Damaging Effects of Total Parenteral Nutrition Formula on Vascular Endothelium.

OBJECTIVES: Sepsis in one of the most serious complications that can occur during total parenteral nutrition (TPN) procedures. In this experimental study, we investigated the effects of TPN, with or without lipid emulsion, on vascular endothelial damage. METHODS: In total, 50 rabbits were used, divided into 5 groups of 10 each. TPN with lipids (group 1), TPN without lipids (group 2), and 0.09% saline (group 3) were given for 10 days via a central venous catheter. Group 4 received no treatment other than placement of a central venous catheter for 10 days. Group 5 was a control group. At the end of day 10, rabbits were sacrificed and tissue samples of liver, kidney, and inferior vena cava were prepared and examined by immunohistochemical methods for vascular cellular adhesion molecule (VCAM)-1 expression. RESULTS: In tissue sections of liver, kidney, and inferior vena cava, VCAM-1 activity was increased prominently in TPN with and without lipids compared with the control group. VCAM-1 activity in the TPN with lipids group was decreased versus the TPN without lipids group (P > 0.05). CONCLUSIONS: The TPN procedure results in vascular endothelial cell damage not only in the vein where the solution is introduced but also in other parts of the vascular system. Even if it is not statistically significant, lipids in the TPN formula may decrease this endothelial cell damage, as shown by immunohistochemistry.

Protective effects of dexpanthenol in an experimental model of necrotizing enterocolitis.

BACKGROUND/PURPOSE: In pathogenesis of necrotizing enterocolitis (NEC), both oxidative stress and inflammation are considerable risk factors. The study was designed to evaluate whether administration of dexpanthenol (Dxp) is able to attenuate intestinal injury through the antioxidant and antiinflammatory mechanisms in a neonatal rat model of NEC. METHODS: Forty newborn pups divided into four groups were included in the study: control, control+Dxp, NEC, and NEC+Dxp. NEC was induced by hyperosmolar formula and additionally the pups were exposed to hypoxia/hyperoxia and cold stress. They were sacrificed on postnatal day four, and their intestinal tissues were analyzed biochemically and histopathologically. RESULTS: Dxp caused a significant decrease in intestinal damage as determined by the histological score, villus height and number of goblet cells in NEC groups (p<0.0001). Tissue malondialdehyde, total oxidant status, and oxidative stress indexes levels were higher in the NEC group than in the control and control+Dxp groups (p<0.001). These values were reduced in the pups treated with Dxp (p≤0.004). Superoxide dismutase, glutathione peroxidase, and reduced glutathione activities were significantly reduced in the NEC group compared to the others (p<0.005). Treatment with Dxp significantly reduced elevations in tissue homogenate levels of tumor necrosis factor-α and interleukin-1ß in the NEC+Dxp group (p=0.002 and p=0.01, respectively). CONCLUSIONS: Dexpanthenol seems to have antiinflammatory and antioxidant properties. Prophylaxis with Dxp has a potential to reduce the severity of intestinal damage in NEC in the animals.

Protective effect of leflunomide against oxidative intestinal injury in a rodent model of sepsis.

BACKGROUND: Sepsis is defined as an uncontrolled inflammatory response in a host. The process may lead to severe sepsis, multisystem organ failure and even death. Leflunomide has important immunomodulatory and anti-inflammatory effects, which may mitigate host response to bacterial translocation. The goal of our study was to measure the effects leflunomide administration had on a variety of biochemical markers upregulated in systemic inflammatory response syndrome, sepsis, and multiple organ failure syndrome. MATERIALS AND METHODS: Wistar albino type rats were randomly divided into five groups: control, sham, leflunomide, sepsis, and sepsis + leflunomide. Sepsis was achieved by means of the cecal ligation and puncture method. Leflunomide 2 × 10 mg/kg/d was administered before the experiment. At the end of 24 h, the tissue levels of superoxide dismutase, catalase activity, malondialdehyde, nitric oxide, and protein carbonyl were measured. RESULTS: The level of the bowel superoxide dismutase and catalase levels of the sepsis group is significantly lower than those of the control, sham, and leflunomide groups (P < 0.05). Malondialdehyde, nitric oxide, and protein carbonyl levels are significantly higher in sepsis compared with other groups (P < 0.05). CONCLUSIONS: Leflunomide's prevention of protein and lipid peroxidation was observed in septic bowel tissue. Use of leflunomide could have protective effects against both the onset and the progressive stages of sepsis.

