabetes-induced decrease in mechanical paw withdrawal threshold was significantly corrected by the LEC treatment. The results of this study show that thermal hyperalgesia and mechanical allodynia induced by diabetes may be associated with alterations in blood glucose level. Depletion of macrophages with LEC in diabetic rats may reduce mechanical allodynia without affecting thermal hyperalgesia. Taken together, these results suggested that depletion of macrophages in diabetes may partially postpone the development of diabetic neuropathic pain.

The effects of the nonsteroidal anti-inflammatory drug diclofenac sodium on the rat kidney, and alteration by furosemide.

INTRODUCTION: Renal physiology is a partially cyclooxygenase (COX)-dependent system. Kidneys express both COX-1 and COX-2 enzymes. In this study, we tried to investigate the effects of diclofenac sodium (D), with or without furosemide (F), on plasma renin activity (PRA), serum and urine electrolytes, creatinine clearance, and COX-1 and COX-2 expression in the renal cortex. METHOD: Forty-two Wistar-albino rats were divided into four groups (G). G1, G2, G3, and G4 were treated with placebo, F (20 mg/kg), F (20 mg/kg) plus D (2.5 mg/kg), and D (2.5 mg/kg), respectively, and followed for seven days. Urinary osmolality and volume, and levels of serum and urinary creatinine, sodium, and potassium were measured. Renal COX-1 and COX-2 expression were examined by the immunohistochemical method. RESULTS: Compared with G1, body weights were significantly reduced in G3 and G4 (P < 0.05 for all). Serum sodium in G2 decreased significantly compared with G1, G3, and G4. Serum potassium in G2 decreased significantly compared with G1 and G3. Urine volume in G2 increased significantly compared with G1, G3, and G4. Urine osmolality in G2 and G4 decreased significantly compared with G1 and G3. Urine Na in G2 increased significantly compared with G4. Although urine K was lowest in G4, there were no statistically significant differences between the groups. Creatinine clearance decreased in G4 compared with the other groups. PRA was similar in all groups. Renal cortical COX-2 expression was lowest in G1. COX-1 expression in cortical collecting tubules was significantly reduced in G3 and G4 compared with G1 and G2 (P < 0.05 for all). Although creatinine clearance in G4 was significantly lower than in G3, COX-1 and COX-2 expression were no different in G3 and G4. DISCUSSION: Acute renal failure was caused by D. F prevented development of renal failure in rats treated with a combination of D and F. The diuretic effect of F was neutralized by D. Whereas COX-1 expression was reduced by D and by the combination of D and F in G3 and G4, renal COX-2 immunoreactivity was increased by F and D and the combination of both. Although creatinine clearance was lower in rats that were given D alone compared with the combination of F and D, COX-1 and COX-2 expression were similar in these groups.

The effect of early statin treatment on inflammation and cardiac events in acute coronary syndrome patients with low-density lipoprotein cholesterol.

We investigated the effects of atorvastatin on inflammation and cardiac events during the inpatient period and initial 6-month follow-up in acute coronary syndrome (ACS) patients with low low-density lipoprotein (LDL) cholesterol level. One hundred and twelve consecutive ACS patients with LDL cholesterol less than 100 mg/dl were included in the study (mean 78.2+/-12.3 mg/dl). While 70 randomly selected patients received a dose of 40 mg atorvastatin within the first 24 h on top of their standard treatment as the atorvastatin group, the remaining 42 patients considered as the control group were given the standard treatment only, i.e., without any lipid-lowering drug therapy. Lipid profile, high-sensitivity C-reactive protein (hsCRP), and plasma amyloid A (SAA) levels were measured in all patients within the first 24 h of chest pain, on the 5th day, and in the 6th month. During the inpatient period and subsequent 6-month follow-up, all episodes of angina, reinfarction, revascularization, heart failure, rehospitalization, cardiac mortality, and total number of cardiac events were recorded. In the atorvastatin group, hsCRP and SAA values on the 5th day and in the 6th month compared to the first 24 h were significantly lower than those of the control group (P<0.0001). Mean LDL cholesterol level was significantly decreased in the atorvastatin group (55.7+/-17.7 mg/dl), but there was no significant change in the control group at the 6th month. The frequency of heart failure during the inpatient period and angina, unstable angina pectoris, heart failure, and revascularization in the first 6 months were also significantly reduced in the atorvastatin group. Atorvastatin started in the first 24 h reduces inflammation and improves the prognosis during both the inpatient period and the first 6 months of clinical follow-up in ACS patients with low LDL cholesterol levels.

Biochemical indicators and cardiac function tests in chronic alcohol abusers.

AIM: To determine the effect of chronic alcohol abuse on cardiac function, antioxidant system, trace elements, and liver function tests. METHODS: Mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), superoxide dismutase (SOD), malondialdehyde (MDA), as well as zinc, magnesium, and copper were assayed in 25 chronic alcoholic patients and their 25 healthy relatives matched in age and gender. Echocardiographic parameters were evaluated for subjects. RESULTS: Mean corpuscular volume (96.7 fL vs 92.4 fL) and mean corpuscular hemoglobin levels (31.4 pg vs 30.5 pg) were found to be significantly increased in the patient group (P=0.002 and P=0.048, respectively). The results of the SOD and MDA assays showed no significant differences between the two groups. AST (38.7 U/L vs 22.1 U/L) and GGT (104.2 U/L vs 34.2 U/L) levels were found to be significantly increased in the patient group compared with controls (P=0.005 and P<0.001, respectively). Magnesium (1.6 mmol/L vs 1.8 mmol/L) and zinc levels (14.9 micromol/L vs 19.2 micromol/L) were significantly decreased, whereas copper levels (19.3 micromol/L vs 17.9 micromol/L) were increased in alcoholics (P=0.042, P<0.001 and P=0.003, respectively). Echocardiographic examination showed a significant decrease in mitral and tricuspid ratio of peak early and atrial flow velocity (E/A ratio) in alcoholics. CONCLUSION: Decrease in mitral and tricuspid E/A ratios accompanied with low levels of magnesium and zinc, and increased levels of copper indicate that alcoholics already have heart muscle disease even chronic alcohol exposure.