Wall Edema Research Articles

Sunitinib-induced small bowel wall edema as a prognostic marker in metastatic renal cell carcinoma.

The aim of this study was to evaluate the presence of small bowel wall edema (SBWE) on computed tomography (CT) images in patients with metastatic renal cell carcinoma (mRCC) treated with sunitinib and to investigate the relationship between the presence of SBWE and survival. We retrospectively evaluated the presence of SBWE on CT images of 27 mRCC patients who received at least one cycle of sunitinib. Then, we analyzed the relationship between the presence of SBWE and progression-free survival (PFS) and overall survival (OS). All 27 patients had SBWE on at least one CT scan. The median value of SBWE thickness was 2.5 mm. SBWE thickness was ≤2.5 mm in 13 patients (group A) and >2.5 mm in 14 patients (group B). The median OS was significantly higher in group B (55 vs. 18 months, respectively, P = 0.02). Although it was not statistically significant (13 vs. 8 months, respectively, P = 0.69), the median PFS was longer in group B than in group A. This study showed that sunitinib treatment caused SBWE in all patients with mRCC who received the drug. Also, this study demonstrated an association between higher SBWE thickness and better survival outcomes.

A Mysterious Case of Abdominal Pain

A Mysterious Case of Abdominal Pain

The correlation between COVID-19 segmentation volume based on artificial intelligence technology and gastric wall edema: a multi-center study in Wuhan.

PurposeThis study aimed to investigate manifestations of the gastric wall and related risk factors in COVID-19 patients with gastrointestinal symptoms by CT.Materials and methodsTwo hundred and forty patients diagnosed with COVID-19 by RT-PCR were enrolled from January 2020 to April 2020. Patients showed gastrointestinal symptoms, including nausea, vomiting, or diarrhea. Results of the initial laboratory examination were performed after admission. Chest CT was performed for all patients, with the lower bound including the gastric antrum. The volume of COVID-19 and lungs was segmented, and the ratio was calculated as follows: PV/LV = Volumepneumonia/Volumelungs.ResultsAmong the 240 patients, 109 presented with gastric wall edema (edema group), and 131 showed no gastric wall edema (non-edema group); the PV/LV values between the two groups were significantly different (P = 0.002). Univariate analysis revealed the following: fibrinogen (Fib), thrombin time (TT), activated partial thromboplastin time (APTT), and albumin (ALB) significantly differed between the two groups (P < 0.05). Binary logistic regression analysis showed that only APTT had a negative effect on gastric wall edema (P = 0.003).ConclusionsSARS-CoV-2 invades the gastrointestinal tract, gastric wall edema is the primary CT manifestation, and gastric wall edema is more likely to occur with a shorter APTT and severe pneumonia, with a slightly longer hospitalization time. Patients with gastric wall edema observed by CT should intervene early, which may improve digestive function, and further strengthen immune potency against COVID-19.

S2489 Differentiating CMV Colitis From GVHD in Post-Transplant Patients: A Case Study

Introduction: Cytomegalovirus (CMV) infection can complicate the clinical course of immunocompromised patients including allogeneic hematopoietic stem cell transplant (allo-HSCT) recipients, where the infection can be serious. CMV can involve different organs including lungs, brain, eyes, and the GI tract. Signs and symptoms of CMV infection may overlap with other conditions including graft-versus-host disease (GVHD), a multisystem disorder commonly seen in allo-HSCT recipients. Case Description/Methods: A 57-year-old female presented with abdominal pain and diarrhea. Past medical history included relapsed acute myeloid leukemia, treated with azacitidine and venetoclax followed by allo-HSCT. She was recently hospitalized for suspected GVHD with skin, liver, and gastrointestinal involvement. She was also found to have a CMV viral load of 920 IU/mL. Endoscopy showed diffuse inflammation across the GI tract, with biopsies revealing apoptotic bodies consistent with acute GVHD. She was treated with ruxolitinib and prednisone for GVHD, and valganciclovir prophylactically for CMV viremia. At this presentation, labs were notable for lymphocytes of 39 x103/uL and platelets of 22 x 103/uL, and CMV viral load of 1,822,242 IU/mL. CT imaging revealed thickened distal small bowel loops, cecum, and right colon, and edematous gastric walls with submucosal enhancement. Infectious work-up, including stool culture, ova/parasite, and clostridium, was negative. She underwent endoscopic evaluation; EGD showed white discoloration that washed off in the esophagus and diffuse erythematous mucosa in the stomach (Figure). Biopsies from gastric mucosa and right colon mucosa revealed focal nuclear changes. Immunohistochemical stains were positive for CMV. She was diagnosed with refractory CMV colitis and treated with maribavir with improvement of symptoms and reduction of viral load, and prior course of steroids was tapered. Discussion: Immunosuppression for GVHD has been identified as an important risk factor for CMV reactivation. Differentiating CMV colitis and GI-GVHD poses a diagnostic challenge, and endoscopic evaluation is needed to address this. Endoscopy can identify cecal ulcers, a reliable finding for CMV colitis in patients with GVHD after allo-HSCT.1 It is important to timely identify CMV colitis to prevent post-transplant morbidity and mortality. This case also demonstrates effectiveness of maribavir, a novel antiviral, for refractory post-transplant CMV colitis.Figure 1.: EGD images showing white discoloration in the entire esophagus and diffuse erythematous mucosa in the entire examined stomach.