Schwannoma with an uncommon upper lip location and literature review.

Schwannomas are usually single, encapsulated, and benign tumors of the nerve sheath that arise from the perineural Schwann cells. Schwannomas are mostly seen in the fourth decade. Despite its location in the head and neck region is 25-45%, lip location of schwannoma are very rare. We present a case of a upper lip schwannoma in the pediatric age and review the literature.

Pain, fentanyl consumption, and delirium in adolescents after scoliosis surgery: dexmedetomidine vs midazolam.

BACKGROUND: The study aim was to compare the efficacy of dexmedetomidine vs midazolam for sedation during the early postoperative period in adolescents who underwent scoliosis surgery. METHODS: We performed a prospective, randomized trial in an intensive care unit (ICU) in a tertiary care center. In this study, 42 patients (American Society of Anesthesiology physical status I and II) who underwent scoliosis surgery were divided into two groups according to sedation protocols: group dexmedetomidine (DEX) (n = 22) and group midazolam (MDZ) (n = 20). Adolescents (12-18 years) requiring mechanical ventilation underwent a continuous infusion of either dexmedetomidine (group DEX; starting dose, 0.4 µg·kg(-1) ·h(-1)) or midazolam (group MDZ; starting dose, 0.1 mg·kg(-1) ·h(-1)) with intermittent fentanyl, as needed. The efficacy of sedation was assessed using the Richmond Agitation Sedation Scale (RASS). Quality of pain relief was measured using the Numeric Visual Analog Scale (NVAS). Delirium was determined in patients in the RASS range of -2 to +1 using the Confusion Assessment Method for the ICU (CAM-ICU). Fentanyl consumption, incidence of delirium, NVAS scores, and hemodynamics were recorded postoperatively at 2, 4, 6, and 24 h in the ICU. RESULTS: The NVAS pain scores and fentanyl consumption at all the evaluation time points were significantly higher in group MDZ than those in group DEX (P < 0.05). Further, total fentanyl consumption in group MDZ was significantly higher than that in group DEX (P < 0.05). Delirium was significantly higher in the group MDZ than that in group DEX (31.3% vs 12.5%) when analyzed as the endpoint of CAM-ICU (P < 0.05). The heart rate was significantly lower in group DEX compared with that in group MDZ at all the evaluation time points (P < 0.05). CONCLUSION: Dexmedetomidine was associated with the decreased postoperative fentanyl consumption, NVAS scores, and a decreased incidence of delirium. These findings may be beneficial for managing sedation protocols in adolescents who have undergone scoliosis surgery.

Effects of tolterodine and trospium chloride on renal damage induced by partial upper urinary tract obstruction.

OBJECTIVE: To examine the efficacy of trospium chloride and tolterodine on the renal parenchymal inflammatory process and upper urinary dilation in rats with chronic partial upper urinary tract obstruction. MATERIALS AND METHODS: A total of 32 rats were divided into 4 groups: group 1, control; group 2, obstruction; group 3, obstruction plus tolterodine; and group 4, obstruction plus trospium chloride. In all groups, except for group 1, partial upper urinary tract obstruction was induced by embedding the upper quarter of the right ureter into the psoas muscle for 14 days. At the end of the experiment, the rats were killed. The catalase, malondialdehyde, and protein carbonyl levels were determined in renal tissue. Tubular dilation and parenchymal inflammation were evaluated using hematoxylin-eosin staining. Smooth muscle actin and cytoglobin were examined with immunohistochemical staining. RESULTS: The obstruction group demonstrated severe pelvic dilation and parenchymal inflammation and increased smooth muscle actin staining in the wall of upper urinary tract (P <.05). The treatment of the rats with tolterodine and trospium chloride markedly attenuated the inflammatory alterations and reduced tubular dilation. This treatment also reduced elevated oxidative stress product levels and restored the depleted renal antioxidant enzyme. CONCLUSION: These findings imply that increased renal pelvic pressure can contribute to renal parenchymal injury in chronic pelvic upper urinary tract obstruction. Antimuscarinic medications such as tolterodine and trospium chloride exert renoprotective effects, probably by prevention of pelvic pressure increases.

