Profile of paediatric umbilical hernias managed at Federal Medical Centre Umuahia.

BACKGROUND: Umbilical hernias are common in children but many resolve spontaneously within the first five years of life. Most umbilical herniorrhaphies in our environment are due to symptomatic hernias which constitute a small percentage of all umbilical hernias. PATIENTS AND METHODS: A retrospective review of all pediatric patients with UH treated at Federal Medical Centre Umuahia, Abia State from February 2001 to February 2011. RESULTS: There were 22 patients but only 20 of the folders were found and analyzed. They were made up of 11 males and 9 females with a mean age of 6.19 +/- 0.83 years and median age of 6 years. Nine(7 males and 2 females) had acute incarcerations, nine (3 males and 6 females) had recurrent umbilical pains without incarceration and two (1 male and 1 female) had recurrent incarcerations. Age range for acute incarceration was 2-8 years (mean: 4.69 years, median: 4 years); recurrent umbilical pains was 4 months -15 years (mean: 7.7 years, median: 8 years) and for recurrent incarceration 2-10 years (mean: 6 years). All had standard umbilical hernia repairs except one whose parents declined surgery after reduction of acute incarceration. One patient with acute incarceration had gangrenous bowel with hernia sac abscess and was offered bowel resection with end-to-end anastomosis. On short-term follow-up, the symptoms resolved in all the patients following surgery. Five patients had six complications: 1 exuberant granulation tissue, 2 stitch reactions, 2 superficial wound dehiscence and one superficial wound infection. There were no mortalities and no recurrence on short-term follow-up. Only one patient (5%) registered under the National Health Insurance Scheme (NHIS). CONCLUSIONS: Active observation of all umbilical hernias at all ages will ensure early detection of complications and prompt treatment. Elective repair of umbilical hernias in patientsabove five years with fascia defect greater than 1.5cm is encouraged. Comprehensive NHIS will ensure early presentation and reduced complications.

Effects of cigarette smoke with different tar contents on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.

The effects of smoke from cigarettes with two different tar contents (32 mg/cigarette, high tar, and 15 mg/cigarette, low tar) on hepatic and pulmonary monooxygenase (MO) activities (aniline 4-hydroxylase [AH]; aminopyrine N-demethylase [AMND]; 7-ethoxyresorufin O-deethylase [EROD]; p-nitroanisole O-demethylase [p-NAOD]), lipid peroxidation (LP) and reduced glutathione (GSH) levels and glutathione S-transferase (GST) activities toward several substrates (1-chloro-2,4-dinitrobenzene [CDNBI; 1,2-dichloro-4-nitrobenzene [DCNB]; ethacrynic acid [EAA]; 1,2-epoxy-3-(p-nitrophenoxy)-propane [ENPP]) were determined in adult male rats. Adult male rats were exposed to smoke of high- or low-tar cigarettes five times a day, with 1-hour intervals, for 3 days in a chamber where smoke and fresh air lead alternatively and were killed 16 hours after the last treatment. Smoke of both high- and low-tar cigarettes (SHTCC and SLTCC) significantly increased hepatic and pulmonary EROD and p-NAOD activities compared to controls. However, the increase noted by SHTCC on pulmonary EROD activity was higher than that of SLTCC. Hepatic AMND and pulmonary AH activities were significantly increased only by SHTCC. LP level was significantly decreased and increased by SHTCC in liver and lung, respectively, whereas it remained unaltered by SLTCC. Only SHTCC significantly increased GSH level in liver. In the lungs, both SHTCC and SLTCC significantly increased GSH level to the same extent. Hepatic GST activity toward EAA was significantly increased by SHTCC but was significantly decreased by SLTCC. ENPP GST activity was significantly decreased by SHTCC and SLTCC in the livers. In the lungs, all the GST activities examined were significantly depressed by SHTCC whereas only GST activity toward DCNB was reduced significantly by SLTCC. These results reveal that the hepatic and pulmonary MOs and GSTs are differentially influenced by SHTCC and SLTCC in rats.

7-ethoxyresorufin O-deethylase (EROD) activity is not capable of reflecting the overall malignant potential of breast cancer tissue.

