Diffuse Thickening Research Articles

Identification of Lupus Podocytopathy with Coexistent Glomerular Diseases – A Case Report

Abstract Introduction/Objective Lupus podocytopathy (LP), featured by nephrotic syndrome, is a unique subtype of lupus nephritis that mimics minimal change disease or primary focal segmental glomerulosclerosis (FSGS) on renal biopsy with diffuse podocyte foot process effacement and no capillary-loop immune deposits. LP usually presents on a background of ISN/RPS class I or class II lupus nephritis, and very rarely may present without immune deposits. Diagnosis of LP, when confounded by other glomerular diseases associated with nephrotic syndrome, can be very challenging and requires thorough clinical and pathology correlations. Methods Here we report a case of LP in a patient with nephrotic syndrome and multiple comorbidities affecting kidneys. A 24-year-old female with type-I diabetes, psoriasis, and intermittent arthritis/rash of unknown etiology, presented with abrupt onset of nephrotic proteinuria attributed to recent low dose prednisone therapy, and renal insufficiency. A renal biopsy showed nodular glomerulosclerosis and FSGS. No immune deposits were identified by immunofluorescence or electron microscopy. Ultrastructurally there was also diffuse glomerular basement membrane thickening and over 90% podocyte foot process effacement. With no established systemic lupus erythematosus (SLE), the case was initially diagnosed as diabetic nephropathy with coexistent FSGS as the etiologies for nephrotic proteinuria, and the patient was put on ACEI and diuretics. However, massive proteinuria persisted, and the patient also developed pancytopenia. Serology concurrent with the biopsy came out later showing positive autoantibodies against dsDNA, Smith, and Histone. With continued worsening of creatinine, a renal biopsy was repeated revealing essentially similar findings to the first biopsy. Results Integrating the serology results and clinical presentation, SLE was favored. The pathology findings were re- evaluated and considered to be most consistent with LP and coexistent diabetic nephropathy, with FSGS either a component of LP or an independent lesion secondary to diabetes or hypertension. The patient was started with high dose prednisone at 60 mg/day. One month later, her proteinuria, serum creatinine, pancytopenia, skin rash, and arthritis were all significantly improved. Conclusion LP can be easily masked by coexistent glomerular diseases. Sufficient awareness of the entity is necessary for the appropriate diagnosis and treatment.

Imaging-based algorithmic approach to gallbladder wall thickening.

Gallbladder (GB) wall thickening is a frequent finding caused by a spectrum of conditions. It is observed in many extracholecystic as well as intrinsic GB conditions. GB wall thickening can either be diffuse or focal. Diffuse wall thickening is a secondary occurrence in both extrinsic and intrinsic pathologies of GB, whereas, focal wall thickening is mostly associated with intrinsic GB pathologies. In the absence of specific clinical features, accurate etiological diagnosis can be challenging. The survival rate in GB carcinoma (GBC) can be improved if it is diagnosed at an early stage, especially when the tumor is confined to the wall. The pattern of wall thickening in GBC is often confused with benign diseases, especially chronic cholecystitis, xanthogranulomatous cholecystitis, and adenomyomatosis. Early recognition and differentiation of these conditions can improve the prognosis. In this minireview, the authors describe the patterns of abnormalities on various imaging modalities (conventional as well as advanced) for the diagnosis of GB wall thickening. This paper also illustrates an algorithmic approach for the etiological diagnosis of GB wall thickening and suggests a formatted reporting for GB wall abnormalities.

DIAGNOSIS OF UROCYSTITIS IN A DOMESTIC CAT (CLINICAL CASE)

Urocystitis, as a nosological unit, explains the inflammatory process of acute or chronic nature in the bladder and urethra. This disease is quite common among cats kept indoors.
 Early diagnosis of urocystitis, in particular differential, is difficult and should be comprehensive, and include: collection of medical history, clinical examination of a sick animal, laboratory examination of urine, ultrasound (ultrasound diagnosis) of the urinary system. The article presents a clinical case from the veterinary practice of diagnosing urocystitis in a domestic cat. The research was conducted according to generally accepted methods, using special equipment. Catheterization of the bladder was performed to select urine. Changes in the clinical condition characterized by oppression of the animal, pale mucous membranes, anorexia, dysuria, forced posture of the animal, hematuria. Urination in a sick animal is frequent and difficult, or no, hyperemia of the penis, there is pain on palpation of the bladder. In the urine of animals with urocystitis revealed a decrease in relative density to 1.017 g / m3 and an increase in pH to 6.6. Epithelial cells of the bladder, leukocytes (up to 10 cells in the field of view) and a significant number of erythrocytes were registered in the sediment. Biochemical examination diagnosed elevated urea content, which corresponded to 18.8 mmol / l and creatinine - 158.1 μmol / l, respectively. The results of ultrasonographic examination of the urinary system in a sick animal are highlighted. Changes in the size of the bladder due to significant filling of urine, diffuse thickening of its walls and the presence of sediment in the form of flakes, which is easily moved and visualized sharply echopositively.
 Diagnostic tests and their analysis confirmed the diagnosis of urocystitis in a domestic cat.

