Necrotising enterocolitis in an adult with anorexia nervosa.

Necrotising enterocolitis (NEC) is a rare cause of the acute abdomen in adults and carries one of the highest mortality rates in gastroenterology. However, its rarity confines research to small case reports. Both its pathogenesis and aetiology remain enigmatic in adult patients, proving timely diagnosis and management a challenge. This paper reports on one case of NEC in an adult patient with underlying anorexia nervosa, following a seven-day period of starvation. She underwent emergency laparotomy for resection of necrotic bowel and subsequently made a good recovery. To date, there have only been eight reports linking NEC with anorexia nervosa. We review our patient in the context of plausible mechanisms hypothesised in these cases. Successful management depends on prompt diagnosis, resuscitation and surgical intervention.

Level and modalities of origin of the small saphenous vein: toward codification of the proximal approach level.

PURPOSE: The proximal approach to the small saphenous vein (SSV) must be performed according to precise anatomical landmarks to respect the esthetic profile of venous insufficiency surgery. In this work, we propose the tip of the lateral malleolus and the lateral edge of the calcaneal tendon as palpable landmarks from which to easily identify the situation of this vein. METHODS: This was a cadaveric dissection study involving 62 members of fresh and embalmed anatomical subjects. We used a horizontal line passing through the tip of the lateral malleolus and the lateral edge of the calcaneal tendon as reference marks. Once the origin of the SSV as dissected, the distances between the saphenous vein and the landmarks were measured. RESULTS: We found that the small saphenous vein was often unique. The origin of this small saphenous vein projected, on average, to 4.40 cm from the horizontal passing through the tip of the lateral malleolus and 1.2 cm from the lateral edge of the calcaneal tendon. CONCLUSION: These two measurements constitute the orthogonal coordinates for the situation of the small saphenous vein origin.

The kidney allocation system does not appropriately stratify risk of pediatric donor kidneys: Implications for pediatric recipients.

Kidney Allocation System (KAS) was enacted in 2014 to improve graft utility, while facilitating transplantation of highly-sensitized patients and preserving pediatric access to high-quality kidneys. Central to this system is the Kidney Donor Profile Index (KDPI), a metric intended to predict transplant outcomes based on donor characteristics but derived using only adult donors. We posited that KAS had inadvertently altered the profile and quantity of kidneys made available to pediatric recipients. This question arose from our observation that most pediatric donors carry a KDPI over 35 and have therefore been rendered relatively inaccessible to pediatric recipients under KAS. Here we explore early trends in pediatric transplantation following KAS, including: (i) use of pediatric donors, (ii) use of Public Health System (PHS) high infectious risk donors, (iii) wait time, and (iv) living donor transplantation. We note some concerning preliminary changes following KAS implementation, including the allocation of fewer deceased donor pediatric kidneys to children and stagnation in pediatric wait times. Moreover, the poor predictive power of the KDPI for adult donors appears to be even worse when applied to pediatric donors. These early trends warrant further observation and consideration of changes in pediatric kidney allocation if they persist.

Anatomical variations in lymphatic drainage of the right lung: applications in lung cancer surgery.

OBJECTIVES: To specify the topography and variations in lymphatic drainage of the right lung to the mediastinum and their therapeutic implications in non-small cell lung cancers (NSCLC). MATERIALS AND METHOD: We injected a dye into the subpleural lymphatic vessels in 65 right lung segments, followed by dissection in 22 subjects. RESULTS: At the upper lobe, we had injected 32 segments. We noted extrasegmental overflow in one case; extrasegmental and extralobar drainage in two cases; drainage to the lymph nodes of another lobe in one case. Fifty-six percent of the segments drained directly (skipping intrapulmonary and hilar lymph nodes) into the right paratracheal lymph nodes, and one dorsal segment drained into the thoracic duct. A ventral segment drained into the inferior tracheobronchial lymph nodes. A contralateral drainage to the recurrent chain was observed in two cases. Sixteen segments of the middle lobe were injected and mainly drained into the inferior tracheobronchial lymph nodes with six direct paths; one medial segment drained into the right anterior mediastinal chain. We noted three contralateral drainages and eight downward abdominal drainages. Out of the 17 segments of the lower lobe injected, 6 segments drained into the lymph nodes of another lobe, 5 segments showed a direct route to the lower quadrant chains. We noted one time a drainage into the paraesophageal lymph nodes. CONCLUSION: The variations in lymphatic drainage of the right lung require to carry out systematically a radical mediastinal lymphadenectomy during the removal of non-small cell lung cancers and to associate an adjuvant treatment.

Eculizumab prevents recurrent antiphospholipid antibody syndrome and enables successful renal transplantation.

