Necrosis In Association Research Articles

Puncture Site Necrosis Over Hemodialysis Native and Prosthetic Vascular Accesses

The aim of this study was to detail our experience in the management of skin necrosis/ulceration over hemodialysis vascular accesses. We collected demographics and operative data about patients undergoing surgery for skin necrosis over native or prosthetic vascular accesses. The different procedural techniques used and outcomes achieved were analyzed. Over a six-year period (2013-2019), 593 hemodialysis accesses were created and 16 patients (50%, 8 male; median age 63.6years, range 42-87; 12 native and 4 prosthetic accesses) were emergently/urgently treated for skin necrosis with danger of rupture (n 9), minor active bleeding (n 4) or life-threatening hemorrhage (n 3). Underlying causes were local infection, aneurysm/pseudo-aneurysm formation and venous stenosis. Most accesses were preserved. Rescue procedures consisted in excision of skin necrosis in association with aneurysmorrhaphy (n 1, 6.3%), simple closure of the venous breach (n 2, 12.5%) or resection and direct re-anastomosis (n 7, 43.8%). Concomitant endoluminal dilatation of venous outflow was needed in 7 (43.8%) cases. No intraoperative complications were observed. At a median of 13months (range 1-39), 90% of rescued accesses were still functional. Skin necrosis/ulceration over vascular access requires prompt surgical intervention ahead the risk of life-threatening hemorrhage. The rescue of a functional access is possible in most patients and provides an efficient dialysis in postoperative period.

Expression of cleaved caspase-3 in renal tubular cells in Plasmodium falciparum malaria patients.

In Plasmodium falciparum malaria, the clinical manifestation of acute kidney injury (AKI) is commonly associated with acute tubular necrosis (ATN) in the kidney tissues. Renal tubular cells often exhibit various degrees of cloudy swelling, cell degeneration, and frank necrosis. To study individual cell death, this study evaluates the degree of renal tubular necrosis in association with apoptosis in malarial kidneys. Kidney tissues from P. falciparum malaria with AKI (10 cases), and without AKI (10 cases) were evaluated for tubular pathology. Normal kidney tissues from 10 cases served as controls. Tubular necrosis was assessed quantitatively in kidney tissues infected with P. falciparum malaria, based on histopathological evaluation. In addition, the occurrence of apoptosis was investigated using cleaved caspase-3 marker. Correlation between tubular necrosis and apoptosis was analyzed. Tubular necrosis was found to be highest in P. falciparum malaria patients with AKI (36.44% ± 3.21), compared to non-AKI (15.88% ± 1.63) and control groups (2.58% ± 0.39) (all p < 0.001). In the AKI group, the distal tubules showed a significantly higher degree of tubular necrosis than the proximal tubules (p = 0.021) and collecting tubules (p = 0.033). Tubular necrosis was significantly correlated with the level of serum creatinine (r = 0.596, p = 0.006), and the occurrence of apoptosis (r = 0.681, p = 0.001). In malarial AKI, the process of apoptosis occurs in ATN.

Interaction between Cucumber mosaic virus 2b protein and plant catalase induces a specific necrosis in association with proteasome activity

Key messageCucumber mosaic virus(CMV) can induce a specific necrosis onArabidopsisthrough the interaction between the CMV 2b protein and host catalase, in which the ubiquitin–proteasome pathway may be involved.We previously reported that the CMV 2b protein, the viral RNA silencing suppressor, interacted with the H2O2 scavenger catalase (CAT3), leading to necrosis on CMV-inoculated Arabidopsis leaves. We here confirmed that CMV could more abundantly accumulate in the CAT3-knockout mutant (cat3), and that CAT3 makes host plants a little more tolerant to CMV. We also found that the necrosis severity is not simply explained by a high level of H2O2 given by the lack of CAT3, because the recombinant CMV, CMV-N, induced much milder necrosis in cat3 than in the wild type, suggesting some specific mechanism for the necrosis induction. To further characterize the 2b-inducing necrosis in relation to its binding to CAT3, we conducted the agroinfiltration experiments to overexpress CAT3 and 2b in N. benthamiana leaves. The accumulation levels of CAT3 were higher when co-expressed with the CMV-N 2b (N2b) than with CMV-Y 2b (Y2b). We infer that N2b made a more stable complex with CAT3 than Y2b did, and the longevity of the 2b–CAT3 complex seemed to be important to induce necrosis. By immunoprecipitation (IP) with an anti-ubiquitin antibody followed by the detection with anti-CAT3 antibodies, we detected a higher molecular-weight smear and several breakdown products of CAT3 among the IP-proteins. In addition, the proteasome inhibitor MG132 treatment could actually increase the accumulation levels of CAT3. This study suggests that the host proteasome pathway is, at least partially, responsible for the degradation of CAT3, which is manifested in CMV-infected tissues.

