Acute Necrosis Research Articles

Hvdroquinone: Assessment of genotoxic potential in the in vivo alkaline comet assay.

Hydroquinone (HQ) exposure is common as it is a natural component of plant-based foods and is used in some fingernail polishes, hair dyes, and skin lighteners. Industrially it is used as an antioxidant, polymerization inhibitor, and reducing agent. The current study was undertaken to determine whether HQ may cause DNA damage in an in vivo comet assay in F344 rats. DNA strand breaks were assessed in the duodenum as a direct tissue contact site, the testes, and the liver and kidneys, which were tumor sites in bioassays. Rats were exposed to HQ by gavage at 0, 105, 210, or 420 mg/kg/day. At all dose levels, mean % tail intensity and tail moment values for all tissues in animals given HQ were similar to the control. There were no statistically significant increases in tail intensity in any tissue following HQ treatment of male and female rat and data for all animals fell within the available historical control ranges for each tissue. There was no evidence of induction of DNA damage in cells isolated from duodenum, kidney or liver of male and female rats or in the testes of male rats following exposure to HQ at a dose levels up to 420 mg/kg/day, which caused acute renal necrosis.

Rickettsioses complicated with dry gangrene and thrombotic thrombocytopenic purpura -a case report

Background: Spotted fever group rickettsioses has become more apparent in certain provinces of Sri Lanka. It has a vast diversity in its clinical presentation. However, toe gangrene and thrombotic thrombocytopenic purpura are rare presentations of rickettsioses and are less reported to date. Case presentation: Acute febrile illness of a 28year old Army Officer was complicated with seizures, acute kidney injury, toe gangrene and skin necrosis. He was treated as for spotted fever group rickettsioses complicated with dry gangrene and thrombotic thrombocytopenic purpura. Accurate clinical diagnosis and specific treatment resulted in dramatic recovery leaving behind only the residual gangrenous toes. Conclusion: This case report highlights the importance of accurate clinical diagnosis along with timely intervention to determine the outcome of certain detrimental and rare complications of spotted fever group rickettsioses.

Acquired deficiency of peroxisomal dicarboxylic acid catabolism is a metabolic vulnerability in hepatoblastoma

Metabolic reprogramming provides transformed cells with proliferative and/or survival advantages. Capitalizing on this therapeutically, however, has been only moderately successful because of the relatively small magnitude of these differences and because cancers may further adapt their metabolism to evade metabolic pathway inhibition. Mice lacking the peroxisomal bifunctional enzyme enoyl-CoA hydratase/3-hydroxyacyl CoA dehydrogenase (Ehhadh) and supplemented with the 12-carbon fatty acid lauric acid (C12) accumulate the toxic metabolite dodecanedioic acid (DDDA), which causes acute hepatocyte necrosis and liver failure. We noted that, in a murine model of pediatric hepatoblastoma (HB) and in primary human HBs, downregulation of Ehhadh occurs in association with the suppression of mitochondrial β- and endosomal/peroxisomal ω-fatty acid oxidation pathways. This suggested that HBs might be more susceptible than normal liver tissue to C12 dietary intervention. Indeed, HB-bearing mice provided with C12- and/or DDDA-supplemented diets survived significantly longer than those on standard diets. In addition, larger tumors developed massive necrosis following short-term DDDA administration. In some HBs, the eventual development of DDDA resistance was associated with 129 transcript differences, ∼90% of which were downregulated, and approximately two-thirds of which correlated with survival in numerous human cancers. These transcripts often encoded extracellular matrix components, suggesting that DDDA resistance arises from reduced Ehhadh uptake. Lower Ehhadh expression was also noted in murine hepatocellular carcinomas and in subsets of certain human cancers, supporting the likely generality of these results. Our results demonstrate the feasibility of C12 or DDDA dietary supplementation that is nontoxic, inexpensive, and likely compatible with more standard chemotherapies.