7-Ethoxylesorufin O-deethylase (EROD) (mainly catalyzed by cytochrome P450 (CYP) 1A1 and used as a marker for CYP 1A1) activity was measured in the breast tumor and surrounding tumor free (normal) tissues of 37 female breast cancer patients with infiltrating ductal carcinoma. About 11% of the tumor and normal breast tissue samples lacked the enzyme activity. Large interindividual variations in the activities of EROD were found in both tumor and normal tissues ranging from 0 to 283 and 0 to 801 fmol/mg/min, respectively. However, no significant difference was noted between the mean EROD activities of tumor and normal breast tissues. This tendency did not change with the stage and grade of the malignancy and menopausal status. No significant correlation was observed between the EROD activity and stage or grade of malignancy (p > 0.05). Thus, it appears that EROD activity is not capable of reflecting the overall malignant potential of breast cancer tissue.

Glutathione and lipid peroxidation levels in human breast tumors.

The levels of reduced glutathione (GSH) and lipid peroxidation (LP) of breast tumor and surrounding tumor free (normal) tissues of 39 breast cancer female patients with infiltrating ductal carcinoma and the relationship between these two parameters were investigated. Large interindividual variations in the levels of GSH and LP were found in both tumor and normal tissues. The mean GSH levels of tumors were significantly higher than those of normal tissues. This tendency did not change with the stage and grade (excluding grade 1) of the malignancy, menopausal status and chemotherapy treatment. No correlation was found between GSH level and stage or grade of malignancy (p > 0.05). However, although more than half of the tumor samples (23/39, 59%) had higher LP levels than their corresponding normal tissues, no significant difference was noted between the mean LP levels of tumor and normal tissues. This tendency did not change with the stage and grade of the malignancy, and menopausal status and chemotherapy treatment. No relationship was observed between the LP level and stage or grade of malignancy (p > 0.05). Overall, no association existed between the levels of GSH and LP in tumors (p > 0.05). These results reveal that the GSH, but not LP, could be a marker of breast malignancy and that the increase in GSH level is not sufficient to lower the LP level in human breast tumors.

Xenobiotic metabolizing and antioxidant enzymes in normal and neoplastic human breast tissue.

An investigation was made of ethoxyresorufin O-deethylase (EROD) activity, a cytochrome P450 (CYP) dependent enzyme mainly catalyzed by CYP1A1, glutathione S-transferase (GST) activity toward the substrates 1-chloro-2,4- dinitrobenzene (CDNB) and ethacrynic acid (EAA), reduced glutathione (GSH) levels, and antioxidant enzyme (AOE) activity namely catalase (CAT) and selenium- dependent glutathione peroxidase (Se-GPx) in tumor and surrounding tumor-free (normal) tissues in female breast cancer patients. Wide interindividual variations were found in the enzyme activities in both tumor and normal breast tissues. No significant differences were noted between mean EROD and CAT activities in tumor and normal breast tissues. The mean activities of CDNB GST, EAA GST and Se-GPx and GSH levels in tumor tissue were significantly higher than those in normal breast tissue. These results show that CYP, GST and AOE behave differentially in breast tumors.

Gender dependent effects of cigarette smoke on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.

The adult male and female rats were exposed to cigarette smoke (CS) 5 times a day, with 1 h intervals, for 3 days in a chamber where smoke and fresh air lead alternatively and were killed 16 h after the last treatments and hepatic and pulmonary monooxygenase (MO) activities (aniline-4-hydroxylase, AH; aminopyrine-N-demethylase, AMND; 7-ethoxyresorufin-O-deethylase, EROD; p-nitroanisole-O-demethylase, p-NAOD), lipid peroxidation (LP) and reduced glutathione (GSH) levels and glutathione-S-transferases (GSTs) activities toward several substrates (1-chloro-2,4-dinitrobenzene, CDNB; 1,2-dichloro-4-nitrobenzene, DCNB; ethacrynic acid, EAA; 1,2-epoxy-3-(p-nitrophenoxy)-propane, ENPP) were determined. CS significantly increased hepatic AMND, EROD and p-NAOD activities whereas it unaltered AH activity in both genders as compared with controls. In the lung, EROD and p-NAOD activities were also significantly increased by CS in both genders. Pulmonary AH activity, however, significantly increased in males but remained unchanged in females. Pulmonary AMND activity significantly increased in females but remained unaltered in males. A significant decrease was noted in the LP level of males, while that of females was unaltered by CS in the liver. Pulmonary GSH and LP, and hepatic GSH levels were significantly increased by CS in both genders. In males, GST activities toward CDNB and DCNB did not alter, whereas GST activities toward EAA and ENPP significantly increased and decreased, respectively, in the liver. In females, CS significantly increased hepatic GST activity toward DCNB but it was ineffective on the other hepatic GST activities. All pulmonary GST activities of males were significantly depressed by CS. In females, however, CS significantly increased pulmonary GST activities toward CDNB and DCNB but was ineffective on GST activities toward EAA and ENPP. These results suggest that gender related differences exist in the modulations of hepatic GST, and pulmonary MO and GST activities but not in those of hepatic MO activities, by CS in rats.