142 Focal full-thickness epidermal necrosis in association with adalimumab in a patient with ulcerative colitis

142 Focal full-thickness epidermal necrosis in association with adalimumab in a patient with ulcerative colitis

Inhibition of lipopolysaccharide-induced liver injury in rats treated with a hepatic drug-metabolizing enzyme inducer p,p′-DDT

Hepatocellular hypertrophy in association with drug-metabolizing enzyme induction is considered to be an adaptive change associated with drug metabolism. To improve our understanding of liver hypertrophy, we determined the effect of a single ip injection of either lipopolysaccharide (LPS) or vehicle in male F344 rats with hepatocellular hypertrophy induced by oral delivery of p,p′-DDT for 2 weeks. The rats were sacrificed 3h or 24h after LPS or vehicle injection. LPS induced a focal hepatocellular necrosis in rats fed the control diet. When rats pre-treated with p,p′-DDT were injected with LPS, necrotic foci surrounded by ballooned hepatocytes were observed in the liver. The change was consistent with reduced LPS-mediated increases in plasma hepatic biomarkers, neutrophil influx, and apoptosis, and also associated with hepatic mRNA levels of TNF-α, CYPs, and NOS2. By contrast, when combined with p,p′-DDT and LPS, faint hepatocellular fatty change was extended, together with a synergistic increase in total blood cholesterol. These results suggest that hepatocytes exposed to p,p′-DDT are protected from the cell-lethal toxic effects of an exogenous stimulus, resulting in cell ballooning rather than necrosis in association with reduced inflammation and apoptosis, but compromised by an adverse effect on lipid metabolism.

Neumomediastino y necrosis cutánea en asociación a dermatomiositis: presentación de un caso clínico y revisión de la literatura

We report a 37 years old male with a dermatomyositis treated with oral cyclophosphamide. He was admitted to the hospital due to a zone of skin necrosis with purulent exudate, located in the second left toe. A complete blood count showed a leukocyte count of 2,600 cells/mm³. A Chest CAT scan showed a pneumomediastinum with emphysema of adjacent soft tissue. Cyclophosphamide was discontinued and leukocyte count improved. The affected toe was amputated and a chest CAT scan showed a partial resolution of the pneumomediastinum. We discuss and review the pathogenesis, clinical presentation and management of pneumomediastinum and cutaneous necrosis in association with dermatomyositis.

Finger Necrosis Due to Cryoglobulinemic Vasculitis in Association with Membranous Nephropathy

Cryoglobulinemic vasculitis is a small vessel vasculitis that has been associated with chronic infections and autoimmune, lymphoproliferative, and neoplastic disorders. When no significant etiological factors are identified, it is called essential mixed cryoglobulinemia. A detailed and thorough laboratory investigation is required to exclude all possible causes of cryoglobulin formation. Although cryoglobulin testing is simple, careful temperature regulation is needed to avoid false-negative results. Consensus diagnosis should be developed and implemented for appropriate cryoglobulin detection and accurate clinical diagnosis for cryoglobulinemic vasculitis. Here we present an interesting, first-ever case report of a 54-year-old Hispanic-American woman with essential mixed cryoglobulinemia presenting with significant digital necrosis in association with membranous nephropathy.

Bilateral striatal necrosis in two subjects with Aicardi–Goutières syndrome due to mutations in ADAR1 (AGS6)

Aicardi-Goutières syndrome (AGS) is a genetic inflammatory disease. The classic neuroradiological picture mimics that of congenital infections in that Aicardi-Goutières syndrome is characterized by leukoencephalopathy, brain atrophy and intracranial calcifications. To date, bilateral striatal necrosis has not been reported in patients with AGS. We report on two patients with clinical diagnosis of Aicardi-Goutières syndrome in which brain MRI and CT scans demonstrated bilateral striatal necrosis. The diagnosis of Aicardi-Goutières syndrome in these two patients was genetically confirmed after the recent discovery that mutations in the ADAR1 (AGS6) gene may cause Aicardi-Goutières syndrome. This is the first report of bilateral striatal necrosis in association with Aicardi-Goutières syndrome. These results expand the neuroradiological phenotype of Aicardi-Goutières syndrome.