Xanthogranulomatous pyelonephritis with unconnected liver lesion.

Xanthogranulomatous pyelonephritis is a chronic renal inflammation characterized by destruction and replacement of its parenchyma with granulomatous tissue. This uncommon condition is rare in children. We report on a 5-month-old male infant with a left renal and hepatic mass detected by ultrasound. The case was preoperatively misdiagnosed as Wilms' tumor and total nephrectomy and biopsy from liver lesion were performed. The subsequent histopathological findings confirmed the diagnosis of xanthogranulomatous pyelonephritis for renal and liver lesions. Increasing awareness of this disease should lead to the diagnosis being suspected preoperatively even if it is with unconnected tissue lesions.

Effect of leflunomide on liver regeneration after partial hepatectomy in rats.

PURPOSE: Partial hepatectomy (PH) can be an inevitable surgical therapy in some conditions, such as hepatic malignancies, trauma or partial liver transplantation. Its capacity for regeneration distinguishes the liver from other essential organs. Regeneration is a complex process involving growth factors, cytokines, transcription factors, hormones, and oxidative stress products. In the event of ineffective or total absent liver regeneration, the life threatening picture of acute liver failure may supervene. In the present research, we studied the effect of leflunomide, a novel immunosuppressive and antiinflammatory agent against autoimmune disease, on hepatic regeneration after PH in Wistar Albino rats. METHODS: Thirty-five Wistar albino rats were divided into five groups: group 1, control; group 2, sham; group 3, drug control (was treated with leflunomide 10 mg/kg/d/i.g.); group 4, PH; group 5, PH + leflunomide. As for PH, approximately 70% of the rat liver was surgically removed under general anesthesia. On postoperative day 3, all rats were humanely killed. Catalase (CAT), superooxide dismutase (SOD) and myeloperoxidase (MPO) activities with malondialdehyde (MDA), nitric oxide and protein carbonyl (PC) levels were determined in remnant liver tissue. Inflammatory process and liver regeneration were evaluated with H&E and KI67, respectively. RESULTS: The tissue levels of MDA, PC and MPO were lower in group 5 than levels in group 1. PH significantly decreased the enzymatic activity of CAT (p < 0.05) and SOD. This reduction was significantly improved by the treatment with leflunomide. Histopathologically the enhancement of the liver parenchymal regeneration in the group 5 was significantly greater than the group 4. CONCLUSION: The findings imply that oxidative stress products play a preventive role in liver regeneration after PH and leflunomide ameliorates the regeneration probably by the radical scavenging and antioxidant activities.

Prevention of renal ischemia/reperfusion-induced injury in rats by leflunomide.

OBJECTIVE: There is increasing evidence to suggest that toxic oxygen radicals play an essential role in the pathogenesis of ischemia/reperfusion (I/R) injury in the kidney. This study was designed to investigate the effects of leflunomide, an isoxazole derivative and a unique immunomodulatory agent, in I/R-induced renal injury in rats. METHODS: Forty female Sprague-Dawley rats were divided equally into four groups: (I) control (only leflunomide 10 mg/kg, intragastrically treated); (II) sham operated (only unilateral nephrectomy); (III) I/R; and (IV) leflunomide (10 mg/kg for two doses prior to experiment) plus I/R groups. In groups III and IV, after unilateral nephrectomy, the rats were subjected to 60 min of left renal pedicle occlusion, followed by 6 h of reperfusion. At the end of the reperfusion period, rats were killed and kidneys and blood were removed. Catalase, myeloperoxidase and xanthine oxidase activities, and malondialdehyde, nitric oxide and protein carbonyl levels were determined in renal tissue. Serum creatinine, blood urea nitrogen and aspartate aminotransferase were measured for the evaluation of renal function. In histopathological examination, renal damage was scored 0-3. RESULTS: Group III animals demonstrated severe deterioration of renal function, renal morphology and a significant renal oxidative stress. Pretreatment of animals with leflunomide markedly attenuated renal dysfunction, morphological alterations, reduced elevated oxidative stress products levels and restored the depleted renal antioxidant enzyme. CONCLUSION: The findings imply that oxygen radicals play a causal role in I/R-induced renal injury, and leflunomide exerts renoprotective effects probably by the radical scavenging and antioxidant activities with immunomodulatory effect.