Gastroprotective, Biochemical and Acute Toxicity Effects of Papaver decaisnei against Ethanol-Induced Gastric Ulcers in Rats

Papaver decaisnei (P. decaisnei) has been used as folkloric medicine for many health issues including gastric problems. The current study investigates the gastroprotective roles of P. decaisnei against ethanol-induced ulcers in rodents. Sprague Dawley rats (30) were separated into five groups: the normal group (G1) and the ulcer control group (G2) were orally administered 0.5% carboxymethylcellulose (CMC); the reference group (G3) was administered 20 mg/kg of Omeprazole; two experimental groups were fed with 200 mg/kg (G4) and 400 mg/kg (G5) of the P. decaisnei extract (PDE), respectively. Next, the rats were given absolute ethanol and sacrificed for the analysis of the gastric mucosal injury through microscopic, enzymatic, histologic, and immunohistochemistry assays. The ulcer controls showed significant superficial hemorrhagic gastric mucosal lesions, with a decreased gastric wall mucus and edema production, whereas fewer were found for the reference and plant-treated rats. Furthermore, the PDE pre-treated rats had a significantly reduced the periodic acid-Schiff (PAS) staining intensity, produced the upregulation of the HSP70 protein, and the downregulation of the Bax protein expressions in the stomach epithelium. P. decaisnei displayed a significant role in the upregulation of endogenous antioxidant enzymes (SOD, CAT, and PGE2), significantly reduced malondialdehyde (MDA), TNF-a, IL-6, and upraised the IL-10 levels. Based on the positive impacts, the PDE can be proposed as the protective/treatment agent against gastric ulcers and stomach lesions.

S3552 Herpes Gastritis: A Rare Cause of Gastric Outlet Obstruction

Introduction: Gastrointestinal tract involvement from herpes simplex virus is commonly associated with esophagitis. However, herpes simplex infection of the stomach is very rare with only a handful of cases being reported in immunocompromised patients. We present a case of herpes gastritis causing gastric outlet obstruction in an otherwise healthy, immunocompetent individual. Case Description/Methods: A 37-year-old male with a recent past medical history of COVID-19 infection, presented to the hospital with intractable nausea, vomiting, bloating, and early satiety for two days. Upon evaluation, CBC and CMP were remarkable for a WBC of 12.5 k/mm3 and ALT and AST of 124 U/L and 129 U/L, respectively. Lipase was 373 U/L. A CT abdomen/pelvis w/contrast showed circumferential wall thickening with edematous changes in the antrum consistent with localized inflammatory response. There was suspicion for gastric lymphoma and patient was admitted for further workup. An EGD was performed which showed exudative esophagitis and antral wall edema with luminal narrowing of gastric antrum. Endoscopic ultrasound (EUS) showed a 2.5 × 3 cm antral wall lesion worrisome for linitis plastica. Esophageal biopsies showed focal cytologic changes consistent with herpes esophagitis. The FNA of the gastric antral wall showed multinucleation of the basal cell layer with classic ground glass nuclei, consistent with herpes infection. No dysplasia or malignancy was seen. Both HSV1 and HSV2 IgG were elevated. HSV IgM was normal. A HSV PCR was ordered but never resulted. Patient was started on Valacyclovir 1 g PO BID for 10 days. He underwent a follow-up EGD 3 months later which showed complete resolution of the gastric antral changes (Figure). Discussion: Herpes gastritis is extremely rare. Literature review has revealed only 3 case reports of herpes gastritis; and all involved immunocompromised patients. To the best of our knowledge, this is the first case of herpes gastritis in an immunocompetent patient. Our patient presented with symptoms of gastric outlet obstruction which was caused by local inflammation from herpes simplex. It is unclear if having a COVID 19 infection altered patient’s immunity and lead to herpes gastritis. This may need further investigation. No established guideline exists for treatment duration. Our patient received 10-day course of Valacyclovir, and his symptoms improved. Furthermore, patient had complete resolution of the herpes infection on follow-up EGD, indicating adequate treatment response.Figure 1.: Panel A: EGD showing circumferential antral erosive gastropathy Panel B: Histology showing multinucleated cells with classic ground glass nuclei Panel C: Post-treatment EGD showing complete resolution of gastric antral erosive gastropathy.

S2671 Upper Gastrointestinal Bleeding Due to Duodenal Ischemia: A Case Series

Introduction: Duodenal ischemia is a rare entity given dual blood supply from branches of the Celiac axis and Superior Mesenteric artery. However, it may present with clinically significant GI bleeding. We present three cases of duodenal ischemia diagnosed on EGD. Case Description/Methods: Case 1: An 84-year-old lady with heart failure presented with abdominal pain and melena. Vitals were BP 90/55, HR 112. She was cachectic with a mildly tender abdomen. Labs were notable for hemoglobin 6.6 g/dL from baseline of 8.2; BUN 65 mg/dL. CT abdomen noted bowel wall edema involving the duodenum. EGD revealed 5 duodenal ulcers with surrounding erythematous and friable mucosa consistent with ischemia (FigureA). She was discharged in stable condition on pantoprazole BID. Case 2: A 63-year-old lady presented with chest pain and was diagnosed with an inferior STEMI. On presentation vitals were BP 76/50 mmHg and HR 43 bpm. Cardiac catheterization was performed with two drug-eluting stents placed in the right coronary artery. Patient was started on aspirin and clopidogrel and developed melena 3 days later. Hemoglobin dripped from 12.4 to 8.4 g/dL. EGD noted pallor of the gastric body with areas of patchy erythema and erosions within the antrum, in addition to several clean based ulcers with erythema within the duodenal bulb through the second portion (FigureB). Admission CT abdomen showed moderate celiac narrowing. Patient was continued on pantoprazole BID and did not have further bleeding episodes prior to discharge. Case 3: A 63-year-old man with ESRD was admitted with endocarditis, MSSA bacteremia and embolic strokes. On day 9, he suffered PEA arrest and was resuscitated. He subsequently developed melena and shock. Hemoglobin dropped from 9.8 g/dL to 6.6 g/dL. Urgent EGD revealed a diffusely hemorrhagic stomach and the duodenum was noted to have spotty areas of necrosis, erosions and ulcerations within the bulb and second portion ( FigureC). CTA revealed moderate to severe stenosis in the proximal SMA and celiac axis. The patient was transitioned to comfort measures after suffering recurrent embolic strokes during admission. Discussion: Clinicians should maintain a high index of suspicion for duodenal ischemia in patients presenting with upper GI bleeding in the setting of a low-flow state, as illustrated in the above three cases. Management is typically supportive; however prognosis may be poor reflecting patients’ systemic illnesses leading to the process.Figure 1.: Endoscopic images demonstrating duodenal ischemia.