Acute renal injury due to rhabdomyolysis: A tertiary hospital experiencee

Aim: Rhabdomyolysis (RML) is a clinical and biochemical syndrome caused by acute necrosis of striated muscle fibers and the subsequent transportation of potentially toxic cellular contents into the systemic circulation. In this study, we present data from rhabdomyolysis patients that developed acute renal failure who were hospitalized and treated in our clinic in 2019. Materials and Methods: We reviewed all cases of RML treated in the tertiary hospital within a 12-month period, which was defined as serum creatinine kinase (CK) levels > five times the upper normal limit. The inclusion criteria were as follow: (a) being aged ≥ 18 years, (b) being treated for RML within the designated time period, (c) AKI development. The exclusion criteria are as follows: (a) being aged 5 time upper normal limit (UNL), 14 conformed to the inclusion criteria and were selected as subjects Results: A total of 14 patients were included in the study, 12 of which were male. The mean age of the patients was 48.1 (18–80). The etiologies were as follows: hypothyroidism, 3; prolonged exposure to sun, 2; electrolyte imbalance due to severe diarrhea, 1; viral upper respiratory tract infection (URTI), 3; intramuscular injection, 1; heavy exercise or falls.Conclusion: Rhabdomyolysis is an interdisciplinary clinical condition that can lead to life-threatening outcomes including AKI. Rapid diagnosis and treatment can be life-saving. AKI is a significant potential complication of RML and renal function should be evaluated irrespective of CK levels or the presence of myoglobinuria.

가리비의 Acute Viral Necrosis Virus (AVNV) 모니터링

가리비의 Acute Viral Necrosis Virus (AVNV) 모니터링

Predictors of Mortality During Initial Liver Transplant Hospitalization and Investigation of Causes of Death.

BackgroundLiver transplant (LT) remains a life-saving procedure with a high mortality rate. The present study investigated the causes of death and sought to identify predictive factors of mortality during the initial LT hospitalization.Material/MethodsWe retrieved data on first-time adult recipients who underwent LT between November 2017 and October 2019 receiving grafts from donation after citizen’s death. The risk factors for mortality during the initial LT hospitalization were confirmed by univariate analysis. We also analyzed the causes of death.ResultsWe enrolled 103 recipients, including 86 males and 17 females, with a mean age of 47.7 years. Thirty-eight (36.9%) recipients were labeled as non-cholestatic cirrhosis-related indications. Approximately 8% of all recipients had diabetes prior to LT. Induction therapy was used in 11 (10.7%) recipients, along with maintenance therapy. The median model for end-stage liver disease score at LT was 32.4 (21.4–38.4). The in-hospital mortality rate of LT recipients was 6.8% (7/103), and infections were responsible for most of the deaths (6/7). The 1 remaining death resulted from primary graft failure. Univariate analysis showed recipients with postoperative pneumonia (p<0.05), acute hepatic necrosis, and intensive care unit (ICU) stay ≥7 days (both p<0.01), postoperative bacteremia, creatinine on day 3 after LT>2 mg/dL, and alanine transaminase on day 1 after LT >1800 μmol/L (all P<0.001) were much more likely to die.ConclusionsIn-hospital mortality of LT recipients was high, due in large part to infections. Acute hepatic necrosis, prolonged post-transplant ICU stays, certain types of postoperative infections, and postoperative liver and kidney dysfunction were potential risk factors for in-hospital mortality of LT recipients.

Type 2 MI induced by a single high dose of isoproterenol in C57BL/6J mice triggers a persistent adaptive immune response against the heart.

