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Spontaneous retroperitoneal haemorrhage is a lethal condition if not detected on time. The abdominal CT scan is the most accurate diagnostic method for detection. Surgical management is necessary in patients with haemodynamic instability.

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Macrophage migration inhibitory factor (MiF) has been associated with the pathogenesis of several rheumatic diseases. in systemic sclerosis (ssc) it has been shown that MiF expression is dysregulated in serum and skin. however, the MiF receptor, Cd74, has been poorly investigated and its potential role in the pathogenesis of ssc remains unknown. this study aimed to analyze mrna, tissue, and serum expression of MiF and Cd74 in patients with limited (lcssc) and diffuse (dcssc) systemic sclerosis. a case-control study in 20 ssc patients and 20 control subjects (Cs) from southern México was conducted. MiF and Cd74 mrna expression levels were quantified by real-time PCr, MiF serum levels were measured by an elisa kit, and MiF and its receptor Cd74 were evaluated by immunohistochemistry of skin biopsies. MiF mrna expression was significantly higher in Cs than in ssc patients (p = 0.02), while Cd74 showed no differences between patients and Cs. MiF serum levels were similar between ssc patients and Cs: dcssc = 3.82 ng/ml, lcssc = 3.57 ng/ml, and Cs = 3.28 ng/ml. in skin biopsies of ssc, MiF and Cd74 were enhanced in keratinocytes, while they showed decreased expression in endothelial cells. on the other hand, the staining of Cd74 was high in fibroblasts of dcssc patients. our findings show MiF and Cd74 deregulation at the transcriptional and translational levels in ssc, which might be associated with the proinflammatory process leading to tissue remodeling and excessive fibrosis in ssc.

Background: Acute renal graft dysfunction (AGD) is one of the primary complications after kidney transplantation. The aim of this study was to identify the systemic oxidative DNA damage and apoptosis markers in patients with AGD, which will aid the understanding of the underlying processes of the complication. Methods: A cross-sectional analytical study was conducted in renal transplant (RT) recipients with and without AGD. The follow-up time of patients was <1 year. Using the ELISA technique, the markers of oxidative DNA damage (8-hydroxy-2-deoxyguanosine and 8-oxoguanine-DNA-N-glycosylase-1) and apoptosis (caspase-3, caspase-8, soluble TNF receptor 1, and cytochrome C) were determined. Results: Donor age was significantly higher in patients with AGD versus those without AGD (43±11 years versus 34.1±10.6 years, respectively; p<0.001). Levels of 8-hydroxy-2-deoxyguanosine were also significantly higher in AGD patients than those without AGD (624.1±15.3 ng/mL and 563.02± 17.4 ng/mL, respectively; p=0.039) and the DNA repair enzyme 8-oxoguanine-DNA-N-glycosylase-1 was significantly diminished in AGD patients versus non-AGD patients (7.60±1.8 ng/mL versus 8.13±1.70 ng/mL, respectively; p=0.031). A significant elevation of soluble TNF receptor levels in AGD patients was also found versus those without AGD (1178.6±25.2 ng/mL versus 142.6±39 ng/mL, respectively; p=0.03). Caspase-3 levels were higher in patients with AGD (1.19±0.21 ng/mL) versus those without AGD (0.79±0.11 ng/mL; p=0.121) and was also significantly augmented in AGD versus healthy control subjects (0.24±0.1 ng/mL; p=0.036). Cytochrome c in AGD patients was 0.32±0.09 ng/mL and 0.16±0.03 ng/mL in those without AGD versus 0.08±0.01 ng/mL in healthy controls (p=0.130 and p=0.184, respectively). Conclusion: These findings suggest that oxidative DNA damage with insufficient DNA repair and higher levels of caspase-3 compared to controls are markers of apoptosis protein dysregulation in AGD patients.

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Postcholecystectomy bile duct injuries (BDI) produce hepatic cholestasis and cause infection of the biliary tract. The biliary cells participate in secreting cytokines and in expression of immune response receptors. Toll-like receptors (TLRs) conduct signalling and activate the innate and adaptive inflammatory response. The objective was to determine the serum levels of TLR-2 and the expression of TLR-1 and TLR-2 and β-defensin in liver biopsies of postcholecystectomy BDI patients. A transverse, analytical study with 2 groups was done. One group included healthy volunteers (control group) and other included 25 postcholecystectomy BDI patients with complete biliary obstruction. Using the Enzyme-linked Immunosorbent Assay (ELISA) technique, serum levels of TLR-2 were determined, and with immunofluorescence the morphologic analysis of TLR-1 and TLR-2 and β-defensin in liver biopsies of postcholecystectomy BDI patients was performed. The average TLR-2 serum level in the control group was 0.0 pg/mL and in the BDI group, 0.023 ± 0.0045 pg/mL (P < 0.0001, bilateral Mann Whitney U). Immunofluorescence was used to determine the expression in liver biopsies, blood vessels, bile ducts, and hepatic parenchyma where 12 hepatic biopsies were positive for TLR-1 with average of 3213057.74 ± 1071019.25 μm2; and 7 biopsies were positive for β-defensin with an average of 730364.33 ± 210838.02 μm2; and 6 biopsies positive for TLR-2, obtaining an average of 3354364.24 ± 838591.06 μm2. In conclusion, TLR-1 and TLR-2 and β-defensin play an important role in the innate antimicrobial defense of the hepatobiliary system.