Engin Günel

Effect of antioxidant therapy on collagen synthesis in corrosive esophageal burns.

Abstract To investigate the efficacy of antioxidant therapy on collagen synthesis in corrosive esophageal burns, 110 Sprague-Dawley rats were divided into five groups of 22 animals each. A standard esophageal caustic burn was produced by 1 ml of 10% sodium hydroxide solution for the rats in groups B to E; group A was instilled only with 0.9% saline after preparation of the distal esophageal segment. Group A animals (controls) were uninjured and untreated. Group B had untreated esophageal burns. Esophageal burns were treated in group C with vitamin E (10 mg/kg IM), in group D with vitamin C (10 mg/kg IP), and in group E with methylprednisolone (30 mg/kg IM) on each of 5 days. Eight rats from each group were killed 4 days after initiation of the study and the abdominal esophagus was studied for tissue malondialdehyde (MDA; μmol/g protein) levels. The other rats were killed 28 days after initiation of the study and determination of hydroxyproline (HP) (μg/g tissue) levels in esophageal tissue was performed for 8 rats in each group. Histopathologic evaluation was also performed in the other 6 rats from each group. MDA levels in esophageal tissue were significantly lower in groups C (9.24 ± 2.62, P < 0.01) and group E (6.26 ± 2.22, P < 0.001) than in group B (12.35 ± 1.80). HP levels were significantly lower in groups A (0.75 ± 0.21, P < 0.001), C (1.11 ± 0.15, P < 0.01), and E (0.96 ± 0.15, P < 0.001) than in group B (1.40 ± 0.20). Histopathologically, collagen deposition in the submucosa and tunica muscularis was lower in groups C and E than in group B (P < 0.05, and 0.01, respectively). Our results demonstrate that treatment with antioxidant drugs such as vitamin E and methylprednisolone decreased tissue HP levels, and thus inhibited new collagen synthesis and stricture formation in rats with alkali-induced caustic esophageal burns.

Treatment of intestinal reperfusion injury using antioxidative agents

BACKGROUND/PURPOSE A number of antioxidants are present in human tissues, which comprise the secondary defence system against the oxygen-free radicals and oxidative stress. Therefore, this study was undertaken in an animal model to investigate the effects of antioxidants such as vitamin E, vitamin C, methyl prednisolone, and mannitol, on the treatment of intestinal reperfusion injury when given during ischemia. METHODS The study was performed on six groups of animals, each composed of six rabbits: Group I, mesenteric ischemia group; group R, ischemia-reperfusion group; group E, ischemia-reperfusion plus Vitamin E treatment; group C, ischemia-reperfusion plus vitamin C treatment; group CS, ischemia-reperfusion plus corticosteroid treatment; and Group M, ischemia-reperfusion plus mannitol treatment. Malondialdehyde (MDA) and glutathione (GSH) levels of the intestinal mucosa were assayed to reflect the free radical formation. RESULTS Mucosal injury scores in the M and C groups were significantly lower than the R group (P< .01 and P< .01, respectively), and in the E and CS groups, mucosal injury scores were not significantly different from R group. MDA levels in the M and C groups were significantly lower than the R group (P < .01 and P < .01, respectively). GSH levels in the E, C, and M groups, were significantly higher than R group (P < .01, P < .05, and P < .01, respectively). CONCLUSION The results of this study showed that antioxidant drugs, such as vitamin C and mannitol, may play a role in attenuating reperfusion injury of the gut demonstrated by depression of tissue MDA levels and by elevation of tissue GSH levels.

Reactive oxygen radical levels in caustic esophageal burns

PURPOSE This study was designed to determine the tissue levels of reactive oxygen radicals in caustic esophageal burns in a rat model. METHODS Forty rats were divided into four groups of 10 animals each. The control rats were uninjured in group A, and the others were injured rats in groups B, C, and D. Through a median laparatomy incision, a 1.5-cm abdominal esophageal segment was isolated and tied with 2-0 chromic sutures in all groups as described by Gehanno. One milliliter of 10% sodium hydroxide solution in groups B, C, and D and 0.9% saline solution in group A were instilled through the isolated segment via a no. 24 cannula for 3 minutes, then the esophagus was rinsed for 1 minute with distilled water. The studied 1.5 cm of the abdominal esophagus was removed from each animal 24 hours after caustic injury in group B, 48 hours after in group C, and 72 hours after in group D. In group A, studied uninjured segments were removed for biochemical investigation. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined for each group. RESULTS The mean MDA levels in esophageal tissue were significantly higher in groups B, C, and D than in group A (P < .05). Moreover, the mean GSH levels in the same esophageal tissues were significantly lower in groups C and D than in groups A and B (P < .05). CONCLUSION The reactive oxygen radicals may be play an important role in early phase of caustic esophageal burns by increasing the tissue damage.