Heart failure is the common final pathway of several cardiovascular conditions and a major cause of morbidity and mortality worldwide. Aberrant activation of the adaptive immune system in response to myocardial necrosis has recently been implicated in the development of heart failure. The ß‐adrenergic agonist isoproterenol hydrochloride is used for its cardiac effects in a variety of different dosing regimens with high doses causing acute cardiomyocyte necrosis. To assess whether isoproterenol‐induced cardiomyocyte necrosis triggers an adaptive immune response against the heart, we treated C57BL/6J mice with a single intraperitoneal injection of isoproterenol. We confirmed tissue damage reminiscent of human type 2 myocardial infarction. This is followed by an adaptive immune response targeting the heart as demonstrated by the activation of T cells, the presence of anti‐heart auto‐antibodies in the serum as late as 12 weeks after initial challenge and IgG deposition in the myocardium. All of these are hallmark signs of an established autoimmune response. Adoptive transfer of splenocytes from isoproterenol‐treated mice induces left ventricular dilation and impairs cardiac function in healthy recipients. In summary, a single administration of a high dose of isoproterenol is a suitable high‐throughput model for future studies of the pathological mechanisms of anti‐heart autoimmunity and to test potential immunomodulatory therapeutic approaches.

A prospective evaluation of hepatic parameters in congestive heart failure patients

Background: Heart failure is heterogeneous and complex clinical syndrome. Passive congestion of liver is associated with increase in direct and indirect serum bilirubin and elevated liver enzyme. Impaired perfusion due to decreased cardiac output is responsible for acute hepatocellular necrosis and serum aminotransferases will be elevated. Present study has been designed to study the prevalence of liver function abnormalities in heart failure patients, pattern of elevation of liver enzymes and correlation of liver function tests with etiology, duration and of heart failure.Methods: All patients enrolled for this study was evaluated clinically and echocardiographically. Various demographic parameters like age sex duration of disease were recorded on predesigned Performa.Results: Serum bilirubin was 3.76±1.62 mg/dl in class IV and least in class I that is 1.125±0.30 mg/dl. Serum AST was highest in class IV 154.64±24.96 IU and least in class I that is 36.21±12.65 IU (p=0.001). Serum ALT was highest in class IV 192.24±34.44 IU and least in class I that is 33.34±11.460 (p=0.001).Conclusions: From present study we can conclude that heart failure was common in fifth and sixth decade of life and there was male predominance. Congested hepatomegaly was common presentation jaundice and ascites was also common. Change in biochemical parameters was increased with severity and duration of heart disease.

ESTABLISH THE INITIAL PROCEDURE FOR DETECTING VIBRIO PARAHAEMOLYTICUS IN THE SHRIMP BY ONE STEP- PCR METHOD

Early Mortality Syndrome (EMS), also known as Acute Hepatopancreas Necrosis Disease (AHPND) in shrimps, has been identified as being caused by a strain of V. parahaemolyticus. This disease has caused enormous damage to the shrimp farming industry among countries in the world in general and Vietnam in particular. One of the main reasons for uncontrollable widespread disease is the process of identifying pathogens is slow and inaccurate, leading to no promptly preventive measurement. In order to enhance the ability to briefly detect disease and improve the current disease status, in this study the PCR process using two specific 16S rRNA and ldh primers has been developed to swiftly diagnose V. parahaemolyticus pathogen in shrimps with a detection threshold of 3.5x103 CFU/ml

Gastrointestinal mucormycosis due to Rhizopus microsporus following Streptococcus pyogenes toxic shock syndrome in an HIV patient: a case report