Clinicopathological characteristics, diagnosis, and treatment of 29 cases of signet ring cell carcinoma of the rectum and sigmoid colon

Objective: To investigate the clinicopathological characteristics and the therapeutic effects of signet ring cell carcinoma (SRCC) of rectum and sigmoid colon. Methods: Clinical data and the follow-up information of 29 SRCC patients treated in our tertiary care center from 2008 to 2018 were retrospectively reviewed. The clinicopathological features, diagnostic and therapeutic effects, and the prognostic outcomes were analyzed. Results: Among the 29 patients, 17 were male, 12 were female. The average age was (48.7±14.3) years. Colonoscopy revealed the features of diffuse circumferential thickening of the bowel wall in 20/29 cases (69.0%), while in 9/29 cases (31.0%), endoscopic biopsies showed false negative results. Twenty-five% (4/16) and 17.6% (3/17) lesions were misdiagnosed as the inflammatory changes by endoscopic rectal ultrasonography exam and rectal MRI scan, respectively. Thirteen of the 29 patients received the neoadjuvant chemoradiotherapy (NCRT), 27 patients underwent the radical resection surgeries, and 8 underwent the postoperative radiotherapy. With a median follow-up of 38.5 (3.5-87.0) months, the cumulative 3-years overall survival (OS) rate was 54.0%, and the cumulative 3-years disease-free survival (DFS) rate was 43.0%. The OS rates of patients treated with or without NCRT (non-NCRT) were 46.2% and 69.2%, respectively, without significant difference (P>0.05). The DFS rates of patients treated with or without NCRT were 45.8% and 39.2%, respectively, without significant difference (P>0.05). Parameters including age younger than 40 years and tumor size larger than 5 cm were independent potential risk factors for shortened OS (P<0.05). Conclusions: SRCC of the rectum and sigmoid colon is a rare malignant tumor with special clinical manifestations. It is younger-onset, highly malignant and with very poor prognosis. Therefore, in-depth researches with focus upon the progress of molecular oncology are urgently needed to substantially improve the therapeutic effect of this disease.

Male genital tract tuberculosis: Acomprehensive review of imaging findings and differential diagnosis.

Urogenital tuberculosis is the most common form of extrapulmonary tuberculosis. Genital organ involvement occurs as a continuum of urinary tract tuberculosis and often presents a diagnostic challenge due to the non-specific nature of the symptoms. Delay in diagnosis may lead to complications such as infertility and perineoscrotal sinuses. Imaging plays an important role in raising timely suspicion of tuberculosis. In this article, we describe the imaging findings of male genital tuberculosis and the differential diagnosis. High-resolution ultrasonography (HRUS) is the best modality for assessing the epididymis, testis, scrotum and vas deferens, whereas MRI is optimal for evaluating the prostate, seminal vesicles and ejaculatory ducts. Epididymis is the most common site of genital tuberculosis, and presents as a nodular lesion limited to the tail or as diffuse enlargement. The proximal vas deferens is also frequently involved due to anatomical contiguity and shows diffuse or nodular thickening. Advanced cases may show pyocele formation and scrotal wall sinuses. Testicular involvement is almost always secondary to epididymal tuberculosis and presents as single or multiple nodules, diffuse enlargement, or the 'miliary' pattern. Isolated testicular involvement should raise suspicion of malignancy. Tuberculosis of the prostate is often asymptomatic. The most common imaging manifestations are nodules and the diffuse forms, which may later evolve into abscesses. Fibrosis and calcification occur with healing. Seminal vesicle and ejaculatory duct involvement with fibrosis may cause infertility. Awareness of the imaging findings would enable the radiologist to raise timely suspicion, so that prompt treatment is initiated and complications are prevented.

Diffuse Hemorrhagic Enterocolitis in the Setting of 2019 Coronavirus

A 47-year-old woman with diabetes diagnosed with COVID-19 was transferred to our institution for extracorporeal membrane oxygenation therapy. Gastroenterology was consulted because of worsening diarrhea, which started before transfer, and new hematochezia after extracorporeal membrane oxygenation was discontinued. Contrast-enhanced computed tomography demonstrated diffuse small and large bowel wall thickening and edema (Figure A, arrows), resulting in ribbon-like bowel. Upper endoscopy and colonoscopy were pursued. Atrophic and friable gastric and duodenal mucosa was found. Diffuse congested, friable, and hemorrhagic mucosa (Figure B) was seen throughout the colon and terminal ileum. Biopsies from the ileum and colon (Figure C) showed complete loss of glandular epithelium without associated increase in lamina propria inflammation despite the degree of epithelial damage. Supportive management was pursued. Extracorporeal membrane oxygenation is associated with immune system activation, leading to a systemic inflammatory response and a procoagulant state that can ultimately cause organ injury, such as ischemic colitis. COVID-19 has demonstrated a wide range of gastrointestinal manifestations. We present a case of diffuse hemorrhagic enterocolitis with endoscopic biopsies showing diffuse mucosal damage with relative lack of inflammatory response. This histologic pattern of injury resembles immunosuppressed states and apoptosis-mediated processes. Based on timeline and findings, the gastrointestinal tract injury is likely related to severe COVID-19.