Penile necrosis in association with chronic renal failure; Calciphylaxis or Calcific uremic arteriolopathy

Penile necrosis in association with chronic renal failure; Calciphylaxis or Calcific uremic arteriolopathy

Vascular limb occlusion in twin-twin transfusion syndrome (TTTS): case series and literature review

The purpose of this study was to evaluate the phenomenon of vascular ischemic limb necrosis in twin-twin transfusion syndrome (TTTS). This was a multicenter retrospective review of ischemic limb necrosis in patients with TTTS. Twenty cases of fetal ischemic limb necrosis in association with TTTS were identified from 10 fetal medicine centers. The recipient was affected in 19 cases, and the lower limb was affected in 17 cases. The extent of the damage correlated with TTTS severity. Eighty percent of limb defects (16/20) clearly were unrelated to laser treatment (3 cases untreated, 7 cases after amnioreduction, 6 cases present at time of laser). The recipient was relatively polycythemic in 5 of 7 cases in which neonatal or fetal hemoglobin/hematocrit levels were available. Ischemic limb necrosis is a rare complication of TTTS. The lesion is unrelated to therapy and may be the result of polycythemia, hypertension, and vasoconstriction.

Challenges in Mammography: Part 2, Multimodality Review of Breast Augmentation—Imaging Findings and Complications

Breast augmentation is common throughout the world; however, there is variation in materials and surgical techniques. This review illustrates the mammographic, sonographic, and MRI characteristics of the different types of breast augmentation, including silicone, saline, polyacrylamide gel, and autologous fat augmentation. The imaging findings of complications such as implant rupture, free silicone, and fat necrosis in association with augmentation will be illustrated.

Acute sleeve gastrectomy for a strangulated paraoesophageal hernia.

Gastric necrosis in association with strangulation of a paraoesophageal hernia is a rare but life-threatening condition. The present article reports a case of strangulated paraoesophageal hernia with gastric necrosis in an obese woman treated successfully by acute sleeve gastrectomy.

Nucleos(t)ide analogue treatment reduces apoptotic activity in patients with chronic hepatitis B

Background Reduction of necroinflammatory activity is a major goal of antiviral therapy of patients with chronic hepatitis B. Serum ALT does not detect all forms of cell death. Objectives To analyze dynamics of novel serum cell death markers for apoptosis and necrosis in association with virologic response to nucleos(t)ide (Nuc) analogue treatment. Study design Quantification of the M30-apoptosis neoepitope and the cytokeratin-18 (M65-necrosis) serum levels before and during treatment of patients with chronic hepatitis B with Nuc ( n = 26). Results Before treatment, M30-apoptotic activity was significantly correlated with M65-necrosis and fibrosis but not with serum ALT. During therapy with Nucs, cell death parameters M30-apoptosis, M65-necrosis, and ALT declined in association with virologic response. The most frequent cell death pattern was simultaneous decline of ALT and M30-apoptosis which occurred more frequently in patients with HBs-Antigen decline than in patients with HBs-Antigen increase during treatment (87.5% vs. 40.0%; p = 0.024). ALT decline in association with increase of M30 apoptosis was frequent in patients with HBs-Antigen increase during treatment (36.3%) but was not observed in patients with HBs-Antigen decline during treatment. Conclusion Decline of cell death parameters in association with decline of HBV-DNA and HBs-Antigen indicates a reduction in overall cell death activity during Nuc treatment supporting the concept that response to Nuc therapy reduces necroinflammatory activity and progression of liver disease.

Prevalence of bone marrow necrosis in Egyptian cancer patients referring to the National Cancer Institute

BackgroundBone marrow necrosis is a relatively rare entity which has been associated with a poor prognosis. It is most commonly found in patients with neoplastic disorders and severe infections. MethodsThe study comprised examination of 5043 bone marrow biopsy specimens performed at the National Cancer Institute, Cairo University, over 7years period (March 2004–March 2011). It included 5years retrospective (2867 archived samples) and 2years prospective (2176 samples). ResultsBone marrow necrosis was diagnosed in fifteen out of 5043 examined specimens with a percentage of 0.3% and ranged from mild to massive according to semiquantitative estimation. Prognosis of all patients was poor with survival not exceeding 6months from the date of marrow necrosis diagnosis. ConclusionIn Egyptian patients, bone marrow necrosis in association with malignancy is a rare disorder which is accompanied by a poor outcome.

Vascular CD39/ENTPD1 Directly Promotes Tumor Cell Growth by Scavenging Extracellular Adenosine Triphosphate