BackgroundGastrointestinal (GI) mucormycosis is a rare and often deadly form of mucormycosis. Delayed diagnosis can lead to an increased risk of death. Here, we report a case of GI mucormycosis following streptococcal toxic shock syndrome in a virologically suppressed HIV-infected patient.Case presentationA 25-year-old Thai woman with a well-controlled HIV infection and Grave’s disease was admitted to a private hospital with a high-grade fever, vomiting, abdominal pain, and multiple episodes of mucous diarrhea for 3 days. On day 3 of that admission, the patient developed multiorgan failure and multiple hemorrhagic blebs were observed on all extremities. A diagnosis of streptococcal toxic shock was made before referral to Siriraj Hospital – Thailand’s largest national tertiary referral center. On day 10 of her admission at our center, she developed feeding intolerance and bloody diarrhea due to bowel ischemia and perforation. Bowel resection was performed, and histopathologic analysis of the resected bowel revealed acute suppurative transmural necrosis and vascular invasion with numerous broad irregular branching non-septate hyphae, both of which are consistent with GI mucormycosis. Peritoneal fluid fungal culture grew a grayish cottony colony of large non-septate hyphae and spherical sporangia containing ovoidal sporangiospores. A complete ITS1–5.8S-ITS2 region DNA sequence analysis revealed 100% homology with Rhizopus microsporus strains in GenBank (GenBank accession numbers KU729104 and AY803934). As a result, she was treated with liposomal amphotericin B. However and in spite of receiving appropriate treatment, our patient developed recurrent massive upper GI bleeding from Dieulafoy’s lesion and succumbed to her disease on day 33 of her admission.ConclusionDiagnosis of gastrointestinal mucormycosis can be delayed due to a lack of well-established predisposing factors and non-specific presenting symptoms. Further studies in risk factors for abdominal mucormycosis are needed.

Acute ozone exposure can cause cardiotoxicity: Mitochondria play an important role in mediating myocardial apoptosis

ObjectiveTo clarify the cardiotoxicity induced by acute exposure to different concentrations of ozone in both gender rats and explore the underlying mechanisms. MethodsA total of 240 rats were randomly sorted into 6 groups with equal numbers of male and female rats in each group. The rats were subjected to ozone inhalation at concentrations of 0, 0.12, 0.5, 1.0, 2.0 and 4.0 ppm, respectively, for 6 h. After ozone exposure, function indicators, myocardial injury indexes and risk factors of cardiovascular disease in blood were assayed. ResultsHigh ozone exposure resulted in sustained ventricular tachycardia in male and female rats. Myocardial apoptosis in male rats started from 1.0 ppm ozone, and that in female rats started from 2.0 ppm ozone (p < 0.05). Caspase-9 increased significantly from 0.12 ppm ozone (p < 0.01) in both gender rats, while caspase-3 was initially activated at 0.5 ppm ozone. From 1.0 ppm ozone, mitochondrial cristae and myofilaments dissolved. The ratio of Bcl-2/Bax decreased significantly from 0.12 ppm and MRCC-IV decreased significantly from 2.0 ppm by ozone. ConclusionAcute ozone exposure can cause paroxysmal ventricular tachycardia in rats. Moreover, the changes of inflammatory factors in the heart tissues of female and male rats after ozone exposure were greater than those of oxidative stress. This study reported for the first time that 6 h ozone exposure does not cause acute cardiomyocyte necrosis, but promotes cardiomyocyte apoptosis in a mitochondrial-dependent manner. Ozone could regulate caspases-3 dependent cardiomyocyte apoptosis by affecting the balance between caspase-9 and XIAP.

Cardiopulmonary Lesions in Sheep Produced by Experimental AcuteClostridium PerfringensType D Enterotoxemia

Enterotoxemia caused by Clostridium perfringens type D is one of the most prevalent clostridial diseases of sheep. The lesions of the acute form of this disease, particularly the cerebral lesions, are well characterized; however, detailed descriptions of the cardiac and pulmonary lesions are lacking. Here we describe cardiopulmonary lesions in experimental acute type D enterotoxemia in sheep and determine the role of epsilon toxin (ETX) in the development of these lesions. Four groups of 6 sheep were intraduodenally inoculated with either a wild-type C. perfringens type D strain; its etx knockout mutant, which is unable to produce ETX; the etx mutant complemented with the wild-type etx gene, which regains the ETX toxigenic ability; or sterile culture medium as a control. All sheep were subjected to postmortem examination within 24 hours of inoculation. Lesion scores were compared between groups for pulmonary edema; hydrothorax; ascites; hydropericardium; endocardial, myocardial and epicardial hemorrhages; microscopic lesions of acute myocardial degeneration and necrosis; and myocardial, endocardial, and epicardial edema, hemorrhage, and inflammation. Only sheep inoculated with the wild-type and complemented ETX-toxigenic bacterial strains developed cardiopulmonary lesions, which were present in varying degrees of severity and proportions. These lesions were not present in sheep inoculated with the etx mutant or in the negative control. We conclude that severe acute cardiopulmonary lesions in sheep with experimental enterotoxemia are associated with the capacity of the strains to produce ETX. These changes are likely contributors to the clinical signs and even death of affected animals.