S2175 Now You See Me, Now You Don’t: A Case of Campylobacter Jejuni Colitis Presenting as a Colonic Mass

Introduction: Campylobacter jejuni is responsible for 3-6% of diarrheal illnesses in the United States. Inoculation follows ingestion of a contaminated source such as poultry, unpasteurized milk, or drinking water. The presentation of a C. jejuni infection may radiographically and endoscopically mimic other pathologies such as colonic malignancy and inflammatory bowel disease (IBD). Case Description/Methods: A 66-year-old man with a past medical history of prostate cancer in remission and a 6mm colonic polyp removed 5 years prior presented to the emergency department with 5 days of watery diarrhea. He complained of 6 watery bowel movements per day associated with colicky abdominal pain and bloating. He was hemodynamically stable with a physical exam notable for severe tenderness in the right lower quadrant. Serum chemistries did not reveal any abnormalities. Computed tomography revealed severe, focal bowel wall thickening in the ascending colon and a 1.7cm hypodense lesion in the right hepatic lobe which was confirmed on magnetic resonance of the abdomen. The radiologist’s interpretation emphasized concern for colonic malignancy with metastasis to the liver (Figure). Endoscopic evaluation revealed diffusely erythematous, granular and ulcerated mucosa throughout the colon with concern for infectious vs inflammatory colitis. Histologic evaluation of ascending colonic mucosal biopsy revealed moderately active chronic colitis with extensive cryptitis and crypt abscesses. Stool polymerase chain reaction was notable for C. jejuni infection and the patient achieved clinical and endoscopic remission without antimicrobial therapy. Discussion: In patients with C. jejuni enterocolitis, radiographic imaging may reveal signs of bowel wall edema or ulcerations which may resemble colonic malignancy or IBD. Endoscopic findings of campylobacter enterocolitis are non-specific, however, may reveal edematous, erythematous, and friable mucosa which may be associated with hemorrhage. Inflamed mucosa can be either isolated or discontinuous. Colonic ulcers may present as either aphthous or linear (may resemble cobblestoning as seen in Crohn's Disease). Histologic evaluation can reveal cryptitis and crypt abscess formation similar to findings of ulcerative colitis. This case highlights the range of radiographic and endoscopic presentations of C. jejuni Colitis. Infectious colitis should remain on the differential for radiographic evidence of colonic edema in the right clinical setting.Figure 1.: A and B: CT Abdomen/Pelvis showing ascending colon wall thickening resembling mass; C: CT of Hypoechoic liver mass; D: T2-weighted MRI Abdomen of ascending colon wall thickening resembling a mass; E: Colonoscopy image revealing inflamed mucosa of ascending colon; F: Ulcerated mucosa of the sigmoid colon.

S2050 Inferior Mesenteric Arteriovenous Fistula Treated with Embolization

Introduction: Inferior mesenteric arteriovenous fistulous malformations are a rare yet reversible cause of ischemic colitis. They can cause increased outflow of blood in the venous circulation and predispose to colon ischemia. We report a case of inferior mesenteric arteriovenous fistula causing ischemic colitis in an atypical distribution in the IMA territory. Case Description/Methods: A 50-year-old gentleman presented to the emergency room with a 3-week history of abdominal pain and bloody diarrhea. His symptoms started with a dull pain, 8/10 in intensity, with radiation to his lower back. He had also been having a low appetite for the duration of his abdominal pain. He described having around 10 bowel movements daily with blood mixed with mucus. CT abdomen showed diffuse circumferential thickening involving the entire sigmoid colon, extending to the upper rectum suggesting non-specific colitis. He came to the hospital 2 weeks prior to his presentation and underwent a colonoscopy which grossly showed diffuse severe inflammation in the distal descending colon, sigmoid colon and proximal rectum, till 30 cm from the anal verge suggesting left-sided colitis. Biopsied from the region showed evidence of ischemic colitis. His CT-angiography showed engorgement of the IMA and IMV, with an early contrast in IMV which suggested IMA to IMV AV fistula within the left hemipelvis. That suggested vascular malformation as the cause of the colorectal findings. Patient subsequently underwent embolization of 2 branches of IMA with stent placement in IMA, causing closure of the AV fistula. Patient tolerated the procedure without any complication (Figure). Discussion: Ischemic colitis is most commonly seen in the watershed areas of the colon such as splenic flexure and rectosigmoid junction due to arterial anastomosis between the mesenteric arteries supplying the colon. In these situations, the colonic involvement is focal involves these specific segments. In this case, patient had diffuse gross ischemic findings from the distal rectum extending to descending colon involving the whole part of ischemic artery supply which is atypical for the distribution of colonic ischemia. In such situations, CT angiography comes as a diagnostic tool for identifying the pathology and in this situation it showed AV fistula between IMA and IMV which hampered the colonic blood supply to the extent to cause ischemic colitis with symptoms.Figure 1.: a. Early filling of dilated mesenteric veins (bottom arrow) with adjacent bowel wall edema due to venous congestion (top arrow) b & c. inferior mesenteric artery (arrows) adjacent to ill-defined area of contrast (dashed arrow) thought to represent arterio-venous fistula d. view from sigmoidoscopy showing ischemic colitis in the sigmoid colon.