Renal transplantation in patients with antiphospholipid antibodies has historically proven challenging due to increased risk for thrombosis and allograft failure. This is especially true for patients with antiphospholipid antibody syndrome (APS) and its rare subtype, the catastrophic antiphospholipid antibody syndrome (CAPS). Since a critical mechanism of thrombosis in APS/CAPS is one mediated by complement activation, we hypothesized that preemptive treatment with the terminal complement inhibitor, eculizumab, would reduce the extent of vascular injury and thrombosis, enabling renal transplantation for patients in whom it would otherwise be contraindicated. Three patients with APS, two with a history of CAPS, were treated with continuous systemic anticoagulation together with eculizumab prior to and following live donor renal transplantation. Two patients were also sensitized to human leukocyte antigens (HLA) and required plasmapheresis for reduction of donor-specific antibodies. After follow-up ranging from 4 months to 4 years, all patients have functioning renal allografts. No systemic thrombotic events or early graft losses were observed. While the appropriate duration of treatment remains to be determined, this case series suggests that complement inhibitors such as eculizumab may prove to be effective in preventing the recurrence of APS after renal transplantation.

Neuropsychological function and cerebral metabolites in HIV-infected youth.

The effects of HIV on brain metabolites and cognitive function are not well understood. Sixteen HIV+youths (15 vertical, 1 transfusion transmissions) receiving combination antiretroviral therapy and 14 age-matched HIV- youths (13-25 years of age) were evaluated with brain two-dimensional (2D) magnetic resonance spectroscopy (MRS) at 3 Tesla (T) and a neuropsychological battery that assessed three cognitive domains (attention/processing speed, psychomotor ability, and executive function). The relationship between brain metabolite ratios and cognitive performance was explored. Compared to HIV- controls, HIV+ subjects had higher sycllo-inositol (Scy)/total creatine (tCr) (+32%, p = 0.016) and higher Scy/total choline (tCho) (+31%, p = 0.018) on 2D-MRS in the right frontal lobe. HIV+ subjects also had higher glutamate (Glu)/tCr (+13%, p = 0.022) and higher Glu/tCho (+15%, p = 0.048) than controls. HIV+ subjects demonstrated poorer attention/processing speed (p = 0.011, d = 1.03) but similar psychomotor and executive function compared to HIV- controls. The attention/processing score also correlated negatively with the ratio of N-acetylaspartate (NAA) to tCr on 2D-MRS (r = -0.75, p = 0.0019) in the HIV- controls, but not in the HIV+ subjects (Fisher's r-z transformation, p < 0.05). Our results suggest that attention/processing speed is impacted by early HIV infection and is associated with right hemisphere NAA/tCr. Scy and Glu ratios are also potential markers of brain health in chronic, lifelong HIV infection in perinatally infected youths receiving antiretroviral therapy.

Relative importance of patient, procedural and anatomic risk factors for early vein graft thrombosis after coronary artery bypass graft surgery.

AIM: The aim of the present study was to investigate the relative importance of a wide array of patient demographic, procedural, anatomic and perioperative variables as potential risk factors for early saphenous vein graft (SVG) thrombosis after coronary artery bypass graft (CABG) surgery. METHODS: The patency of 611 SVGs in 291 patients operated on at four different hospitals enrolled in the Reduction in Graft Occlusion Rates (RIGOR) study was assessed six months after CABG surgery by multidetector computed tomography coronary angiography or clinically-indicated coronary angiography. The odds of graft occlusion versus patency were analyzed using multilevel multivariate logistic regression with clustering on patient. RESULTS: SVG failure within six months of CABG surgery was predominantly an all-or-none phenomenon with 126 (20.1%) SVGs totally occluded, 485 (77.3%) widely patent and only 16 (2.5%) containing high-grade stenoses. Target vessel diameter ≤ 1.5 mm (adjusted OR 2.37, P=0.003) and female gender (adjusted OR 2.46, P=0.01) were strongly associated with early SVG occlusion. In a subgroup analysis of 354 SVGs in which intraoperative graft blood flow was measured, lower mean flow was also significantly associated with SVG occlusion when analyzed as a continuous variable (adjusted OR 0.984, P=0.006) though not when analyzed dichotomously, <40 mL/min versus ≥ 40 mL/min (adjusted OR 1.86, P=0.08). CONCLUSION: Small target vessel diameter, female gender and low mean graft blood flow are significant risk factors for SVG thrombosis within six months of CABG surgery in patients on postoperative aspirin therapy. This information may be useful in guiding revascularization strategies in selected patients.

New technologies and therapies for cardiac arrhythmias.

Catheter ablation of cardiac arrhythmia has evolved to an important treatment modality for patients with various cardiac rhythm abnormalities. Over the past three decades, the understanding of arrhythmia mechanisms and technology for catheter based diagnostic and ablation procedures have evolved rapidly. New technologies and therapies for treatment of cardiac arrhythmia include ablation catheters designed to destroy targeted tissue with improved precision and safety, robotic systems to guide accurate catheter movements, electrical mapping systems, and improved imaging to complement such systems. This review focuses on improved imaging modalities used in the modern electrophysiology laboratory.