ORGANOPHOSPHORUS POISONING PRESENTING WITH ACUTE CORTICAL NECROSIS: A RARE COMPLICATION OF A COMMON DISORDER IN INDIAN SETTING

Organophosphorus poisoning in the form of insecticides and pesticides acts by inhibition of anticholinesterase activity at the neuromuscular junction leading to overstimulation of the nicotinic and muscarinic receptor. Renal involvement usually manifests as increased urination, urinary incontinence, strangury due to overstimulation of urinary bladder . Acute kidney injury in the form of acute cortical necrosis is an extremely rare complication of OP poisoning. Here we highlight a case 31 year old male who presented to Emergency with Dichlorvos poisoning with anuria due to cortical necrosis requiring hemodialysis with gradually improving renal function thus representing an uncommon complication of Organophosphorus poisoning thus making it as a rare and interesting presentation.&#x0D; Keywords: Organophosphorus poisoning, Acute cortical necrosis, Granular casts

S2672 Influenza a Virus as a Trigger for Autoimmune Hepatitis

INTRODUCTION: Autoimmune hepatitis (AIH) is a chronic liver disease caused by an immune-mediated destruction of the hepatocytes. Studies have shed the light on the important role of infections in triggering AIH as many viral infections and vaccines have been associated with it. We present an atypical case of AIH possibly triggered by Influenza A virus. To our knowledge, this is the first case report showing autoimmune hepatitis induced by influenza A virus. CASE DESCRIPTION/METHODS: A 52-year-old previously healthy female presented with new-onset jaundice after Influenza A viral infection. Initial laboratory investigations revealed an aspartate aminotransferase level of 1211 U/liter, an alanine aminotransferase level of 1506 U/liter, an alkaline phosphatase level of 305 U/liter, a total bilirubin level of 5.1, a direct bilirubin level of 3.4 and an international normalized ratio of 1. Serologic testing for hepatitis A, B, and C, HSV, CMV, and EBV were negative. Influenza A PCR was detected on nasopharyngeal sampling. Covid-19 test was negative. ASMA was positive with a titer of 1:80. ANA was positive with a titer of 1:80. Anti-mitochondrial antibody was negative. IgG, Alpha 1 antitrypsin, ceruloplasmin levels were within normal limits. No acetaminophen was detected in the blood. A CT abdomen showed normal biliary tree with no biliary strictures and no cirrhotic changes of the liver. Her liver biopsy showed acute hepatitis with moderate acute hepatocellular injury and hepatocellular necrosis with mixed portal infiltrates which include both plasma cells and eosinophils. Based on the revised International Autoimmune Hepatitis Group Scoring System for the Diagnosis of Autoimmune Hepatitis, her pretreatment score was 13 points. She was started on prednisone and had significant biochemical improvement. Her steroids were tapered and steroid sparing therapy with azathioprine was initiated. DISCUSSION: Influenza virus and vaccine have been proposed to cause autoimmune disease in the literature such as type 1 diabetes, narcolepsy, recurrent ITP, and multiple sclerosis. There has been an association as well between influenza vaccine and AIH. In a study published by Saski et al, they describe two cases of middle-aged women who developed autoimmune hepatitis after receiving influenza vaccine. We suggest that in our patient, the influenza A virus infection triggered autoimmune hepatitis. Autoimmune hepatitis should be considered in patients with persistently elevated liver enzymes following infections such as influenza.Figure 1.: Liver biopsy cores show findings suggestive of acute hepatitis. Dense portal inflammatory infiltrates are present, comprised of macrophages, lymphocytes, neutrophils, eosinophils and plasma cells. Piecemeal acute hepatocellular necrosis is also noted at the limiting plate (H&E, original magnification 10x).Figure 2.: Prominent bile stasis with sinusoidal Kupffer cell hyperplasia (H&E, original magnification 10x).