P38 The gut that leaks

Introduction/BackgroundSystemic lupus erythematosus is a chronic inflammatory autoimmune disease which can affect multiple organ systems. Symptoms of intestinal involvement in SLE may vary from common and non-specific such as heartburn, oral ulcers and dysphagia to less common but more serious including abdominal pain due to serositis and intestinal vasculitis.Description/MethodA 20 year old girl was referred to the gastroenterology team for the management of ascites. Her past medical history included SLE diagnosed aged 10, class IV lupus nephritis, autoimmune haemolytic anaemia secondary to SLE, Haemoglobin H, gastrostomy feeding due to poor growth.At the time of the transition from paediatric to adult service her SLE was under good control. She was on Prednisolone 6 mg on alternate days, Mycophenolate (MMF) 750 mg BD, Septrin 240 mg OD and Enalapril 2.5 mg OD. After the transition, MMF was reduced to 500 mg OD. The rest were unchanged. Serum total protein was 57 (60-80), serum albumin 32 (35-50). Weight was 41.2 kg.Ten months after the transition, she presented with bilateral leg swelling and subsequently tense ascites over 3 weeks. Serum total protein reduced to 31, albumin 13.24 hour urine total protein was 0.15 (0-0.1), urine volume 1.7 L. Serum creatinine 20 µmol/L and eGFR >90. Urine PCR was 16 mg/mmol.Total protein in ascites drain fluid was <20 g/L, albumin <10 g/L, glucose 5.7 mol/L. There were no malignant cells and no growth on enrichment culture.She was referred to the dietitians who advised that her oral intake was adequate.There was no evidence of heart failure on echocardiogram.Small bowel meal showed oedematous bowel wall but no abnormalities in terminal ileum. Coeliac serology was negative.CT abdomen and pelvis showed normal appearances to the liver, hepatic and portal veins; no features of Budd-Chiari syndrome; normal size kidneys; incidental finding of non-occlusive right internal jugular thrombus and moderate lymphadenopathy in mesenteric and retroperitoneal regions.She developed swelling in the right calf. Doppler ultrasound confirmed major DVT with occlusive thrombus extending to distal superficial femoral veins. Clots in inferior vena cava and portal veins were excluded.Discussion/ResultsDuodenal biopsy confirmed villous oedema and dilated lymphatics consistent with changes seen in protein losing enteropathy. She was referred to Rheumatology. Prednisolone was increased to 15 mg. The response was rapid with reduction in ascites. MMF was increased to maximum tolerable dose 750 mg AM and 500 mg PM.Hb had been persistently low around 50 during this illness. She had longstanding hypocomplementaemia. C3 dropped to 0.37 (baseline 0.6). C4 remained low around 0.04. IgG was 5.9 (baseline >7). Serology showed DsDNA was 5 (normal range 0-15), positive ANA, trace positive RNP and negative Rheumatoid factor and APL antibodies. CRP was 10.Abdominal lymphadenopathy was felt to be due reactive changes due to active lupus.With increased steroids and immunosuppressants, she improved significantly both clinically and biochemically within a few weeks. Hb rose to over 90, serum albumin > 25 and serum protein above 50 by the end of 3 months after treatment escalation.Warfarin was stopped upon completion of 6 month anticoagulation.On repeat CT, previous abdominal lymphadenopathy had resolved completely. Splenomegaly measuring 17.6 cm was noted. This was discussed in haematology MDT and thought to be due to the haemoglobinopathy and haemolysis.Haemolysis continued to be a challenge. She remained on relatively high dose steroids varying between 20 mg and 10 mg over the years. Vitamin D was prescribed. Weight was very low but stable just above 38 kg.Protein Losing Enteropathy (PLE) is rare but recognised in SLE. It typically occurs in young women with clinically severe disease with multi organ involvement. Clinical presentation is characterised by the onset of profound oedema, hypoalbuminaemia in the absence of nephrotic range proteinuria. Severe diarrhoea is present in 50% of the patients. It is important to investigate and exclude other causes of hypoalbuminaemia (e.g cardiac failure, liver diseases, malnutrition) and PLE.Key learning points/ConclusionPLE can be the initial manifestation of SLE.Lupus nephritis and PLE can be present successively or simultaneously in a lupus patient.Stringent diagnostic evaluation is required to exclude other mimicking conditions.Multidisciplinary team involvement is crucial in the management of patients with multi-organ involvement.PLE associated with SLE usually responds well to corticosteroids. However additional immunosuppressant(s) are generally required to treat other SLE symptoms as well as to help with the steroid reduction regime.As well as treating the underlying disease, advice from dietitians is important to improve and maximise the nutritional status of these patients.A clinically significant hyper-coagulable state is reportedly attributed to PLE associated with SLE. Therefore, VTE prophylaxis especially in hospitalised patients is recommended. Moreover, clinicians should have high index of suspicion for VTE in these patients with multiple risk factors to arrange early appropriate investigations and treatment plan.