Hepatic damage in biliary-obstructed rats is ameliorated by leflunomide treatment.

Cholestasis, or impaired bile flow, occurs in a wide variety of liver diseases and causes hepatic damage by retention and accumulation of toxic hydrophobic bile salts inducing persistent inflammation and oxidative stress. In the present research, we studied the effect of leflunomide, a novel immunosuppressive and anti-inflammatory agent against autoimmune disease, on hepatic damage produced by double ligature of the extrahepatic biliary duct in Wistar Albino rats. Cholestasis was done by double ligature and section of the extrahepatic biliary duct (BDL). Leflunomide was given i.g. 10 mg/kg/day. The severity of cholestasis and hepatic injury was determined by changes in the plasma enzyme activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and levels of direct bilirubin. Malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) were determined to the oxidative status in the liver tissue. Myeloperoxidase (MPO) activity and levels of tissue hydroxyproline (HPR) were determined to neutrophil activation and collagen accumulation, respectively. Further, histological changes were studied. Treatment with leflunomide markedly reduced serum transaminase activities as compared to BDL rats. At the same time leflunomide significantly inhibited increases in liver MDA, PC and NO levels and also attenuated the depletion of CAT and SOD in the liver after bile duct ligation. Similarly, increase in tissue MPO activity and HPR due to BDL was also attenuated by leflunomide treatment. These findings were supported by histopathological findings. These findings suggested that leflunomide can attenuate hepatic damage in extrahepatic cholestasis by prevention of oxidative stress and inflammatory process.

Polyenylphosphatidylcholine pretreatment ameliorates ischemic acute renal injury in rats.

AIM: Polyenylphosphatidycholine has been demonstrated to have antioxidant, cytoprotective and anti-inflammatory effects. Whether polyenylphosphatidycholine pretreatment affects ischemia/reperfusion-induced renal damage in vivo is not known and was investigated here in rats. METHODS: Forty female Sprague-Dawley rats were divided into three groups. Group 1 (n = 10) was given saline (control, sham operated). Group 2 (n = 15) were given saline, and Group 3 (n = 15) were given polyenylphosphatidycholine (100 mg/day for 10 days prior to experiment). Groups 2 and 3 were subjected to bilateral renal ischemia (60 min) followed by reperfusion (6 h). After the reperfusion period, the rats were sacrificed and kidney tissue superoxide dismutase, glutathione, total nitrite and nitrate, malondialdehyde and myeloperoxidase levels, plasma aspartate aminotransferase, blood urea nitrogen and creatinine concentrations, and nuclear factor kappa beta expression were determined. RESULTS: Serum levels of aspartate aminotransferase, blood urea nitrogen and creatinine were significantly decreased (P < 0.05) in the treatment group compared to those in the ischemic group. There were significant differences between treatment and ischemic groups regarding the tissue superoxide dismutase, glutathione, total nitrite and nitrate, malondialdehyde, and myeloperoxidase levels (P < 0.05). In addition, polyenylphosphatidycholine pretreatment reduced nuclear factor kappa beta expression in ischemic kidney tissue. Kidneys obtained from rats pretreated with polyenylphosphatidycholine demonstrated marked reduction of the histological features of renal injury compared to kidneys obtained from Group 2 rats, including a little vacuolization, pyknosis and necrosis. CONCLUSIONS: Polyenylphosphatidycholine pretreatment provided significant protection against ischemia/reperfusion injury to the kidney. This treatment could be therapeutic in kidney transplantation and other conditions associated with ischemia/reperfusion injury to the kidney.

Urethral polyps in children: a review of the literature and report of two cases.

A solitary polyp of the urethra is a rare benign fibroepithelial growth and has often been described in boys. Its occurrence in girls is exceptional. In the present paper, two children with solitary polyps of the urethra are presented and discussed. The first case was an 18-month-old boy with a posterior urethral polyp arising from the posterior urethra and extending to the bladder. It was excised by cystostomy because of an unsuccessful endoscopic removal attempt. The second case was a 2-year-old girl with an interlabial mass arising from the posterior wall of urethra and protruding from the external urethral meatus. It was excised transurethrally.