Age dependent differential effects of cigarette smoke on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.

The effects of cigarette smoke (CS) on hepatic and pulmonary monooxygenase (MO) activities (aniline 4-hydroxylase, AH; aminopyrine N-demethylase, AMND; 7-ethoxyresorufin O-deethylase, EROD; p-nitroanisole O-demethylase, p-NAOD), lipid peroxidation (LP), and reduced glutathione (GSH) levels and glutathione S-transferase (GST) activities toward several substrates (1-chloro-2,4-dinitrobenzene, CDNB; 1,2-dichloro-4-nitrobenzene, DCNB; ethacrynic acid, EAA; 1,2-epoxy-3-(p-nitrophenoxy)-propane, ENPP) were determined in 20-, 90- and 360-day-old male rats. The animals were exposed to CS five times a day, with 1 h intervals, for 3 days in a chamber supplied alternatively with smoke and fresh air, and were killed 16 h after the last treatments. The hepatic AH activity increased significantly in 20-day-old rats and remained unaltered in older age groups. The hepatic AMND activity unaltered, significantly increased and decreased in 20-, 90- and 360-day-old rats, respectively. The pulmonary AH activity increased significantly in 20- and 90-day-old rats whereas no alteration was noted in 360-day-old rats. CS was ineffective on pulmonary AMND activity at all ages. CS increased hepatic and pulmonary EROD and p-NAOD activities significantly in all age groups compared to controls. In liver, LP level was significantly increased, decreased, and unaltered in 20-, 90- and 360-day-old rats, respectively. CS increased hepatic GSH level significantly in 90-day-old rats but was not effective in the other age groups. In lung, LP level was increased in 90- and 360-day-old rats and unaltered in 20-day-old rats. CS increased pulmonary GSH level significantly in 90-day-old rats and did not have any effect in the other age groups. The hepatic GST activities toward CDNB and DCNB decreased significantly in 360-day-old rats and were unaltered in the younger age groups. The hepatic GST activity toward EAA was unaltered, significantly increased and decreased in 20-, 90- and 360-day-old rats, respectively. The hepatic GST activity toward ENPP decreased significantly in 20- and 90-day-old rats but was unaltered in the oldest group of rats. In 20-day-old rats, the pulmonary GST activity toward ENPP increased significantly whereas the other GST activities did not alter. In 90-day-old rats, however, CS significantly decreased all the pulmonary GST activities studied. Unaltered DCNB GST, significant increase in EAA GST and decrease in CDNB and ENPP GST activities of lung were noted in 360-day-old rats. These results reveal that the regulation in rats of hepatic and pulmonary MO and GST activities are differentially influenced by CS as a function of age.

Combined effects of ethanol and cigarette smoke on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.

The combined effects of ethanol (EtOH) and cigarette smoke (CS) on hepatic and pulmonary monooxygenase (MO) activities (aniline 4-hydroxylase (AH), aminopyrine N-demethylase (AMND), 7-ethoxyresorufin O-deethylase (EROD), p-nitroanisole O-demethylase (p-NAOD)), lipid peroxidation (LP) and reduced glutathione (GSH) levels and glutathione S-transferase (GST) activities toward several substrates (l-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), 1,2-epoxy-3-(p-nitrophenoxy)-propane (ENPP)) were determined and compared with those of EtOH or CS alone in rats. When the male adult rats (225-275 g) were treated with 10% EtOH (v/v) in their drinking for 21 days AH, AMND and EROD activities and LP and GSH levels increased significantly whereas GST activity for EAA decreased significantly in liver as compared to controls. EtOH did not change the hepatic p-NAOD and GST activities toward CDNB, DCNB and ENPP. In lung, EtOH increased GST activities toward CDNB and ENPP and LP level but decreased GST activity toward DCNB, significantly. No alterations were noted in pulmonary MO activities and GST activity toward EAA and GSH level by EtOH treatment. When the animals were exposed to CS five times a day, with 1 h intervals, for 3 days in a chamber where smoke and fresh air lead alternatively, AMND, EROD and p-NAOD activities, GST activity toward EAA and GSH level increased but LP level and GST activity for ENPP decreased significantly in liver. CS did not alter the hepatic AH and GST activities toward CDNB and DCNB. In lung, CS increased AH, EROD and p-NAOD activities and LP and GSH levels and decreased all the GST activities studied significantly. CS had no influence on pulmonary AMND activity. For the combined treatment, the animals were treated with 10% EtOH (v/v) in their drinking water for 21 days and during the last 3 days they were exposed to CS five times a day, with 1 h intervals, in a chamber where smoke and fresh air lead alternatively. In these animals, augmentation of elevations were noted in AH and p-NAOD activities and LP and GSH levels but not in EROD and AMND activities in liver. Combined treatment significantly decreased GST activity toward CDNB, ameliorated the alteration caused by either EtOH or CS treatment alone on GST activity toward EAA and potentiated the depression of GST activity toward ENPP to a greater degree. No change was observed in GST activity toward DCNB. In lung, combined treatment potentiated the elevations of AMND and p-NAOD activities and LP level and not those of AH and EROD activities. GST activities toward CDNB, DCNB and ENPP were highly elevated by the combined treatment. No changes were observed in pulmonary GSH level and GST activity for EAA by the combined treatment. These results reveal that the regulations of the hepatic and pulmonary MO and GST are differentially influenced by EtOH, CS and the combined treatment.