S2978 Intrathoracic Gastric Incarceration Following Laparoscopic Nissen Fundoplication

INTRODUCTION: Nissen fundoplication is the most performed surgical treatment for GERD. Given the complex anatomy of the EG junction, structural complications occur in up to 30% of cases following fundoplication. Our case is that of post fundoplication paraesophageal hernia with intrathoracic gastric incarceration. CASE DESCRIPTION/METHODS: A 57yo F with PMHx of GERD and type III paraesophageal hiatal hernia who had undergone laparoscopic surgery with primary diaphragm repair and Nissen fundoplication 7mo prior presented with acute onset of dysphagia and epigastric pain. CT revealed superoposterior migration of the Nissen wrap above the diaphragm and a well-circumscribed pouchlike sac to the left of the Nissen fundoplication containing an air-fluid level, without evidence of perforation. GI was consulted and the patient underwent EGD revealing a tight Nissen wrap that was barely traversable. The gastric mucosa was congested, inflamed, and ulcerated from the GE junction to the gastric body concerning for acute incarceration and necrosis. Surgery was urgently consulted, and the patient underwent emergent exploratory laparoscopy which revealed incarcerated herniation of the previously performed fundoplication into the chest. The fundus and upper body of the stomach were necrotic. Laparoscopic subtotal linear gastrectomy with mediastinal abscess drainage and closure of the diaphragmatic defect was performed followed by intraoperative EGD. The patient was discharged a few days later and is currently doing well. DISCUSSION: Nissen fundoplication is a widely accepted and commonly performed anti reflux surgical procedure. The gastric fundus is wrapped around the intraabdominal esophagus, after mobilizing the esophagus and reducing the hiatal hernia, if present. The rate of serious complications has been documented as less than 5%. Incarceration post fundoplication is usually a late diagnosis as it presents with non-specific symptoms of abdominal pain, nausea, and vomiting. EGD with comprehensive retroflexed examination of the fundoplication and barium esophagram are the primary tests to assess for structural complications. Paraesophageal hernia is one of the complications reported after laparoscopic Nissen fundoplication, and it requires emergency operation when associated with incarceration, obstruction, or strangulation of the stomach. There should be high index of suspicion for complications in patients with history of Nissen fundoplication for early detection, prompt treatment, and satisfactory outcomes.Figure 1Figure 2Figure 3

