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S Nalbant

Publications and source records attributed to S Nalbant.

6 recordsLinked to original sources

Synovial fluid features and their relations to osteoarthritis severity: new findings from sequential studies.

OBJECTIVE: Many factors are involved in the osteoarthritic process. It is not yet known which are initiators, promoters or simply results. Thus, we have evaluated some of those potentially important factors in osteoarthritis (OA) as observed sequentially for the first time in synovial fluids. DESIGN: Synovial fluids (SF) obtained between 1992-2002 were all routinely evaluated for gross appearance, leukocyte counts and microscopic examination of wet drop preparations. We used regular and polarized light and alizarin red s stains. We separated out all OA patients, then we looked for patients who had more than two synovial fluid analyses to get sequential information. Time between first and final aspiration ranged from 2 to 7 (3.6+/-1.6) years and number of analyses per patients from 3 to 6 (3.3+/-0.7). We related synovial fluid crystals, fibrils and white blood cell count (WBC) to age, sex, disease duration and radiographic assessment according to the Kellgren-Lawrence radiographic rating system. RESULTS: Of 4523 synovial fluid examinations, we found 855 in patients with knee OA; 330 patients with adequate clinical details for comparison were included in our study. Twenty-six patients (one woman and 25 men) had sequentially examined SF. We found that 52% of those OA patients with effusions studied had crystals identified in their synovial fluid. Twenty-one percent of all the patients had CPPD crystals, 47% had hydroxyapatite, also called basic calcium phosphate (BCP) crystals and 16% had both types of crystals. Microscopically identifiable fibrils were found in 60% of SF. In sequentially examined patients, CPPD crystals and apatite (BCP) were found in 19% and 23%, respectively, at the first aspiration and, in 34% and 58% at the final aspiration. Fibrils were seen in 54% at first examination and 85% later. Apatite and fibrils showed more significant correlation with time (r=0.51,r =0.92) than did CPPD (r=0.32). SF WBC correlated only with CPPD crystals and did not increase with OA duration or severity. CPPD, apatite and fibrils all correlated with higher radiographic grades of OA. CONCLUSIONS: As noted before CPPD and apatite crystals were more common in patients with more severe OA. New findings are that our sequential cases showed that there were some patients with no crystals at onset but that crystals appeared with progression of the disease. Fibril presence in SF also correlated with progression of the disease.

Aged↗

Hospital-acquired infections following the 1999 Marmara earthquake.

In this study, medical records of all casualties admitted to our hospital following the Marmara earthquake, which struck northwest Turkey and resulted in the destruction of several towns in the Marmara region, were evaluated retrospectively. The time buried under the rubble, demographic data, type of medical and surgical therapies performed, type of injury and data on infection were analysed. Between 17 August and 25 September 1999, 630 trauma victims were received at our hospital and 532 (84%) of them were hospitalized. The mean age of hospitalized patients (312 males, 220 females) was 32 years (2-90 years). Two hundred and twenty patients were hospitalized for more than 48 h. Forty-one of them (18.6%) had 43 hospital-acquired infection (HAI) episodes, which were mostly wound infections (46.5%). A total of 143 culture specimens was collected and 48 yielded the following potential pathogens: 15 Acinetobacter baumanii (31.2%), nine Staphylococcus aureus (18.7%), seven Pseudomonas aeruginosa (14.6%), six Escherichia coli (12.5%), six Klebsiella pneumoniae (12.5%), two Stenotrophomonas maltophilia (4.2%) and three various Pseudomonas spp. (6.3%). All S. aureus strains were found to be resistant to methicillin in vitro. Two strains of A. baumannii and one P. aeruginosa were found to be resistant to all antimicrobials including carbapenems. Fifty-three victims died (10%) and 36 of those died during the first 48 h because of severe injuries and multi-organ failure. After 48 h of hospitalization, the mortality rate was significantly higher in those patients with HAI (14/41) than those without (3/179) (34.1% vs. 1.7%, P<0.05). In conclusion, trauma is the significant factor associated with HAI and a high incidence of Acinetobacter strains was responsible for HAI in trauma patients.

Acinetobacter↗

Comparison of the therapeutic efficacy of 4-methylpyrazole and N-acetylcysteine on acetaminophen (paracetamol) hepatotoxicity in rats.

Obtaining effective analgesia with a minimal erosive effect on gastric mucosal tissue has increased the consumption of acetaminophen (paracetamol), especially among the elderly. However, the hepatotoxic effects of acetaminophen have also increased. We aimed to compare the effects of 4-methylpyrazole (4-MP), N-acetylcysteine (NAC) and their combined use on the hepatotoxicity of acetaminophen in a rat model. Male Wistar Albino rats were divided into six groups. Groups 1-5 received 2,000 mg/kg acetaminophen by gavage while the control group was group 6. Group 2 animals were given NAC (loading dose 140 mg/kg followed by seven doses at 4 h intervals); group 3 received 50 mg/kg 4-MP; group 4 received 200mg/kg 4-MP; and group 5 received NAC as in group 2 plus 200 mg/kg 4-MP. Blood samples were taken for measurements of serum AST and ALT levels. The livers of the rats were removed for microscopic examination and grading of hepatic necrosis. AST and ALT levels in groups 2-5 were lower than that of group 1 (p < 0.001), although no significant difference was noted between groups 2-5 (p > 0.05). Higher levels of ALT were found in group 5 than in group 2 (p < 0.05), and higher levels of AST were found in group 5 than in group 3 (p < 0.01). Median necrosis scores were 3.36 for rats receiving acetaminophen alone (p < 0.001, compared with groups 2-6), 1.45-1.81 for groups 2-5 (p > 0.05, compared with each other), and 0.18 for control rats (p < 0.001, compared with groups 1-5). In conclusion, the administration of 4-MP and/or NAC after 4 h of administering toxic dose of acetaminophen, inhibits hepatotoxicity in rats. There was no difference between the 4-MP and NAC-treated groups as reflected by comparable levels of serum transaminases and the degree of hepatic necrosis. Combining of 4-MP and NAC offers no benefit.