Protective effects of leflunomide against ischemia-reperfusion injury of the rat liver.

Hepatic ischemia-reperfusion (I/R) injury may be developed in some conditions, such as trauma, major hepatic resection, hemorrhagic shock or liver transplantation. I/R injury of the liver causes hepatocellular damage that may lead to hepatic failure. A considerable body of evidence indicates that reactive oxygen species (ROS) and inflammation may contribute to hepatocellular injury in liver I/R. Leflunomide is an isoxazole derivative, and a unique immunomodulatory agent. In the present study, we examined the effects of leflunomide on the neutrophil activation with oxidative stress and some antioxidant enzymes in the reperfusion following I/R in the rat liver. Thirty-two rats divided into four groups: group 1 (control); was given leflunomide 10 mg/kg, i.g.; group 2 (SHAM), animals were only laparotomized; group 3 (liver I/R), and group 4 (liver I/R + Leflunomide). In group 4, rats were pretreated with leflunomide (10 mg/kg, i.g.) two doses prior to experiment. In groups 3 and 4, occluding the hepatic pedicel for 60 min induced ischemia and reperfusion was allowed thereafter for 60 min. At the end of the reperfusion period, rats were sacrificed. superoxide dismutase, catalase, nitric oxide, xanthine oxidase, malondialdehyde, protein carbonyl and myeloperoxidase levels were determined in hepatic tissue as well as histological examination with H and E staining. Group 3 animals demonstrated severe deterioration of liver morphology and a significant liver oxidative stress. Pretreatment of animals with leflunomide markedly attenuated morphological alterations and neutrophil activation, reduced elevated oxidative stress products levels and restored the depleted hepatic antioxidant enzyme. The findings imply that ROS play a causal role in I/R-induced hepatic injury, and leflunomide exerts hepatoprotective effects probably by the anti-inflammatory effect with radical scavenging and antioxidant activities.

Glial cell line-derived neurotrophic factor and synaptophysin expression in pelviureteral junction obstruction.

OBJECTIVES: To examine the expression of neuronal markers in congenital pelviureteral junction (PUJ) obstruction as a causative factor. The findings from some investigations have suggested that defective neuronal innervation may play an important role in the pathogenesis of PUJ obstruction. METHODS: Using specific antibodies, we studied the neuronal markers of specimens from 12 cases of PUJ obstruction and 10 normal PUJs by immunohistochemistry using glial cell line-derived neurotrophic factor (GDNF), synaptophysin, S-100, and neurofilament. RESULTS: In the PUJ obstruction specimens, staining with hematoxylin-eosin and Masson's trichrome revealed muscular hypertrophy and an increase in collagen tissue and fibrosis in the lamina propria and tunica muscularis. The most striking finding on immunohistochemistry was the marked nuclear staining of cells with synaptophysin in all layers of the PUJ obstruction specimens that was totally absent in the normal PUJ specimens. In addition, significantly less intense staining for GDNF was found in the PUJ obstruction specimens compared with the normal PUJ specimens. The underexpression of GDNF in PUJ obstruction specimens was localized in the muscular layer especially. Immunohistochemical staining for S-100 and neurofilament showed no differences in the expression level of these neuronal markers in normal and PUJ obstruction specimens. CONCLUSIONS: Because GDNF is a survival factor for central and peripheral neurons, defective expression of GDNF could play an important role in the defective neuronal innervation of PUJ obstruction. Intense nuclear expression of synaptophysin in all layers of obstructed PUJ specimens suggested that obstructed PUJs have a serious structural abnormality.

Polyenylphosphatidylcholine pretreatment protects rat liver from ischemia/reperfusion injury.