A RARE CASE OF FULMINANT MYOCARDITIS CAUSED BY MYCOPLASMA PNEUMONIAE SUCCESSFULLY TREATED WITH IVIG

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Fulminant myocarditis (FM) is a clinical condition which main characteristic is a rapidly progressive clinical course associated with hemodynamic compromise and high mortality risk.It is associated with an infectious process but rarely reported alongside Mycoplasma pneumoniae infection.It is unclear if the primary problem is ongoing damage from a virus, post-infectious inflammatory reactions, or both. Therefore,immunosuppressive therapy such as IVIG could be of potential benefit for treating FM.We report a rare case of FM caused by M.pneumoniae in a 27 y/o F showing improvement with IVIG therapy. CASE PRESENTATION: 27 y/o F with DM1 presented to ED with lethargy,hypotension,and tachycardia.Labwork showed DKA.She was intubated, transferred to the ICU and then started on insulin drip.On day 2, the she developed ST segment elevations,along with elevated troponin(11.86 ug/L).Echocardiogram showed EF of 42% along diffuse hypokinesis. Cardiac angiogram revealed nonobstructive CAD.On day 3, DKA resolved and patient was transitioned off insulin drip. Echocardiogram revealed worsened EF of 10-15%.Her workup showed positive M. pneumoniae IgM serology and doxycycline therapy was started, however she developed hemodynamic instability and was started on IVIG therapy.On day 4,she was weaned off vasopressor support and extubated.Repeat echocardiogram revealed EF>50% without wall motion abnormalities.Patient completed 2 days of IVIG therapy and was discharged after 8 days of hospitalization. DISCUSSION: Despite FM’s rareness, up to 12% of cases of sudden death in patients aged <40 years exhibit myocarditis.Our patient was admitted to the ICU with severe DKA, and within 24 hours she developed FM with positive M. pneumoniae IgM serology. M. pneumoniae is among the most common bacterial causes of respiratory tract infections and also associated with carditis. Myocarditis should be suspected in patients with or without cardiac signs and symptoms who present a rise in cardiac biomarker levels; changes in ECG or abnormalities of ventricular systolic function. Definitive diagnosis of myocarditis is achieved via endomyocardial biopsy(EMB).Yet, 2013 ACCF/AHA guidelines suggest excluding other causes of HF as EMB might be helpful when the results influence the management.Therefore,our patient underwent heart catheterization to rule out obstructive CAD upon the documented STEMI findings.IVIG therapy was started when she worsened hemodynamically.Yet, the use of IVIG for acute myocarditis should not be part of routine practice as its use is obscured by poor quality evidence making its use for infectious myocarditis debatable. CONCLUSIONS: The response to IVIG therapy suggests that the rapid decline of this case of infectious FM may be caused in part by an autoimmune process.Immunosuppressive treatment with IVIG in FM associated to M.pneumoniae may reduce the mortality rate and prevent irreversible myocardial injury. Reference #1: Veronese, G. (2018). Fulminant myocarditis: Characteristics, treatment, and outcomes. The Anatolian Journal Of Cardiology. https://doi.org/10.14744/anatoljcardiol.2017.8170 Reference #2: Tretjak, M., Verovnik, F., Vujkovac, B., Slemenik-Pusnik, C., & Noc, M. (2003). Severe Diabetic Ketoacidosis Associated With Acute Myocardial Necrosis. Diabetes Care, 26(10), 2959-2960. https://doi.org/10.2337/diacare.26.10.2959 Reference #3: Gupta, A., Ghimire, G., & Hage, F. (2013). Guidelines in review: 2013 ACCF/AHA Guideline for the Management of HF. Journal Of Nuclear Cardiology, 21(2), 397-399. https://doi.org/10.1007/s12350-013-9832-x DISCLOSURES: No relevant relationships by Sabree Abedrabo, source=Web Response No relevant relationships by Violeta Alvarez-Retamales, source=Web Response No relevant relationships by Mukul Bhattarai, source=Web Response No relevant relationships by Phyo Kyaw, source=Web Response No relevant relationships by Odalys Lara-Garcia, source=Web Response No relevant relationships by Suhayb Ranjha, source=Web Response No relevant relationships by Mingchen Song, source=Web Response

Rotavirus infection in a racing pigeon (Columba livia) in Great Britain during 2018

We report the first diagnosis of fatal rotavirus A (RVA) infection in a racing pigeon in Great Britain. In August 2018, a small group of racing pigeons (Columba livia) from...