Corticosterone promotes increased heme oxygenase-2 protein and transcript expression in the newborn rat brain.

Heme oxygenase-2 (HO-2) is the predominant heme oxygenase isozyme in neurons in the brain, the enzyme cleaves the heme molecule at the alpha-meso carbon bridge to form CO, Fe and biliverdin. Recently, in the promotor region of the HO-2 gene a consensus sequence of the glucocorticoid response element (GRE) has been identified. Presently, we have investigated the potential relevance of the GRE to the expression of the isozyme, at the transcript and protein levels, in the 14 day old rat brain, by examining the effect of postparturition corticosterone treatment (4 days, starting 24-36 h after birth) on the developmental pattern of HO-2 expression. Northern blot analysis showed that HO-2 transcripts (approximately 1.3 and approximately 1.9 kb) in brain increase with age. In many brain nuclei, HO-2 protein, as visualized by immunohistochemistry, was detected at low levels in neurons in the 14 day old rat brain. Postparturition exposure to corticosterone resulted in a marked enhancement of HO-2 immunoreactivity in several neuronal populations, including, among others, the cerebellum, the hippocampal formation, and the oculomotor and red nuclei. The response to elevated levels of corticosterone was particularly striking in the Purkinje neurons of the cerebellum and the CA3 region of the hippocampus. This was linked to an increase in gene transcription, as indicated by in situ hybridization analysis, which revealed an increase in the signal for HO-2 transcripts in these regions. Elevated levels of heme oxygenase activity and HO-2 protein were consistent with an increase in catalytically active protein expression. These data point to the intimate involvement of the adrenal steroids in developmentally-linked HO-2 expression in the neurons involved in motor function and cognition, and hence, identify a potentially important aspect of the adrenal steroids' effect on brain growth and differentiation.

Differential responses of hepatic monooxygenases and glutathione S-transferases of mice to a combination of cadmium and nickel.

The acute combined effects of cadmium (Cd) and nickel (Ni) on hepatic monooxygenase activities (ethylmorphine N-demethylase, EMND; aminopyrine N-demethylase, AMND; aniline 4-hydroxylase, AH), cytochrome P-450, cytochrome b5, microsomal heme and reduced glutathione (GSH) levels and glutathione S-transferase (GST) activities toward several substrates (1-chloro-2,4-dinitrobenzene, CDNB; 1,2-dichloro-4-nitrobenzene, DCNB; ethacrynic acid, EAA; 1,2-epoxy-3-(p-nitrophenoxy)-propane, ENPP) were determined and compared with those of Cd or Ni alone in mice. Male adult mice (25-30 g) were administered either a single dose of Cd (3.58 mg CdCl2.H2O/kg, i.p.) 48 hr prior to killing or a single dose of Ni (59.5 mg NiCl2.H2O/kg, s.c.) 16 hr prior to killing. For the combined treatment, the animals received the single dose of Ni 32 hr after the single dose of Cd and were then killed 16 hr later. Cd treatment alone significantly decreased EMND, AMND, and AH activities and cytochrome P-450 and heme levels as compared with controls. Cytochrome b5 level was not altered by Cd treatment. Cd also inhibited GSH level and the GST activities toward CDNB, EAA and ENPP significantly. No significant change was observed in the GST activity for DCNB by Cd. Ni treatment alone, however, decreased the monooxygenase and GST activities studied, and cytochrome P-450, cytochrome b5, heme and GSH levels significantly. Combined treatment significantly depressed the monooxygenase activities and cytochromes and heme levels. GSH level was not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)