P33 The successful use of Belimumab in recurrent small bowel obstruction secondary to Lupus Enteritis

P33 The successful use of Belimumab in recurrent small bowel obstruction secondary to Lupus Enteritis

P30 A case of small bowel and leukocytoclastic vasculitis associated with acitretin therapy

Introduction/BackgroundAcitretin is an oral retinoid that is used to treat a number of skin conditions including acne. It is generally well tolerated and common side-effects such as gastrointestinal upset, mucosal and skin reactions are usually mild. However, we present what we believe to be the first reported case of small bowel and leukocytoclastic vasculitis (LCV) caused by acitretin and this required prompt treatment with intravenous glucocorticoids and cyclophosphamide to induce remission.Description/MethodA 53-year-old caucasian male presented to the Emergency Department with severe bilateral foot pain for four days and a purpuric rash which initially affected the soles of his feet and spread to affect all four limbs, both hands and abdomen. He was three weeks into his second course of acitretin 20mg daily for a flare of psoriasis, having ceased treatment three months before due to a suspected iatrogenic rosacea type reaction. He had generalised abdominal pain and recent constipation. Observations demonstrated a sinus tachycardia at 130 beats per minute only and examination revealed widespread patchy non-blanching palpable purpura and deep ulcers over the soles of both feet. There was mild abdominal distension and global tenderness but no peritonism. The remainder of the physical examination was unremarkable. Initial blood tests showed: haemoglobin 156 g/L, white cell count 13 x 109/L (neutrophilia: 10.6 x 109/L), platelets 514 x 109/L, CRP 123 mg/L, ESR 12 mm/hr, normal renal and liver function. Detailed immunology, microbiology and viral screens were negative including anti-neutrophil cytoplasmic antibodies (ANCA) and cryoglobulins. Urine dipstick was unremarkable. Abdominal x-ray showed distended small bowel loops and CT demonstrated significant intestinal wall oedema suggestive of small bowel vasculitis. Skin biopsy demonstrated typical changes of leukocytoclastic vasculitis. After surgical review he was managed conservatively on the high dependency unit with intravenous methylprednisolone 1g daily for three days followed by intravenous hydrocortisone and one dose of cyclophosphamide (15mg/kg). Total parenteral nutrition was initiated, and his bowel symptoms settled after two weeks. His skin significantly improved and he was discharged after four weeks’ inpatient stay. Actretin was stopped indefinitely, and he has remained in remission over three years later. Prednisolone was successfully tapered at a slow rate, and no further cyclophosphamide was required. His psoriasis is currently managed well with oral methotrexate.Discussion/ResultsLCV is a small vessel vasculitis which mostly occurs in the cutaneous form but can be life-threatening with systemic involvement. Around 50% of cases are idiopathic, with infections (15-20%), autoimmune diseases (15-20%) and malignancy (<5%) being well-recognised causes.Drug-induced LCV accounts for nearly 15% of cases and antibiotics, non-steroidal anti-inflammatories, anti-epileptics and TNF-alpha blockers are well-known precipitants. It usually occurs within three weeks after commencement of the medication, and the timing of re-introduction of acitretin in our patient makes it likely to be the cause. Up to 90% of LCV cases resolve within weeks to months after addressing the precipitating cause, with or without oral steroids. However, a 2% mortality is reported, likely due to systemic involvement and given the severity of our patient’s presentation, it was decided to commence immunosuppression in view of the skin biopsy and CT findings. (A biopsy of the small bowel was considered but would have delayed treatment).To our knowledge there are no published case reports linking LCV and small bowel vasculitis to acitretin therapy. However, there have been several case reports of LCV and other vasculitides caused by all-trans-retinoic acid (ATRA) and isotretinoin (first generation retinoids). Yamada et al. (1999) reported a severe case of haemonecrosis of the ileum, as a complication of ATRA treatment for acute promyelocytic leukaemia. Surgical intervention was required and histology demonstrated LCV.Isotretinoin was attributed to cause 5 out of 11 LCV cases reviewed by Dwyer et al. (1989). Turan et al. (2012) reported a case of a Henoch-Schonlein Purpura secondary to isotretinoin that improved with discontinuing treatment and three weeks of fluocortolone 20mg daily. More recently, a case of diffuse alveolar haemorrhage due to isotretinoin-induced granulomatosis with polyangiitis was described by Assuncao et al. (2018), which remitted with intravenous methylprednisolone and cyclophosphamide.Key learning points/ConclusionAlthough very rare, consider retinoids including acitretin in cases of drug-induced LCV and small bowel vasculitis.Symptoms usually improve on cessation of the treatment alone, but immunosuppression might be required for more severe cases.Future case series could help guide treatment choices.

OA19 A case of severe refractory lupus enteritis and nephritis that remitted with Obinutuzumab