Acetaminophen↗

Is there a role for Chlamydia pneumoniae infection in systemic lupus erythematosus and in the associated atherosclerotic cardiovascular disease?

OBJECTIVE: To search for molecular evidence of Chlamydial infection in systemic lupus erythematosus (SLE) subjects and to assess if there is an association of this infectious agent with coronary artery calcification (CAC), a marker of total atherosclerotic burden. METHODS: 28 SLE subjects had blood samples drawn and DNA extracted from peripheral blood mononuclear cells (PBMC) and an electron beam computed tomography (EBCT) scan. Polymerase chain reaction (PCR) analysis was performed for Chlamydia trachomatis 16srRNA and major outer membrane protein (MOMP) and for C. pneumoniae 16srRNA, MOMP, as well as nested PCR for MOMP. RESULTS: Four of 28 subjects (14.2%) had evidence of C. pneumoniae nucleic acid in PBMC. The 16srRNA primers detected C. pneumoniae in one patient (3.57%) and the nested PCR MOMP primers in 3 subjects (10.71%). None were positive for Chlamydia trachomatis. Two of the 4 subjects with C. pneumoniae DNA had abnormal EBCT scans and 2/11 (18.3%) subjects with abnormal EBCT were positive for C. pneumoniae. There were significant associations of C. pneumoniae DNA with smoking (OR = 3) and corticosteroid use. The odds ratio for subjects with abnormal CAC and detectable C. pneumoniae was 1.67. CONCLUSION: This pilot study demonstrates for the first time that C. pneumoniae DNA can be identified in the PBMC of some SLE subjects and there may be an association with CAC. Smoking may be an additional risk factor for infection in this population. Determination of pathogenicity of this organism in atherosclerotic coronary vascular disease in SLE will require further study.

Adult↗

Does rofecoxib increase TNF-alpha levels?

OBJECTIVE: Rofecoxib (Vioxx), the first COX-2 selective non-steroidal anti-inflammatory drug (NSAID), was recently withdrawn from the market due to the increased risk of acute myocardial infarction. The precise mechanism responsible for this phenomenon still remains unknown. Tumor necrosis factor alpha (TNF-alpha) is a cytokine, possibly most responsible for mortality in patients with acute myocardial infarction. However, this study was designed to study possible effects of rofecoxib on the level of TNF-alpha by using MSU crystal induced inflammation in the rat subcutaneous air pouch model. METHODS: Rat subcutaneous air pouches were produced and examinations commenced 6 days later. Control groups received only MSU crystals, or no crystals or drugs. To begin with, rofecoxib (30 mg/kg), indomethacin (20 mg/kg) or diclofenac (3 mg/kg) were administered to groups of 5 rats each. Thirty minutes later, MSU crystals were injected into air pouches, except for the negative control group. Twenty-four hours later, the rats were sacrificed for aspiration of fluid and for the dissection of pouch walls to determine leukocyte counts, pouch wall histology, and to assay IL-10 and TNF-alpha. RESULTS: Intra-pouch injection of MSU crystals, compared to non-injected pouches, caused an increase in white blood cell count (WBC) (30 +/- 44.7 versus 4508 +/- 792.3 cells/mm3), in the numbers of pouch wall vessels (vascular index) (4.8 +/- 0.3 versus 11.4 +/- 1.5 vessels/high-power field) and in TNF-alpha (50.0 +/- 13.4 versus 70.34 +/- 20.9 ng/mL), but not in interleukin-10 (IL-10) (60.6 +/- 63.0versus 61.48 +/- 7.1). WBC and vascular index were significantly reduced in all study groups compared to the control group (p < 0.05). Levels of TNF- in fluids were unexpectedly and significantly (p < 0.05) increased in all cases. The highest level of TNF-alpha was found in the rofecoxib group. In contrast to TNF-alpha, IL-10 levels were significantly (p < 0.05) decreased in all three drug groups. Indomethacin tended to suppress inflammation more effectively. However, there was no significant difference between the groups for IL-10 (p > 0.05). CONCLUSION: All three NSAIDs exhibited anti-inflammatory activity against MSU crystal induced inflammation. The difference in anti-inflammatory effects of these three non-steroidal drugs is seen not only in the anti-inflammatory effect on MSU induced inflammation but also in the nature of the effects. Refocoxib tended to increase the TNF-alpha level. Whether increased TNF-alpha levels can help explain the side effect of COX-2 specific inhibitors still requires further studies.

Animals↗