Isolated Duodenal Rupture due to Go-Karting Accidents – Braking News

INTRODUCTION

Isolated duodenal injury due to blunt abdominal trauma is extremely rare. We present a series of three such injuries due to go-karting accidents, which presented to our hospital over 5 months.

CASE REPORTS

Between October 2007 and February 2008, three cases of D3/D4 duodenal rupture presented to our hospital after go-karting accidents. Trauma occurred as a result of the steering wheel impacting on the abdomen. All patients presented similarly with symptoms of epigastric and right upper quadrant pain. In all cases, computed tomography scanning was highly suggestive of duodenal injury and, in particular, demonstrated presence of retroperitoneal air centred around the duodenum. Treatment required laparotomy and operative repair in all cases.

CONCLUSIONS

Duodenal injury presents insidiously due to its retroperitoneal position. A low threshold for investigating patients presenting with epigastric and right upper quadrant pain should be adopted along with active clinical vigilance to exclude serious and life-threatening trauma after go-karting accidents.     

Henoch Schonlein purpura in childhood: clinical analysis of 254 cases over a 3-year period

We aimed to evaluate the patients who were diagnosed as Henoch Schonlein purpura (HSP) for disease characteristics and prognosis of those with joint, gastrointestinal (GI), and renal involvement. Two hundred and fifty-four children who were followed up with the diagnosis of HSP in the Pediatric Nephrology Clinics of Meram Medical Faculty of Selcuk University and Medical Faculty of Gazi University between January 2003 and June 2006 were retrospectively evaluated. The clinical follow-up and treatment regimens of patients in whom renal biopsy was performed were evaluated in detail. The study group consisted of 254 children, 147 boys (57.8%) and 107 girls (42.2%), and the ratio of boys to girls was 1.37. The percentages of skin, joint, GI, and renal manifestations were 100%, 66%, 56%, and 30%, respectively. Eight patients had intussusception. Five of them recovered with steroid treatment only while three patients were operated on. Sixty-four patients (44%) with GI involvement had severe disease and were successfully treated with steroids. Renal biopsy was performed in 26 patients. Among those 26 patients, two of them recovered spontaneously within 3 and 4 weeks. Ten patients improved with only steroid treatment while 12 patients recovered with steroid and cyclophosphamide treatment. Two patients were resistant to steroid and cyclophosphamide treatment and were treated with cyclosporine A. We believe that steroid therapy given to the HSP patients with GI manifestations might be helpful to prevent probable complications such as GI bleeding and intussusception. In addition, combined therapy with steroid and cyclophosphamide can usually be an appropriate treatment for patients with nephrotic proteinuria.     

Real-time immune cell interactions in target tissue during autoimmune-induced damage and graft tolerance

Real-time imaging studies are reshaping immunological paradigms, but a visual framework is lacking for self-antigen-specific T cells at the effector phase in target tissues. To address this issue, we conducted intravital, longitudinal imaging analyses of cellular behavior in nonlymphoid target tissues to illustrate some key aspects of T cell biology. We used mouse models of T cell–mediated damage and protection of pancreatic islet grafts. Both CD4⁺ and CD8⁺ effector T (T_eff) lymphocytes directly engaged target cells. Strikingly, juxtaposed β cells lacking specific antigens were not subject to bystander destruction but grew substantially in days, likely by replication. In target tissue, Foxp3⁺ regulatory T (T_reg) cells persistently contacted T_eff cells with or without involvement of CD11c⁺ dendritic cells, an observation conciliating with the in vitro “trademark” of T_reg function, contact-dependent suppression. This study illustrates tolerance induction by contact-based immune cell interaction in target tissues and highlights potentials of tissue regeneration under antigenic incognito in inflammatory settings.Tissue damage by self-antigen–specific T lymphocytes causes autoimmune diseases such as type 1 diabetes. In these disorders, defective central tolerance (Mathis and Benoist, 2004) and peripheral regulation (Josefowicz et al., 2012) lead to initiation of autoantigen-specific responses in a cascade of molecular and cellular interactions between antigen-presenting cells and T lymphocytes. During the effector phase, activated CD4⁺ and CD8⁺ T_eff cells migrate to target tissues to inflict damage. The immune destruction at this phase can be suppressed by CD4⁺Foxp3⁺ T_reg cells (Josefowicz et al., 2012), as demonstrated in models of autoimmune diabetes (Chen et al., 2005; Feuerer et al., 2009). Extensive studies have contributed to the understanding of immune responses at the induction phase in lymphoid organs; however, the behavior of immune cells in nonlymphoid target tissues remains murky.High-resolution imaging of live cells in lymphoid organs has elucidated key features of cellular dynamics during the initiation phase of immune responses (Germain et al., 2012). A major gap of knowledge remains, however, in understanding immune cell action and interaction in nonlymphoid target tissues, except in some infection models. In particular, noninvasive real-time evidence of how pathogenic immune cells at the effector phase engage target cells, how immune damage is controlled, and how target tissue cells respond remains scanty. This is largely a result of technical limitations that make most target tissues inaccessible to noninvasive visualization at cellular levels. Researchers often have to resort to surgical exposure of tissue or invasive insertion of a probe during imaging. Surgical wounds, however, create a two-pronged limitation on imaging analyses. First, they make longitudinal analyses difficult, if possible. Second, the acute surgical wound leads to immediate release of an array of inflammatory cytokines that may confound the interpretation of immune cell behavior uncovered in a traumatic setting. As a result, key events in the cascade of CD4⁺ and CD8⁺ T cell–mediated immune damage or protection in target tissue remain poorly delineated.A recently established imaging platform, intravital microscopy of pancreatic islets engrafted in the anterior chamber of the mouse eye (ACE), facilitated high-resolution visualization of immune cells noninvasively and longitudinally (Speier et al., 2008a,b; Abdulreda et al., 2011). In this study, we take advantage of this imaging platform, along with a series of reductionist animal models. We established models of effective immune responses in the ACE imaging site versus the native pancreas, in terms of equivalent kinetics of tissue damage and regulatory T (T_reg) cell–mediated protection. Using this noninvasive imaging approach, we studied in real time how self-antigen–specific T cells interacted with target tissue cells in vivo. We depicted the behavior of three major T cell lineages (CD4⁺ effector T [T_eff] cells, CD4⁺ T_reg cells, and CD8⁺ T_eff cells), analyzed the regulatory effect of CTLA4 on their behavior, and examined tissue responses in destructive settings.     