BACKGROUND: Hepatic injury induced by ischemia/reperfusion following surgery, transplantation, or circulatory shock combined with resuscitation is a major clinical problem. Polyenylphosphatidylcholine (PPC) has strong antioxidant, cytoprotective and anti-inflammatory effects. AIM: In this study, the influence of PPC pretreatment on ischemia-reperfusion (I/R) injury of the liver was examined in rats. METHODS: The animals were divided into three groups: control (n=10), I/R (n=15) and I/R+PPC (n=15). PPC was given 100mg/day for 7 days before experiment. Several parameters of hepatic damage, oxidative stress, neutrophil infiltration and nuclear factor kappa beta (NF-kappaB) expression were measured as well as microscopic examination. RESULTS: We observed that a significant reduction in AST and ALT values in the PPC treated group when compared with the ischemic group. The increases in hepatic total NO(2)+NO(3) and MDA, and decreases in SOD and GSH levels after reperfusion were partially, but significantly, inhibited by PPC pretreatment. I/R induced increase in hepatic myeloperoxidase content and NF-kappaB expression were also lowered by PPC pretreatment. Animals pretreated with PPC presented minimal hemorrhage and reduced signs of liver injury. CONCLUSION: PPC pretretament provided significant protection againts I/R injury to the liver. This treatment could be therapeutic in liver transplantation and other conditions associated with I/R injury.

Does pneumoperitoneum always require laparotomy? Report of six cases and review of the literature.

The presence of intraperitoneal free air signals perforation of a hollow viscus in over 90% of the patients. Rarely, however, the presence of pneumoperitoneum may not indicate an intra-abdominal perforation and thus may not require laparotomy. This condition, which poses a dilemma to the surgeon faced with this problem, is termed "nonsurgical", "spontaneous" or "idiopathic" pneumoperitoneum. Six cases of nonsurgical pneumoperitoneum admitted over a 2-year period to our institution are reported, and the etiological mechanisms and the pathophysiology of the appearance of intra-abdominal free gas are reviewed. Two of the six children with nonsurgical pneumoperitoneum underwent exploratory laparotomy when clinical examination suggested an acute abdomen; no intra-abdominal pathology was documented in one of these patients. In the other children, malrotation was found. Four patients, on ventilatory support, were managed conservatively after performing a diagnostic peritoneal lavage and/or contrast studies those were negative. An appreciation of the condition and its likely etiological factors should improve awareness and possibly reduce the imperative to perform emergency laparotomy on an otherwise well patient with an unexplained pneumoperitoneum.

Delayed gastric emptying in gastroesophageal reflux disease: the role of malrotation.

The association between gastroesophageal reflux (GER) and intestinal malrotation (IM) has been well described. Delayed or impaired gastric emptying in IM is thought to be a contributing factor in the development of gastroesophageal reflux disease (GERD). The current study assessed the role of malrotation in delayed gastric emptying in children with GERD. We also evaluated the interactions between GERD, malrotation, gastric pH abnormalities, and gastric dysmotility. Sixty-seven patients between 1 and 5 years of age (mean 3.08+/-1.2) and with symptoms of GER, such as emesis, reactive or recurrent lung disease, and/or growth retardation, were studied in 2001-2005. Upper and lower gastrointestinal contrast studies were performed for the diagnosis of malrotation. Gastric motility was evaluated with a liquid gastric emptying protocol. GER was documented by upper gastrointestinal studies, scintigraphy, and/or 24-h pH monitoring. In our series of 44 children with GERD, there was an unexpectedly high incidence of IM: 54.5% (24/44). IM has previously been known to occur in 25% of patients with GERD. GERD was found in 24 (82.7%) of 29 patients with IM. Mean nuclear gastric emptying (MNGE) was 51.6+/-8.04 min in patients with isolated GERD and 96.6+/-20.5 min in children with IM and GERD. There was a statistically significant difference in MNGE time (p<0.05) between children with primary GERD and in those with GERD and IM. Esophageal pH monitoring showed that mean fraction time below pH 4 was 7.06+/-1.1% in patients with isolated GERD and 14.7+/-4.1% in patients with IM and GERD. GERD is common in children between 1 and 5 years old. Using gastric emptying studies and esophageal pH monitoring, we have shown that gastric dysmotility and esophageal pH abnormalities are highly prevalent, especially in children with malrotation compared with children with isolated GERD. These findings suggest that malrotation is an important factor responsible for delayed gastric emptying in GERD. Hence, we recommend that all infants and children with GERD and delayed gastric emptying undergo careful evaluation for malrotation.

Plasma D-lactic acid level: a useful marker to distinguish perforated from acute simple appendicitis.