Serum D-lactate levels as a predictor of intestinal ischemia-reperfusion injury

Abstract Currently, no serum marker has proved helpful in diagnosing intestinal ischemia and reperfusion (I/R) injury. An experimental study was conducted to determine the value of serum D-lactate in detecting intestinal I/R injury. Thirty New Zealand White rabbits were divided into three groups of 10 animals each: sham-operation controls (S); I/R; and I/R plus mannitol treatment (M). Serum samples were obtained before operation (T0), at the end of the ischemic period (T1), after the first 30 min of reperfusion (T2), and at the end of the reperfusion period (T3). In Group S, mean D-lactate levels for T0, T1, and T2 were 0 μg/dl, while T3 was 5.8 ± 4.7 μg/dl. Before the operation (T0), serum mean D-lactate levels were 0 μg/dl in all groups (S, I/R, M). Levels increased after 1 h of ischemia (T1) in groups I/R (83.5 ± 25.6 μg/dl) and M (89.8 ± 19.9 μg/dl), but not in group S (0 μg/dl). The mean T2 level in group I/R (231.6 ± 78.6 μg/dl) was statistically higher than in group M (140.1 ± 53.5 μg/dl) (P = 0.007). At the end of the reperfusion period, the mean T3 level in group I/R (698.4 ± 360.4 μg/dl) was significantly higher than in group M (158.7 ± 61.4 μg/dl) (P = 0.000). In group I/R, mean D-lactate levels changed significantly at each time point (T1 vs T2, P = 0.001; T2 vs T3, P = 0.004). However, in group M the increase from T1 to T2 was significant (P = 0.012), but that from T2 to T3 was not (P = 0.293). As a result, the mean T3 level was significantly higher than the T2 level in group I/R (P = 0.004), but not in group M. This study confirmed a significance rise in D-lactate levels in animals with I/R injury compared to sham-operated and I/R injury plus M treatment. We suggest that serum D-lactate levels could be a useful marker of intestinal I/R injury before laparatomy.

Intestinal ischemia-reperfusion and plasma enzyme levels.

Abstract Determination of blood levels of intracellular enzymes is an appropriate method to evaluate tissue and organ damage. To show systemic tissue damage resulting from intestinal ischemia-reperfusion, New Zealand rabbits underwent 60 min intestinal ischemia and 60 min reperfusion. Plasma samples were obtained before and at 55, 70, and 120 min after operation and enzyme levels were determined. Plasma aspartate aminotransferase (AST) showed a significant increase during reperfusion while lactate dehydrogenase (LDH) and creatine kinase (CK) levels were significantly increased at the end of ischemia and continued to be so throughout reperfusion. It is difficult to claim that enzymes arise from the intestine, but an increase of CK, LDH, and later of AST without any increase in alanine aminotransferase levels during ischemia suggests that their primary source is the injured intestine. Increased levels of plasma enzymes do not provide exact information about the location, but do reveal the presence of an injury.

Acute-phase changes in children recovering from minor surgery

Abstract The metabolic response to surgical stress is a nonspecific increase in hepatic synthesis of some specialized acute-phase proteins and a decrease in plasma concentrations of visceral proteins following surgical trauma. This study was undertaken determine which specific proteins were the better clinical indices in monitoring the metabolic response to surgical stress in children recovering from minor surgery. Forty-four patients undergoing elective inguinal surgical procedures under general anesthesia were studied. Blood samples were collected preoperatively (−1) and at 1(+1) and 5(+5) days postoperatively to determine albumin (AL), Prealbumin (PA), C-reactive protein (CRP), and a1-acid glycoprotein (AGP) values, and to calculate the prognostic inflammatory and nutritional index (PINI). Mean AL values were the same on all days. Mean PA  +1 was significantly lower than PA −1 and PA +5 (P < 0.001). Median CRP +1 and mean AGP +1 values were significantly higher than median CRP −1 and mean AGP −1 (P < 0.0001), respectively. Although there was a decrease after postoperative day 1, median CRP +5 and mean AGP +5 values were still significantly higher than preoperative values (P < 0.01 and P < 0.0001). Moreover, the median PINI +1 was also greater than PINI −1 and PINI +5 (P < 0.0001), but the median PINI+5 was significantly higher than PINI −1 (P < 0.01). Median percent changes of PINI values were significantly higher than those of the other parameters from both preoperatively to postoperative day 1 and preoperatively to postoperative day 5. Although several specific proteins (AL, PA, CRP, and AGP) have been evaluated as indicators of the acute metabolic response, we suggest that the PINI is more valuable for reflecting the response to surgical stress in patients recovering from minor surgery.