Introduction/BackgroundSystemic lupus erythematosus (SLE) is an autoimmune disease that can affect almost any organ system but gastrointestinal (GI) involvement is very rare. Obinutuzumab is a humanised type II anti-CD20 monoclonal antibody that is licensed to treat haematological malignancies. It has been used in a small number of SLE patients with secondary non-depletion non-response (2NDNR) to Rituximab and appears to be effective in lupus nephritis (LN) as outlined in the NOBILITY trial. We present a case of refractory lupus enteritis (LEn) and LN in a patient with 2NDNR to repeated Rituximab cycles that achieved remission with Obinutuzumab.Description/MethodA 19-year-old African woman was diagnosed with SLE in 2018 after presenting with polyarthritis without systemic involvement. Blood tests showed leucopenia, positive antinuclear antibody, anti-double-stranded DNA >200 IU/ml and hypocomplementaemia. Prednisolone and Methotrexate were commenced. However, one month later she presented to hospital with generalised abdominal pain, vomiting and diarrhoea. CT abdomen demonstrated significant small bowel wall thickening with mucosal hyperenhancement. Multidisciplinary team (MDT) input confirmed likely LEn. She was treated successfully with intravenous Methylprednisolone and Rituximab. Total parenteral nutrition was required for two weeks.Unfortunately, four further hospital admissions followed over the next six months due to GI symptoms, transient acute kidney injury and moderate proteinuria. Small bowel oedema persisted on MRI, three months after the CT. Renal biopsy demonstrated class 2 LN. Intravenous methylprednisolone helped and further Rituximab was given but she had infusion reactions. Six months later she re-presented with abdominal pain, synovitis and had nephrotic range proteinuria. She was treated again for LEn after gastroenterology input. Further Rituximab was given (MabThera instead of Truxima) but reactions still occurred and her B cells were non-deplete. Repeat renal biopsy confirmed class 4 LN and intravenous Cyclophosphamide (Euro-Lupus regimen) was commenced. This was repeated seven months later due to persisting high disease activity and proteinuria despite a short trial of intravenous Belimumab. However, she was admitted to hospital with colitis on CT after completing the second course of Cyclophosphamide. MDT decision was to treat with Obinutuzumab. Since commencing treatment eighteen months ago, her SLE has dramatically improved and she feels well for the first time. SLEDAI-2K score is 2 (16 pre-treatment), renal function has recovered with mild proteinuria. Anti-double-stranded DNA has reduced from >200 to 52.9 IU/ml and complements normalised. She remains on Prednisolone 5mg daily and Tacrolimus and a third maintenance dose of Obinutuzumab is planned.Discussion/ResultsLEn has been reported in only 0.2-5.8% of SLE cases. It is defined by the British Isles Lupus Assessment Group (BILAG 2004) by either vasculitis or inflammation of the small bowel supported by imaging or histology. Its pathogenesis is poorly understood but thought to be related to immune complex deposition and complement activation resulting in intestinal capillary leak and submucosal oedema. Symptoms are non-specific and a review by Janssens et al. (2013) suggested abdominal pain (97%), ascites (78%), nausea (49%), vomiting (42%) and diarrhoea (32%) were the most common symptoms in patients with LEn. They reported the ileum and jejunum were most commonly affected in LE (84% and 83% respectively), followed by colon (19%), duodenum (17%) and rectum (4%).Abdominal CT is considered to be the first line investigation and ‘classic’ radiological findings are bowel wall oedema (“target sign”), engorgement/increased number of mesenteric vessels (“comb sign”) and increased attenuation of the mesenteric fat (Ha et al. 2000, and Kim et al. 2006). These were all demonstrated on our patient’s initial CT abdomen which showed engorgement of the mesenteric vessels from the proximal jejunum to the proximal ileum.LEn seldom occurs in isolation and usually presents in the context of high disease activity and other systemic involvement. It is often responsive to glucocorticoids and bowel rest but further immunosuppression with Cyclophosphamide or Rituximab might be warranted in refractory cases as in our patient’s case.Obinutuzumab has been shown to be safe, effective and steroid-sparing in renal and non-renal SLE patients with 2NDNR to Rituximab from a case series of 9 patients by Arnold et al. (2022). This applied to LN in our patient and we believe this to be the first case where refractory LEn was treated successfully with Obinutuzumab.Key learning points/ConclusionAlthough very rare, have a high index of suspicion of LEn in SLE patients who present with GI symptoms and typical radiological findings.LEn often occurs with other systemic manifestations including LN and it is important to assess for these at the time of diagnosis of LEn.Obinutuzumab is an emerging treatment for severe SLE particularly 2NDNR to Rituximab and can improve both LN and LEn. We eagerly await results from the current REGENCY and ALLEGORY clinical trials which are assessing Obinutuzumab in renal and non-renal SLE patients respectively.

Early diagnostic markers in predicting the severity of dengue disease

The aim of the present study was to determine whether the serum ferritin, the biomarker of an acute phase reactant and the gall bladder wall edema, an early indicator of capillary leakage can predict the severity of dengue fever. This study included 131 patients, who were between the age group of 18–80 years. The patients presented to our department with an acute illness, within the first four days of high temperature. The statistical analysis of this study was performed by using the Chi-square and independent Student’s t tests. The diagnostic markers are considered statistically significant, if the serum ferritin level is higher than 500 ng/ml and the gall bladder wall thickness is more than 3 mm. The present study observed that, 39 patients (89%) who had severe dengue (n = 44) revealed a significant gall bladder wall thickening, and this correlation was significant statistically (p < 0.000). It was also observed that, the ferritin levels have a highly significant positive correlation with the severity of dengue. The severe dengue patients had a mean ferritin level of 9125.34 μg/l, whereas the non-severe group had 4271 μg/l. This comparison was also statistically significant, as the p value was 0.003. We report that the serum ferritin levels have a highly significant positive correlation with the severity of dengue. The gall bladder wall edema during the third and fourth day of the illness was also associated with severe dengue. However, diffuse gall bladder wall thickening and high serum ferritin levels are also reported in various other conditions and their exact cause have to be determined by the correlation of associated clinical findings and imaging features.