S2857 Intestinal Behcet’s Disease Involving Terminal Ileum

INTRODUCTION: Behcet’s Disease (BD) is a rare, chronic, inflammatory vasculitis that affects several organ systems. Gastrointestinal involvement occurs in 3 to 25% of patients, with prevalence of 1–2/1,000,000 in the United States. We present a case of a patient with BD developing abdominal pain, diarrhea, and weight loss. CASE DESCRIPTION/METHODS: 57-year-old man with known oral and genital BD presented with fever, 1-week 15lb weight loss, abdominal pain and non-bloody diarrhea. He had been on infliximab, colchicine and prednisone. Laboratory studies exhibited iron deficiency anemia and leukopenia. Abdominal CT showed wall thickening of terminal ileum with fat stranding consistent with terminal ileitis. Tuberculosis, Cytomegalovirus and Histoplasma on serum were negative. Colorectal surgery was consulted, and in light of refractory ileitis patient underwent laparoscopic right hemicolectomy with ileocolic anastomosis. Histopathology demonstrated acute ischemic necrosis with ileal ulceration. After surgery, he was continued on low dose prednisone and infliximab infusions with resolution of intestinal symptoms. DISCUSSION: Intestinal BD presents with abdominal pain, anorexia, vomiting, diarrhea, dyspepsia, and bloody/non-bloody stools. Mucosal ulcerations are thought to be the underlying factor behind the symptoms, likely secondary to a combination of vein and venule vasculitis and large vessel involvement leading to ischemia and subsequent infarction. Diagnosis can be challenging given clinical similarities with Inflammatory Bowel Disease (IBD), however findings of vasculitis on biopsy favors intestinal BD over IBD. Imaging modalities are useful in its diagnosis including barium swallow, CT, and MRI which demonstrate colonic wall thickening. Endoscopy often reveals large deep punched out ulcers with discrete margins usually in the ileocecal region. Treatment is similar to IBD, including medical and surgical modalities. First line agents are sulfasalazine, mesalamine and corticosteroids. Second line are infliximab and adalimumab. Colectomy is indicated if medical therapy fails or with presence of bowel perforation, fistulae or GI bleeding. After surgery, recurrence is seen up to 40–80% of cases, with 80% requiring re-operation. Keep in mind that patients with history of BD can develop colitis.Image 1.: Pre-operative CT showing the coronal sequence of images. Notice the circumferentially thickened, irregular terminal ileum in the right lower quadrant. There is secondary luminal narrowing and adjacent fat stranding compatible with transmural involvement.Image 2.: Pre-operative CT as above. Image series.

Multiple extra-splanchnic venous thromboses - an unusual vascular complication of acute pancreatitis.

Acute pancreatitis (AP) is an acute inflammatory process of the pancreas with variable clinical presentations. Splanchnic venous thrombosis is a well-known vascular complication of AP and commonly present as thrombosis of the splanchnic venous system: splenic vein (SplV), portal vein (PV) and superior mesenteric vein (SMV), either separately or in combinations. Involvement of extra-splanchnic vessels is rare and associated with morbidity and mortality. Vascular complications are late phenomena and usually associated with local complications of AP, namely acute fluid collections, necrotizing pancreatitis and walled-off pancreatic necrosis. Pathogenesis of venous thrombosis is multifactorial in which pancreatic inflammation and systemic inflammatory response play a key role. At present, there are no consensus guidelines on treatment and use of anticoagulation for venous thrombosis in the setting of AP. Limited literature suggests the use of anticoagulation in presence of PV with or without SMV thrombosis and extrasplanchnic vessel involvement. Literature on extra-splanchnic vessels involvement in acute pancreatitis is sparse. Here we present two cases with multiple extra-splanchnic vessels involvement and their management.

Spontaneous Necrotizing Hepatic Arteriopathy in Male Sprague-Dawley Rats.

Differentiating test article-related vascular changes from spontaneous findings is important for microscopic interpretation in drug safety evaluation studies intended for regulatory submission. Here, we report background spontaneous hepatic artery degeneration and necrosis in up to 20% of 3- to 9-month-old control male Sprague-Dawley rats in 23 individual safety studies. The vascular degeneration occurred in one cross section of a medium-sized hepatic artery near the hilus and ranged from acute intramural hemorrhage and fibrinoid necrosis to chronic fibrosis of the vascular wall with perivascular edema, hemorrhage, and inflammatory cell infiltrates. The cause was uncertain. Many microscopic features were consistent with systemic necrotizing arteriopathy (SNA) or polyarteritis; however, there was no change in arteries commonly affected in SNA/polyarteritis (mesenteric, pancreatic, or testicular arteries) and hepatic artery degeneration/necrosis occurred in younger rats which is unusual for SNA/polyarteritis. Spontaneous hepatic artery degeneration/necrosis represents a sporadic background finding that may be confused with a test article's toxicologic effect.