High-resolution,noninvasive longitudinal live imaging of immune responses

Intravital imaging emerged as an indispensible tool in biological research, and a variety of imaging techniques have been developed to noninvasively monitor tissues in vivo. However, most of the current techniques lack the resolution to study events at the single-cell level. Although intravital multiphoton microscopy has addressed this limitation, the need for repeated noninvasive access to the same tissue in longitudinal in vivo studies remains largely unmet. We now report on a previously unexplored approach to study immune responses after transplantation of pancreatic islets into the anterior chamber of the mouse eye. This approach enabled (i) longitudinal, noninvasive imaging of transplanted tissues in vivo; (ii) in vivo cytolabeling to assess cellular phenotype and viability in situ; (iii) local intervention by topical application or intraocular injection; and (iv) real-time tracking of infiltrating immune cells in the target tissue.     

Donor islet endothelial cells in pancreatic islet revascularization

OBJECTIVE

Freshly isolated pancreatic islets contain, in contrast to cultured islets, intraislet endothelial cells (ECs), which can contribute to the formation of functional blood vessels after transplantation. We have characterized how donor islet endothelial cells (DIECs) may contribute to the revascularization rate, vascular density, and endocrine graft function after transplantation of freshly isolated and cultured islets.

RESEARCH DESIGN AND METHODS

Freshly isolated and cultured islets were transplanted under the kidney capsule and into the anterior chamber of the eye. Intravital laser scanning microscopy was used to monitor the revascularization process and DIECs in intact grafts. The grafts’ metabolic function was examined by reversal of diabetes, and the ultrastructural morphology by transmission electron microscopy.

RESULTS

DIECs significantly contributed to the vasculature of fresh islet grafts, assessed up to 5 months after transplantation, but were hardly detected in cultured islet grafts. Early participation of DIECs in the revascularization process correlated with a higher revascularization rate of freshly isolated islets compared with cultured islets. However, after complete revascularization, the vascular density was similar in the two groups, and host ECs gained morphological features resembling the endogenous islet vasculature. Surprisingly, grafts originating from cultured islets reversed diabetes more rapidly than those originating from fresh islets.

CONCLUSIONS

In summary, DIECs contributed to the revascularization of fresh, but not cultured, islets by participating in early processes of vessel formation and persisting in the vasculature over long periods of time. However, the DIECs did not increase the vascular density or improve the endocrine function of the grafts.Clinical islet transplantation can restore endogenous insulin production and glycemic control in patients with type 1 diabetes, yet increased knowledge, and hence refinement, would allow for a wider application of this therapy (1). Pancreatic islets are interspersed by a dense and tortuous capillary network that facilitates an efficient exchange of oxygen, nutrients, and hormones between the endocrine cells and the bloodstream. Transplanted islets are revascularized by blood vessels that grow into the islets from the host organ via angiogenesis (2), although the acquired vasculature has a significantly lower vessel density compared with the endogenous islets (3). Furthermore, during the initial avascular engraftment period, a dramatic reduction in insulin content and high rate of cell death occur within the islets (4). Therapies that enhance the angiogenic capacity of islets by overexpression of vascular endothelial growth factor-A (VEGF-A) can increase the vascular density of islet grafts and improve metabolic function (5,6).Recently, we and others showed that donor islet endothelial cells (DIECs) can form functional vessels within transplanted islets (7,8). Immediately after isolation (i.e., in freshly isolated islets), a large number of intraislet endothelial cells (ECs) are present (7–9). However, if the islets are cultured, the intraislet ECs rapidly disappear, and by 4 days, only ∼5% of the initial content is detected (7). Therefore, freshly isolated islets, in contrast to cultured islets, contain an extra pool of ECs that potentially could promote islet revascularization and function after transplantation. Here, we have performed a detailed characterization of the role of DIECs in the revascularization of transplanted islets.     