Role Of Ultrasound For The Diagnosis Of Complications Of Dengue Fever In Gujrat

Background : The purpose of this study is to evaluate if ultrasonography may be used as an useful addition to clinical and radiology profiles in diagnosing dengue fever and predicting virus severity by comparing imaging findings. The difference in sonographic characteristics observed in patients of various ages was also investigated. &#x0D; Objective : The goal of this study is to determine role of ultrasound for diagnosis of complications of dengue fever in Gujrat &#x0D; Materials and Methods: This is a retrospective study. From October and December 2021, 79 patients who were serologically confirmed with dengue fever were referred for ultrasound scanning of the abdomen at Aziz bhatti shaheed hospital Gujrat, and the imaging data were evaluated. The statistical kit for social science (spss) is used for data analysis.&#x0D; Results: out of 76 positive dengue patients there are 71(89.9%) male and 8(10%) are female .48 (60.8%) patients showed splenomegaly, 24(30%) patients showed ascites in which 8 (10%) have pelvic ascites and 16 (20.3%) abdominal ascites, 63 (79.7%) patients showed edematous GB wall thickening, 21(26.6%) showed pleural effusion while 18 (22.8 %) have bilateral pleural effusion and 3 (3.8%) have right sided. &#x0D; Conclusion: In patients presenting with fever and concomitant symptoms, sonographic signs of thickening GB wall, pleural effusion (bilateral or right side), ascites, and splenomegaly should strongly help in early diagnosis of dengue fever, especially during an outbreak. &#x0D;

P9.54: Graft Versus Host Disease Following Liver Transplantation: A Serious Complication

Introduction: Graft-versus-host-disease (GVHD) after liver transplantation (LT) is a severe complication with high mortality rate (85%). Risk factors, diagnosis and management is challenging. Donor T-lymphocytes play a main role in the immunological attack against the host. We report a case and a comprehensive review of the literature. Around 160 patients are reported in literature with an estimated incidence of 0.5 to 2% of liver transplant. Liver transplantation from hepatocellular carcinoma (HCC) and alcoholic liver disease seems to be the main prevalent diagnosis of patients who developed GVHD. Method: We present a 62-years old male patient with hepatitis C-virus (HCV) cirrhosis and successfully downstaged to Milan criteria HCC. Orthotopic liver transplantation was performed after 6 months of surveillance and discharged uneventfully after 7 days. One month later patient developed abdominal cramps, diarrhea and cutaneous erythema. Mild leukopenia with normal liver and renal function, blood and stool samples were negative, clostridium and other pathogens were also ruled out. Abdominal CT-scan showed moderate distal ileum and colon wall edema. At colonoscopy stellate ulcers was found, biopsy was taken as well to skin lesions. Colon biopsy showed acute inflammation with severe mucosal damage and apoptosis. Skin biopsy showed interphase vacuolar dermatitis. GVHD was suspected and donor lymphocyte chimerism was positive with 5%.Results: Methylprednisolone was initiated then anti-thymocyte globulin and adalimumab were added. Bacterial, viral and fungal prophylaxis were given. The patient recovered and discharged in good conditions. Five months later the patient developed acute severe pneumonia with extensive lung necrosis that required mechanical ventilation but progressed to refractory respiratory distress and the patient died after 6 months following liver transplantation. Conclusion: This is the first GVHD case after liver transplantation reported in Mexico. The diagnosis requires a high level of clinical suspicion. There is no strong consensus about the best management, but literature agrees that steroids, IL-2 antibodies, alpha-tumor necrosis factor inhibitors and antibiotics for opportunistic pathogens must be considered.

Look Out for Fever: Clinical Profile of Dengue in Young Adults in a Tertiary Care Center in North India.

Background Dengue fever (DF) is a common viral disease, clinical manifestations of which vary from influenza-like illness (DF) to life-threatening dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). The aim of this article was to study the clinical profile of DF in young adults. Material and Methods This was an observational study conducted in the department of medicine over a period of 2 years (January 1, 2013-December 31, 2014). Patients aged between 18 and 30 years with serology proven (nonstructural protein 1 [NS1]/dengue immunoglobulin M [IgM]) DF were included in this study. The clinical and laboratory data was recorded and analyzed. Results Out of 418 cases, the incidence of DF, DHF, and DSS was 87.32, 7.66, and 5.02%, respectively. The most common presentations were fever (99.76%) followed by vomiting (29.43%), pain abdomen (17.94%), myalgias (13.16%), petechial rash (12.92%), and bleeding (10.29%). Dengue NS1 and IgM antibodies were positive in 87.3% and 88.12% of the patients, respectively. Ascites, splenomegaly, hepatomegaly, pleural effusion, gall bladder wall edema, and pericardial effusion were present in 8.13, 6.94, 6.70, 5.98, 2.63, and 0.72% of the patients, respectively. Complications included bleeding (10.29%), acute respiratory distress syndrome (1.67%), myocarditis (1.44%), seizures (1.44%), hemarthrosis (0.24%), and encephalopathy (0.24%). The mortality rate was 3.35% with death of 14 patients. Shock, bleeding, and elevated serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase levels predicted adverse outcome. Conclusion DF can present with a plethora of clinical manifestations in endemic areas. Adverse outcome is more likely if patients have elevated SGOT levels, shock, and bleeding. Continuous seroepidemiological surveillance is essential to control outbreak and minimize morbidity and mortality.

A Protective Role of NOD2 on Oxazolone-induced Intestinal Inflammation Through IL-1β-mediated Signalling Pathway.