Extracellular adenosine triphosphate (ATP) is known to boost immune responses in the tumor microenvironment but might also contribute directly to cancer cell death. CD39/ENTPD1 is the dominant ectonucleotidase expressed by endothelial cells and regulatory T cells and catalyzes the sequential hydrolysis of ATP to AMP that is further degraded to adenosine by CD73/ecto-5'-nucleotidase. We have previously shown that deletion of Cd39 results in decreased growth of transplanted tumors in mice, as a result of both defective angiogenesis and heightened innate immune responses (secondary to loss of adenosinergic immune suppression). Whether alterations in local extracellular ATP and adenosine levels as a result of CD39 bioactivity directly affect tumor growth and cytotoxicity has not been investigated to date. We show here that extracellular ATP exerts antitumor activity by directly inhibiting cell proliferation and promoting cancer cell death. ATP-induced antiproliferative effects and cell death are, in large part, mediated through P2X(7) receptor signaling. Tumors in Cd39 null mice exhibit increased necrosis in association with P2X(7) expression. We further demonstrate that exogenous soluble NTPDase, or CD39 expression by cocultured liver sinusoidal endothelial cells, stimulates tumor cell proliferation and limits cell death triggered by extracellular ATP. Collectively, our findings indicate that local expression of CD39 directly promotes tumor cell growth by scavenging extracellular ATP. Pharmacological or targeted inhibition of CD39 enzymatic activity may find utility as an adjunct therapy in cancer management.

Small bowel necrosis in association with jejunal tube feeding

Early recognition and appropriate treatment of bowel ischemia is imperative to reduce morbidity and mortality in any situation, including in conjunction with enteral tube feeding. GI intolerance can manifest as increased nasogastric tube output, unexplained abdominal pain/distension, and pneumatosis intestinalis in critically ill patients who are on tube feedings and may be experiencing periods of splanchnic hypotension. Recommendations are to immediately cease tube feedings when these signs and symptoms are recognized, and total parenteral nutrition should be considered. Surgical exploration during the early stages should be considered to prevent the usual and fatal catastrophic cascade of widespread bowl infarction.

Clinical guidelines for testing for heritable thrombophilia

Trevor Baglin, Elaine Gray, Mike Greaves, Beverley J. Hunt, David Keeling, Sam Machin, Ian Mackie, Mike Makris, Tim Nokes, David Perry, R. C. Tait, Isobel Walker and Henry Watson Addenbrooke’s Hospital, Cambridge, NIBSC, South Mimms, University of Aberdeen, Aberdeen, Guy’s and St Thomas’, London, Churchill Hospital, Oxford, University College Hospital, London, Royal Hallamshire Hospital, Sheffield, Derriford Hospital, Plymouth, Glasgow Royal Infirmary, Glasgow and Aberdeen Royal Infirmary, UK

β2-Toxin of Clostridium perfringens in a Hamadryas Baboon (Papio hamadryas) with Enteritis

An 11-yr-old female hamadryas baboon (Papio hamadryas) that died with a history of diarrhea and anorexia was submitted for necropsy. Major pathologic changes were restricted to the gastrointestinal tract. The small intestinal contents were watery and sanguinous, with a deepening of the red color in the large intestines. The intestinal mucosa was hyperemic. Microscopically, lesions consisted of surface epithelial cell necrosis in association with numerous rod-shaped bacteria and high numbers of Trichuris cynocephalus nematodes. Culturing of the small intestine yielded Clostridium perfringens. No other pathogenic bacteria were cultured using routine bacteriologic techniques. Polymerase chain reaction (PCR) analysis classified the Clostridium perfringens as type A cpb2-positive. Immunohistochemical examination with anti-beta2-toxin antibodies revealed beta2-toxin in close approximation with the intestinal lesions.

Non-Occlusive Small Bowel Necrosis in Association with Feeding Jejunostomy After Elective Upper Gastrointestinal Surgery

Non-occlusive small bowel necrosis (NOSBN) has been associated with early postoperative enteral feeding. The purpose of this study was to determine the incidence of this complication in an elective upper gastrointestinal (GI) surgical patient population and the influence of both patient selection and type of feeding jejunostomy (FJ) inserted, based on the experience of two surgical units in affiliated hospitals. The records were reviewed of 524 consecutive patients who underwent elective upper GI operations with insertion of a FJ for benign or malignant disease between 1997 and 2006. One unit routinely inserted needle catheter jejunostomies (NCJ), whilst the other selectively inserted tube jejunostomies (TJ). Six cases of NOSBN were identified over 120 months in 524 patients (1.15%), with no difference in incidence between routine NCJ (n = 5; 1.16%) and selective TJ (n = 1; 1.06%). Median rate of feeding at time of diagnosis was 105 ml/h (range, 75-125 ml/h), and diagnosis was made at a median of 6 days (range, 4-18 days) postoperatively. All patients developed abdominal distension, hypotension and tachycardia in the 24 h before re-exploratory laparotomy. Five patients died and one patient survived. The understanding of the pathophysiology of NOSBN is still rudimentary; nevertheless, its 1% incidence in the present study does call into question its routine postoperative use especially in those at high risk with an open abdomen, planned repeat laparotomies or marked bowel oedema. Patients should be fully resuscitated before initiating any enteral feeding, and feeding should be interrupted if there is any evidence of feed intolerance.

A 32‐year‐old woman with arthralgias and severe hypotension

A 32‐year‐old woman with arthralgias and severe hypotension