Early diagnosis of perforated appendicitis is important for reducing morbidity rates. The aim of this study was to determine the value and utility of plasma D-lactic acid levels in identifying the type of appendicitis. In this clinical study, plasma D-lactic acid levels were assessed in 44 consecutive paediatric patients (23 with acute appendicitis, 21 with perforated appendicitis) before laparotomy. D-lactic acid levels were determined by an enzymatic spectrophotometric technique using a D-lactic acid dehydrogenase kit. Patients with perforated appendicitis had higher D-lactic acid levels (3.970 +/- 0.687 mg/dL) than patients in the control group (0.478 +/- 0.149 mg/dL) and patients with acute appendicitis (1.409 +/- 0.324 mg/dL; p < 0.05). For a plasma D-lactic acid level greater than 2.5 mg/dL, the sensitivity and specificity of the D-lactic acid assay were 96% and 87%, respectively. The positive predictive value was 87%, the negative predictive value was 96%, and the diagnostic value was 91%. These results suggest that the measurement of plasma D-lactic acid levels may be a useful adjunct to clinical and radiological findings in distinguishing perforated from acute non-perforated appendicitis in children.

Small-dose capsaicin reduces systemic inflammatory responses in septic rats.

We investigated the influence of small- and large-dose capsaicin in modulating systemic inflammatory responses during different stages of sepsis in rats. Rats were divided into six groups: group C, control; group S, sepsis; group CLC, small dose of capsaicin (1 mg/kg subcutaneously); group SLC, small dose of capsaicin plus sepsis; group CHC, large dose of capsaicin (150 mg/kg subcutaneously); group SHC, large dose of capsaicin plus sepsis. Rats were made septic by cecal ligation and puncture (CLP). Each group was subdivided into two subgroups. The animals were killed at 9 or 18 h after CLP. Plasma concentrations of calcitonin gene-related peptide (CGRP), tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, and total nitrite/nitrate (NOx) were measured. Superoxide dismutase and malondialdehyde (MDA) were determined in liver, lung, and heart tissues. CGRP was increased in groups S, CLC, and SLC when compared with the other groups. In the SLC group, plasma concentrations of TNF-alpha, IL-6, NOx, and tissue MDA levels were reduced and IL-10 level was increased when compared with groups S and SHC 18 h after CLP (P < 0.05). Small-dose capsaicin treatment increased antiinflammatory IL-10 levels and attenuated the increases in proinflammatory cytokines, NOx, and tissue MDA in septic rats.

Effects of polyenylphosphatidylcholine on cytokines, nitrite/nitrate levels, antioxidant activity and lipid peroxidation in rats with sepsis.

OBJECTIVES: To determine the effect of pretreatment with polyenylphosphatidylcholine (lecithin, PPC) on plasma levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-10, total nitrite/nitrate (NOx), and tissue levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in septic rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University laboratory. SUBJECTS: Forty-five Spraque-Dawley rats were divided into three groups: group C, sham-operated; group S, sepsis; and group P, sepsis pretreated with PPC. INTERVENTIONS: Rats were made septic by cecal ligation and puncture (CLP). Group P rats were treated with PPC (100 mg/day orally) for 10 days before sepsis. Twenty-four hours later CLP, plasma concentrations of TNF-alpha, IL-6 and IL-10 and plasma levels of NOx were measured. SOD and MDA were determined in liver, lung and heart homogenates. MEASUREMENTS AND MAIN RESULTS: All rats in group P survived during the 24-h observation time after CLP, whereas survival rate in group S was 66.7% (10/15; P<0.05). PPC significantly reduced plasma levels of TNF-alpha (P=0.006), IL-6 (P=0.007), IL-10 (P=0.016), NOx (P<0.001), and tissue levels of MDA (P<0.001) in group P with respect to in group S. Tissue levels of SOD significantly increased in group P when compared with group S (P<0.001). CONCLUSIONS: These results show that PPC pretreatment exerts cumulative effects in decreasing the levels of cytokines, NOx, and tissue MDA concentrations, with a concomitant increase in survival in septic rats. Lecithin therapy may be a useful adjuvant therapy in controlling of the excessive production of the inflammatory cytokines in patients with severe sepsis. DESCRIPTOR: SIRS/sepsis, experimental studies.