NOD2 has emerged as a critical player in the induction of both Th1 and Th2 responses for potentiation and polarisation of antigen-dependent immunity. Loss-of-function mutations in the NOD2-encoding gene and deregulation of its downstream signalling pathway have been linked to Crohn's disease. Although it is well documented that NOD2 is capable of sensing bacterial muramyl dipeptide, it remains counter-intuitive to link development of overt intestinal inflammation to a loss of bacterial-induced inflammatory response. We hypothesised that a T helper bias could also contribute to an autoimmune-like colitis different from inflammation that is fully fledged by Th1 type cells. An oedematous bowel wall with a mixed Th1/Th2 response was induced in mice by intrarectal instillation of the haptenating agent oxazolone. Survival and clinical scoring were evaluated. At several time points after instillation, colonic damage was assessed by macroscopic and microscopic observations. To evaluate the involvement of NOD2 in immunochemical phenomena, quantitative polymerase chain reaction [PCR] and flow cytometry analysis were performed. Bone marrow chimera experimentation allowed us to evaluate the role of haematopoietic/non-hematopoietic NOD2-expressing cells. Herein, we identified a key regulatory circuit whereby NOD2-mediated sensing of a muramyl dipeptide [MDP] by radio-resistant cells improves colitis with a mixed Th1/Th2 response that is induced by oxazolone. Genetic ablation of either Nod2 or Ripk2 precipitated oxazolone colitis that is predominantly linked to a lack of interferon-gamma. Bone marrow chimera experiments revealed that inactivation of Nod2 signalling in non-haematopoietic cells is causing a biased M1-M2 polarisation of macrophages and a decreased frequency of splenic regulatory T cells that correlates with an impaired activation of CD4 + T cells within mesenteric lymph nodes. Mechanistically, mice were protected from oxazolone-induced colitis upon administration of MDP in an interleukin-1- and interleukin-23-dependent manner. These findings indicate that Nod2 signalling may prevent pathological conversion of T helper cells for maintenance of tissue homeostasis.

CT features of confirmed and presumed gastric wall edema in dogs.

Postcontrast computed tomographic (CT) characteristics of gastrointestinal (GI) wall edema in humans have been described as GI wall thickening with a thickened submucosal layer and thin enhanced inner and outer layers. Published studies describing CT features of gastric wall edema in dogs are currently lacking. The aim of this retrospective, case series was to describe CT features of gastric wall edema in a group of dogs. Medical records were searched for dogs with postcontrast abdominal CT scans and a diagnosis of gastric wall edema based on histopathology (group I) or CT characteristics consistent with those reported in humans (group II). Clinical diagnosis, mean serum albumin concentration, and histopathological diagnosis were recorded. The following CT characteristics were recorded: numbers of wall layers, attenuation and contrast enhancement, presence of blood vessels, locations, distribution, and thickness. Twelve dogs (3 in group I and 9 in group II) were included. The most common clinical finding was hypoalbuminemia. In group I, a well-defined three-layer appearance with a non-enhancing fluid-attenuating middle layer was observed in three dogs and thin blood vessels in the middle layer in two dogs. In group II, nine dogs had a three-layer appearance with a non-enhancing fluid-attenuating middle layer. Locations of gastric wall thickening were diffuse in two, focal concentric in six, and focal asymmetric in four dogs. Findings supported including gastric wall edema as a differential diagnosis for dogs with hypoalbuminemia and CT characteristics of a three-layer appearance in the gastric wall, with a non-enhancing fluid-attenuating middle layer and thin blood vessels.

Ultrasonographic assessment of dengue fever and its correlation with platelet count

&lt;p&gt;&lt;em&gt;Background:&lt;/em&gt; Dengue virus infections are a significant threat to human populations particularly in the tropical and subtropical regions. This is mainly transmitted by Aedes aegypti mosquito from humans to humans. The main pathological mechanisms associated include thrombocytopenia, haemorrhagic diathesis with haemoconcentration. Ultrasonography is used because of its ability to detect plasma leakage signs and prediction of disease severity.&lt;/p&gt; &lt;p&gt;&lt;em&gt;Objective:&lt;/em&gt; To evaluate the usefulness of ultrasonographic findings of dengue fever and its correlation with platelet count.&lt;/p&gt; &lt;p&gt;&lt;em&gt;Methods:&lt;/em&gt; It was a prospective observational study, carried out in Bangladesh Medical College Hospital, Dhaka from May 2019 to August 2019. A total of 213 patients of suspected dengue fever during the epidemic were included in this study. All the cases were serologically diagnosed and evaluated with ultrasonographic findings. Platelet counts were estimated in all the cases and compared with findings recorded on ultrasonographic findings.&lt;/p&gt; &lt;p&gt;&lt;em&gt;Results:&lt;/em&gt; The mean age of the study population was 28.7 years. The male female ratio was 1.7:1. The common features on ultrasonography were thickened and oedematous gall bladder wall, mild to moderate ascites, pleural effusion (unilateral and bilateral), and hepatosplenomegaly. Thickened and oedematous gall bladder wall were observed in 68.8%, mild to moderate ascites 65.3%, bilateral pleural effusion 58.2 %, unilateral pleural effusion 40.4%, hepatomegaly 34.3 % and splenomegaly 13.6 % Platelet counts were significantly lower in abnormal ultrasonographic findings (&lt;em&gt;p&lt;/em&gt;=0.001).&lt;/p&gt; &lt;p&gt;&lt;em&gt;Conclusion:&lt;/em&gt; In a febrile patient with thrombocytopenia and positive dengue serology, ultrasonography of the abdomen is a useful tool to evaluate the severity of illness. Ultrasound findings of gall bladder wall oedema, ascites, and pleural effusion were correlated with the severity of thrombocytopenia. In epidemic scenarios, Ultrasonographic features may help in roughly estimating the platelet count even before serology and platelet results are available. Thus, it helps in treatment planning without waiting for the laboratory results.&lt;/p&gt; Bangladesh Med Res Counc Bull 2021; 47(1): 23-28