Emergence and distribution of the ilioinguinal nerve in the inguinal region: applications to the ilioinguinal anaesthetic block (about 100 dissections).

The variations in the emergence and distribution of the ilioinguinal nerve are the cause of the failures of the ilioinguinal block and the difficulties at interpreting the ilioinguinal nerve syndrome. In order to identify its variations and set reliable anatomical landmarks for performing the ilioinguinal block, we dissected 100 inguinal regions of 51 adult corpses. The nerve was absent in seven cases and double in one case. The ilioinguinal nerve emerged from the internal oblique muscle, passing at 1 +/- 0.8 cm of the inguinal ligament and 3.33 +/- 2 cm of the ventral cranial iliac spine. It appeared behind the inguinal ligament and/or the ventral cranial iliac spine in 19 cases and presented a common trunk with the iliohypogastric nerve in 13 cases. In 47 cases, the nerve appeared in the form of a single trunk. Sixteen modes of division and eight types of predominantly anterior scrotal topographic distribution could be noted. These results show the high variability of the emergence and the sensory distribution of the ilioinguinal nerve. They enable us to propose techniques for ilioinguinal block performance using more accurate anatomical landmarks formed by the inguinal ligament and the ventral cranial iliac spine and a better diagnostic approach of ilioinguinal neuropathies.

Anatomical basis of neuropathies and damage to the ilioinguinal nerve during repairs of groin hernias. (about 100 dissections).

Surgical access to the inguinal region, notably during hernia repairs, exposes the ilioinguinal nerve to the risk of damage at the origin of the neuralgia. The incidence of these post-operative neuropathies and their medicolegal consequences justify this study about the anatomical variations of the ilioinguinal nerve. With the aim of preventing its damage during repairs of groin hernias and identifying the factors of onset of chronic spontaneous neuropathy of the ilioinguinal nerve, we dissected 100 inguinal regions of 51 fresh adult corpses. The nerve was absent in seven cases and double in one case. Out of the 94 ilioinguinal nerves observed, we analyzed the path in relation to the inguinal ligament and the connections with the walls of the inguinal canal and its content. The ilioinguinal nerve travels along the superficial surface of the internal oblique muscle, passing on average 1.015 cm from the inguinal ligament. In one case, the fibers of the internal oblique muscle spanned it in several places. The nerve was antero-funicular in 78.72% of cases and perforated the fascia of the external oblique in 28.72% of cases. The terminal division took place in the inguinal canal in 86% of cases, with terminal branches that sometimes perforated the fascia of the external oblique. These results enabled us to better understand the etiopathogenic aspects of certain neuropathies of the groin and to propose techniques useful for the protection of the nerve during repairs of groin hernias.

Myxoma virus M-T5 protects infected cells from the stress of cell cycle arrest through its interaction with host cell cullin-1.

The myxoma virus (MV) M-T5 gene encodes an ankyrin repeat protein that is important for virus replication in cells from several species. Insight was gained into the molecular mechanisms underlying the role of M-T5 as a host range determinant when the cell cycle regulatory protein cullin-1 (cul-1) was identified as a cellular binding partner of M-T5 and found to colocalize with the protein in both nuclear and cytosolic compartments. Consistent with this interaction, infection with wild-type MV (vMyxlac) or a deletion mutant lacking M-T5 (vMyxT5KO) differentially altered cell cycle progression in a panel of permissive and nonpermissive cells. Cells infected with vMyxlac transitioned rapidly out of the G0/G1 phase and preferentially accumulated at the G2/M checkpoint, whereas infection with vMyxT5KO impeded progression through the cell cycle, resulting in a greater percentage of cells retained at G0/G1. Levels of the cul-1 substrate, p27/Kip-1, were selectively increased in cells infected with vMyxT5KO compared to vMyxlac, concurrent with decreased phosphorylation of p27/Kip-1 at Thr187 and decreased ubiquitination. Compared to cells infected with vMyxlac, cell death was increased in vMyxT5KO-infected cells following treatment with diverse stimuli known to induce cell cycle arrest, including infection itself, serum deprivation, and exposure to proteasome inhibitors or double-stranded RNA. Moreover, infection with vMyxlac, but not vMyxT5KO, was sufficient to overcome the G0/G1 arrest induced by these stimuli. These findings suggest that M-T5 regulates cell cycle progression at the G0/G1 checkpoint, thereby protecting infected cells from diverse innate host antiviral responses normally triggered by G0/G1 cell cycle arrest.

Stroke education by utility bill inserts.

