Gallic acid ameliorates busulfan-induced testicular toxicity and damage in mature rats.

Here, we studied the protective effect of gallic acid (GAL) as a potent anti-oxidant and anti-inflammatory agent against damage caused by busulfan (BUS) in the testes of adult rats. The adult Wistar rats were assigned as control, BUS: was intraperitoneally (i.p.) treated with busulfan (15 mg/kg, day 7 and 14), GAL + BUS: was co-treated with busulfan (i.p., 15 mg/kg, day 7 and 14) and orally treated (per os) with gallic acid (60 days, 20 mg/kg) and GAL: was treated with gallic acid (per os, 60 days, 20 mg/kg). The results showed that GAL co-treatment increased the numbers of spermatogonia (Type A and B), spermatocytes (primary and secondary) and round spermatids, along with the tubular diameter, epithelial height and gonado-somatic index. In addition, BUS-induced increase in 3ß-hydroxysteroid dehydrogenase and γ-glutamyl transpeptidase activities were inhibited on GAL co-treatment. Similarly, BUS-induced decrease in gluthathione concentration, catalase and superoxide dismutase activities along with increase in myeloperoxidase activity and malondialdehyde concentration were significantly normalized to control values on GAL co-treatment. Busulfan-induced elimination of tubular germ cells was completely prevented by GAL. Overall, GAL may inhibit BUS-mediated spermatogenesis arrest via decreasing inflammatory-mediated oxidative stress in a rat experimental model.

Effect of Fe and Cd Co-Exposure on Testicular Steroid Metabolism, Morphometry, and Spermatogenesis in Mice.

The mechanism of testicular toxicity of simultaneous multiple exposures to metals is poorly understood. Previous studies reported that the toxic effect of cadmium (Cd) is modified by tissue concentration of iron (Fe). Using the mice (Mus musculus) model in the present study, we demonstrated that combined Cd (25 mg kg-1 bw) and Fe (100 mg kg-1 bw) treatment increased both Cd and Fe testicular concentrations much more than separate exposures to either of the metals. Intratesticular Cd and Fe concentrations were inversely correlated (r = - 0.731, p < 0.05) on administration of Fe but not on combined exposure to both metals when they were positively correlated (versus Cd; r = 0.793, versus Fe; r = 0.779, p < 0.05). Additionally, Cd + Fe treatment increased testicular lipid peroxidation and depleted intratestesticular testosterone, cholesterol and glutathione concentrations much more than their separate treatment. This was also associated with decreased activity of the germ cell marker, testicular lactate dehydrogenase, and increased testicular myeloperoxidase activity. These changes resulted in decreased seminiferous epithelial height, tubular diameter, germ cell (spermatogonia, spermatocytes, and spermatids) numbers, and severe tissue damage. In conclusion, Cd + Fe intake have synergistic toxic effects on testicular steroid formation and spermatogenesis due to the high testicular concentrations of both metals.

Para-spinal abscess following gallstones spillage during laparoscopic cholecystectomy: an unusual presentation.

Gallbladder perforation with subsequent gallstone spillage can occur with higher frequency in laparoscopic cholecystectomy than in traditional open approach. Gallstone abscess formation from stone spillage post-cholecystectomy is extremely rare. We present a case of para-spinal abscess formation 5 years after spilled gallstones following laparoscopic cholecystectomy.

Chronic cholestasis in patients on parenteral nutrition: the influence of restoring bowel continuity after mesenteric infarction.

BACKGROUND/OBJECTIVES: Patients with a short bowel and receiving parenteral nutrition (PN) have an increased risk of chronic cholestasis (CC). Restoration of bowel continuity after a mesenteric infarction results in PN requirements being reduced or stopped. This study aimed to determine the prevalence of CC and whether restoring bowel continuity reduced the risk of CC. SUBJECTS/METHODS: A retrospective review of patients with a short bowel owing to mesenteric infarction from 2000 to 2012. CC was defined as two of bilirubin, alkaline phosphatase and gamma-glutamyl transferase being 1.5 times the upper limit of normal for >6 months. RESULTS: We identified 104 (55 females, median age 54 years) patients. Seventy-three (70%) patients had restoration of bowel continuity; of these, 25 (34%) had abnormal liver biochemistry (liver function test (LFT)), with 15 (21%) having CC. Following restoration of bowel continuity, 8 (53%) of 15 patients with CC and 10 (100%) of 10 patients with abnormal LFT but not CC had a return of liver function within normal range within a year. Univariate analysis showed restoring bowel continuity (P=0.002) and cessation of PN (P=0.006) were associated with a reduction in prevalence of CC. Multivariate analysis showed that cessation of PN was a significant factor in reducing CC (P=0.02). CONCLUSIONS: The prevalence of CC is 29% for patients with a short bowel receiving PN following a mesenteric infarction. CC resolves in 53% after continuity is restored, and this is most likely due to stopping or reducing the PN.

Mortality after acute primary mesenteric infarction: a systematic review and meta-analysis of observational studies.

AIM: The primary aim of this study was to determine whether the in-hospital mortality for acute mesenteric infarction has reduced in the last decade. The secondary aim was to determine if there was a statistical difference in mortality between patients having acute primary mesenteric infarction due to different causes. METHOD: A literature search was performed of PubMed, Ovid (Embase) and Google Scholar databases. Studies on acute mesenteric infarction of primary vascular pathology were included for pooled analyses while studies that had reported comparative mortality between arterial, venous and non-occlusive mesenteric infarction (NOMI) were included in meta-analyses. Their quality was assessed using the National Institute for Health and Care Excellence assessment scale. Odds ratios (ORs) of mortality were calculated using a Mantel-Haenszel random effect model. RESULTS: The total number of patients was 4527 and the male/female ratio was 1912/2247. The pooled in-hospital mortality was 63%. There was no significant reduction of in-hospital mortality rate in the last decade (P = 0.78). There was a significant difference in in-hospital mortality between acute arterial mesenteric infarction (73.9%) compared with acute venous mesenteric infarction (41.7%) [OR 3.47, confidence interval (CI) 2.43-4.96, P < 0.001] and NOMI (68.5%) compared with acute venous mesenteric infarction (44.2%) (OR 3.2, CI 1.83-5.6, P < 0.001). There was no difference in mortality between acute arterial mesenteric infarction and NOMI (OR 1.08, CI 0.57-2.03, P = 0.82). CONCLUSION: In-hospital mortality rate has not changed in the last decade. Patients with arterial mesenteric infarction or with NOMI are over three times more likely to die during the first hospital admission compared with those with venous mesenteric infarction.