Hepatoblastoma in a child with neurofibromatosis type I.

A major hallmark of NF1 is the development of benign tumors, including peripheral neurofibromas, plexiform neurofibromas, gliomas of the optic tract, other low grade gliomas, and pheochromocytomas. Hepatoblastoma have not been previously reported in patients with neurofibromatosis type 1. We present a case of a 9‐month‐old boy diagnosed with both hepatoblastoma and neurofibromatosis type 1. Hepatoblastoma occurs in association with several well‐described cancer predisposition syndromes, including familial adenomatous polyposis, Beckwith–Wiedemann syndrome, Li‐Fraumeni syndrome, trisomy 18, and glycogen storage disease type I. This paper describes a case of hepatoblastoma diagnosed in association with neurofibromatosis type 1. Pediatr Blood Cancer 2007;49:357–359.

Mesenchymal hamartoma of the liver mimicking hepatoblastoma.

Mesenchymal hamartoma of the liver is a cystic benign liver mass occurring in children. Diagnostic confusion with hepatoblastoma may arise when alpha-feto-protein (AFP) level is elevated. We report an extremely rare case of mesenchymal hamartoma in an 11-month-old boy. Serum AFP was elevated and fine-needle aspiration biopsy suggested the lesion as hepatoblastoma, so he received preoperative chemotherapy. At the end of the preoperative chemotherapy, the tumor size and AFP level decreased. A right hepatectomy was performed. The pathologic examination of the specimen revealed mesenchymal hamartoma. Mesenchymal hamartoma of the liver with increased serum AFP levels may mimic hepatoblastoma if a cytological examination samples only the hepatocellular component of mesenchymal hamartoma. According to our knowledge, this is the first case of the mesenchymal hamartoma of the liver, which showed reduction in serum levels of AFP and involution of the tumor size by preoperative chemotherapy.

Ultrasound-guided percutaneous drainage in the treatment of children with hepatic hydatid disease.

Abstract The present study was designed to establish the safety and efficacy of ultrasound-guided percutaneous drainage in the treatment of hepatic hydatid cysts in children. A total of 14 cysts in eight patients were drained under aseptic conditions and continuous ultrasound guidance. An 18-G needle was used for puncture and silver nitrate solution as the scolecoidal agent. All procedures were successful. During follow-up, repeated ultrasound examinations revealed a progressive decrease in cyst size and an alteration in the cyst echopattern. None of the patients had a rise in hydatid antibody titer. There were no immediate or late complications. We conclude that the safety and efficacy of ultrasound-guided percutaneous drainage are satisfactory for the treatment of hepatic hydatid cysts in children.

Helicobacter pylori and hypergastrinemia in children with recurrent abdominal pain

Abstract Recurrent abdominal pain (RAP) is a significant problem in the pediatric population, and there has been much recent interest in the role that Helicobacter pylori (Hp) might play in this disorder. In this case control study, the authors aimed to determine whether Hp is an agent responsible for RAP, and to assess fasting gastrin concentrations in children with and without RAP in the Hp-positive and -negative groups. The study was conducted in 42 patients with RAP and 50 healthy children attending routine day-case surgery as a control group, aged 3 to 15 years, over a 12-month period. Of the 42 children with RAP, 30 were seropositive (71.4%) for Hp IgG, and of 50 children in the control group, 32 were seropositive (64%) for Hp IgG (P > 0.05). We found that Hp infection was as high in healthy children as in children with RAP. The mean fasting gastrin levels in 62 Hp-seropositive children (60.4 ng/l) were not different from those in 30 Hp-seronegative children (57.3 ng/l) and those in 42 children with RAP (58.2 ng/l) were also not significantly different from those in 50 healthy children (62.9 ng/l). Thus, no association between childhood Hp infection, hypergastrinemia, and RAP was found in our Turkish population.