To assess the usefulness of utility bill inserts in stroke education, a stroke fact sheet was included in the bills of 13,000 customers of a rural electric cooperative in eastern Arkansas. Recipients were asked to return their responses to four questions based on the fact sheet via a postage-paid postcard. Two hundred eleven people responded, for an overall 1.65% response rate. Seventy-seven percent responded correctly with all four "S" stroke symptoms. Hypertension was correctly identified by 88% and smoking by 72%. Fifty-seven percent said they would immediately dial 911 at the onset of symptoms, while 36% said they would contact their doctor.

Is testing for inherited coagulation inhibitor deficiencies in young stroke patients worthwhile?

OBJECTIVE: To test the hypothesis that in patients under age 50, with a first, arterial, ischemic cerebral infarct, whose family history and medical history do not suggest an inherited coagulation inhibitor deficiency, the yield of a laboratory search for these disorders will be low. MATERIALS AND METHODS: In 55 such patients under age 50, we systematically searched for deficiencies of protein C, protein S, and antithrombin III. RESULTS: No abnormalities of protein C or antithrombin III were found. One patient had a deficiency of protein S, which was most likely acquired rather than inherited. CONCLUSIONS: In patients who lack clinical features of a prothrombotic state, the yield of testing for protein C, S and AT III deficiency is likely to be low.

Immunosuppressant PG490 (triptolide) inhibits T-cell interleukin-2 expression at the level of purine-box/nuclear factor of activated T-cells and NF-kappaB transcriptional activation.

PG490 (triptolide) is a diterpene triepoxide with potent immunosuppressive and antiinflammatory properties. PG490 inhibits interleukin(IL)-2 expression by normal human peripheral blood lymphocytes stimulated with phorbol 12-myristate 13-acetate (PMA) and antibody to CD3 (IC50 of 10 ng/ml), and with PMA and ionomycin (Iono, IC50 of 40 ng/ml). In Jurkat T-cells, PG490 inhibits PMA/Iono-stimulated IL-2 transcription. PG490 inhibits the induction of DNA binding activity at the purine-box/antigen receptor response element (ARRE)/nuclear factor of activated T-cells (NF-AT) target sequence but not at the NF-kappaB site. PG490 can completely inhibit transcriptional activation at the purine-box/ARRE/NF-AT and NF-kappaB target DNA sequences triggered by all stimuli examined (PMA, PMA/Iono, tumor necrosis factor-alpha). PG490 also inhibits PMA-stimulated activation of a chimeric transcription factor in which the C-terminal TA1 transactivation domain of NF-kappaB p65 is fused to the DNA binding domain of GAL4. In 16HBE human bronchial epithelial cells, IL-8 expression is regulated predominantly by NF-kappaB, and PG490 but not cyclosporin A can completely inhibit expression of IL-8. The mechanism of PG490 inhibition of cytokine gene expression differs from cyclosporin A and involves nuclear inhibition of transcriptional activation of NF-kappaB and the purine-box regulator operating at the ARRE/NF-AT site at a step after specific DNA binding.

Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. The Veterans Affairs Stroke Prevention in Nonrheumatic Atrial Fibrillation Investigators.

BACKGROUND: Cerebral infarction in patients with atrial fibrillation may vary from being clinically silent to catastrophic. The prevalence of silent cerebral infarction and its effect as a risk factor for symptomatic stroke are important considerations for the evaluation of patients with atrial fibrillation. METHODS AND RESULTS: This Veterans Affairs cooperative study was a double-blind controlled trial designed primarily to determine the efficacy of warfarin for the prevention of stroke in neurologically normal patients with nonrheumatic atrial fibrillation. It also was designed to evaluate patients with silent cerebral infarction. Computed tomography scans of the head were performed at entry, at the time of any subsequent stroke, and at termination of follow-up on all patients who completed the study without a neurological event. Of 516 evaluable scans performed at entry, 76 (14.7%) had evidence of one or more silent cerebral infarcts. Age (P = .011), a history of hypertension (P = .003), active angina (P = .012), and elevated mean systolic blood pressure (P < .001) were associated with the presence of this finding. Silent cerebral infarction occurred during the study at rates of 1.01% and 1.57% per year for the placebo and warfarin treatment groups, respectively (NS). Silent cerebral infarction at entry was not an independent predictor of later symptomatic stroke, but active angina was a significant predictor; 15% of the placebo-assigned patients with angina developed a stroke compared with 5% of the placebo-assigned patients without angina. CONCLUSIONS: Silent cerebral infarction is frequently seen in asymptomatic patients with atrial fibrillation. Age, history of hypertension, active angina, and elevated mean systolic blood pressure were associated with silent infarction at entry. The sample size was too small to determine whether warfarin had an effect on the incidence of silent infarction during the trial. Active angina at baseline was the only significant independent predictor for the later development of symptomatic stroke.