Late-presenting congenital diaphragmatic hernia associated with ectopic thoracic kidney

Although congenital defects of diaphragma often occur in the period immediately following birth, 10–20% of these cases are diagnosed later. We report on a 7-month-old male infant with late-presenting congenital diaphragmatic hernia associated with a thoracic ectopic kidney. We conclude that congenital diaphragmatic defects should be considered in young children with respiratory distress and that computerized tomography is a noninvasive and accurate diagnostic method in the evaluation of additional abnormalities in these patients.     

The evaluation of carotid intima-media thickness in children with familial Mediterranean fever

The aim is to investigate whether pediatric familial Mediterranean fever (FMF) patients have an increased risk of premature atherosclerosis and to determine the possible strength of association between atherosclerosis and Mediterranean fever (MEFV) gene mutation gene type. Demographic characteristics and MEFV mutations were defined in 49 children diagnosed with FMF (26 female, 23 male; mean age, 10.71 ± 3.69 years). Twenty-six age-, sex-, and body-mass-index-matched healthy children constituted the control group. We evaluated the blood counts and acute-phase proteins during attack-free periods. Mean C-reactive protein (CRP), serum amyloid-A (SAA), homocysteine (Hcy), lipoprotein-a (Lp-a), and common carotid artery intima-media thickness (CCA-IMT) were 10.75 ± 15.29 vs 4.03 ± 1.20, 23.22 ± 41.94 vs 3.53 ± 1.04, 10.36 ± 3.36 vs 8.64 ± 3.15, 20.84 ± 23.89 vs 8.56 ± 7.48, and 0.038 ± 0.007 vs 0.032 ± 0.004, respectively, and significantly higher than the mean values of control group (p < 0.05). However, no correlation was found between CCA-IMT and CRP, SAA, Hcy, and Lp-a. Twenty-nine patients had M694V mutation, and 13 patients had other mutations. There was no correlation between CCA-IMT and MEFV mutation subgroups. In conclusion, because of the nature of the disease, FMF patients should be considered to have an increased risk of early vascular alteration and atherosclerosis. For this reason, CCA-IMT measurement can be recommended as a noninvasive and early diagnostic method.     

A case of homozygous familial hypercholesterolemia with focal segmental glomerulosclerosis

Familial hypercholesterolemia (FH) is a common autosomal dominant inherited disorder characterized by increased levels of circulating plasma low-density lipoprotein cholesterol (LDL-C), tendon xanthomas, and premature atherosclerotic cardiovascular disease. Homozygous FH occurs in only one in a million people. Focal segmental glomerulosclerosis (FSGS) is clinically characterized by proteinuria, which is marked in the majority of cases and accompanied by nephrotic syndrome, high incidence of hypertension, and progression to renal failure. To our knowledge, we herein report for the first time a case of homozygous FH associated with FSGS. A seven-and-a-half-year-old boy was referred to our hospital due to cutaneous xanthomata and growth retardation. He had multiple nodular yellowish cutaneous xanthomatous lesions each 1 cm in size over his knees and sacral region. Laboratory data included cholesterol level of 1,050 mg/dl, low density lipoprotein cholesterol (LDL-C) 951 mg/dl, high-density lipoprotein cholesterol (HDL-C) 29 mg/dl, triglycerides 168 mg/dl, total protein 6.3 g/dl, and albumin 3.2 g/dl. Urinary protein excretion was 78 mg/m² per hour. A percutaneous renal biopsy was performed, and histological findings showed FSGS. Treatment with cholestyramine and atorvastatin was unsuccessful in terms of lowering lipids, and he was placed on weekly sessions of plasmapheresis. Total cholesterol was reduced from 1,050 mg/dl to 223 mg/dl, LDL-C from 951 mg/dl to 171 mg/dl, and urinary protein excretion from 78 mg/m² per hour to 42 mg/m² per hour after eight sessions of plasmapheresis. It is our belief that plasmapheresis is a treatment of choice in patients with FSGS associated with FH.