S2797 First Case of Isolated Angioedema of the Bowel Caused by Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

INTRODUCTION: Visceral angioedema (VA) has been widely reported as a side-effect of angiotensin-converting enzyme inhibitors (ACEI). We report the first case of VA from NSAIDs. CASE DESCRIPTION/METHODS: An 80 y/o F with history of multiple abdominal surgeries, hypertension on lisinopril, and lumbago on aspirin 325 mg twice daily presented with acute epigastric pain, nausea, and vomiting. A CT scan showed moderate thickening and dilation of the distal small bowel (SB), without transition point. Symptoms resolved within days with supportive measures. One month later, while asymptomatic, a non-contrast MRI for pancreatic cyst surveillance showed normal SB. Two weeks after the MRI, her abdominal symptoms recurred. CT scan revealed multiple dilated, edematous fluid-filled stretches of SB, without transition point. Symptoms resolved spontaneously within days. Two months later, symptoms returned, with CT showing similar edema in the colon wall (Figure 1). Due to sharp angulations from edematous bowel, only a gastroscope could traverse the colon, with normal appearance of mucosa from the anus to the hepatic flexure. No SB evaluation was attempted due to SB edema. She improved after conservative management. She discontinued her lisinopril. One month later, symptoms recurred, with CT scan showing worsened bowel wall edema from prior CT (Figure 2). Labs were unremarkable for serum complement C4, C1 esterase inhibitor functional assay, extended stool pathogen panel, complete blood count, monoclonal gammopathy screen, and serum cytomegalovirus DNA. Aspirin was stopped. Symptoms abated within 24 hours. Five weeks later, while asymptomatic, her CT showed normalization of bowel wall (Figure 3). In no episode did the patient experience constitutional symptoms, dermatologic changes, dyspnea/wheezing, diarrhea, melena, or hematochezia. She had no new exposure to medications, travel, or dietary changes. In all cases where intravenous contrast was used, splanchnic vessels were patent. DISCUSSION: Episodic bowel obstructive symptoms associated with bowel thickening—and interval clinical improvement paralleling radiologic improvement of bowel thickening—illustrate the cadence of VA. As the VA occurred one month after stopping her ACEI, and symptoms resolved after stopping NSAIDs, it was likely triggered by her NSAID use. The shared pathogenesis and presentation of angioedema and enteropathy caused by NSAIDs provide a rationale for NSAID-induced VA. In patients without resolution of VA after stopping ACEI, NSAID cessation is the next step.Figure 1.: Computed tomography scan of the abdomen with intravenous contrast showed diffuse wall thickening of the descending and rectosigmoid colon. No transition point observed. Wall thickening, edema, and increased mucosal enhancement of multiple loops of the ileum and distal jejunum were observed, as well.Figure 2.: Computed tomography scan of the abdomen with intravenous contrast showed worsened evaluation compared to the previous scan. Diffuse wall thickening of the descending and rectosigmoid colon can be seen. No transition point can be seen. Wall thickening, edema, and increased mucosal enhancement of multiple loops of the ileum and distal jejunum were observed as well.Figure 3.: Five weeks after discontinuing her twice-daily aspirin, the patient underwent computed tomography scan with oral contrast (no intravenous contrast used), which showed interval resolution of the small bowel and colon wall thickening.

S2881 Lupus Enteritis as the Unique Manifestation of Lupus Flare - Report of 2 Cases

INTRODUCTION: Gastrointestinal (GI) symptoms are common in patients with systemic lupus erythematous (SLE) but real GI involvement is rare. Lupus enteritis refers to either vasculitis or inflammation of the bowel wall. It is present in 0.2–5.8% of patients usually in the context of high-SLE activity. The symptoms are nonspecific and can be life-threatening especially if the treatment is delayed. We present two cases of lupus enteritis as the sole manifestation of SLE flare. CASE DESCRIPTION/METHODS: Case 1. 19-year-old female with no prior SLE diagnosis was admitted with four months of persistent diarrhea, vomiting, and epigastric pain. Workup revealed Mg 0.5 mg/dl, K 2.5 mEq/l, Hb 11.2 g/dl, CRP 1.40 mg/dl, and subnephrotic proteinuria. Infectious workup was negative. CT scan showed diffuse thickening and enhancement of the small and large bowel wall. Upper and lower endoscopy with biopsy revealed nonspecific edema and chronic inflammation. Further evaluation showed low complement levels, positive ANA ( > 1:160), anti-dsDNA ( > 300 IU/ml), SSA, SSB, anti-histone Ab, and lupus anticoagulant. IV methylprednisolone was started with marked improvement, later transitioned to hydroxychloroquine, azathioprine, and prednisone with taper dose. Case 2. 49-year-old female, SLE diagnosed in 2017, no treatment for 2 years was admitted with one month of persistent vomiting and abdominal pain. Evaluated initially with upper and lower endoscopy which revealed Barret’s esophagus. Workup revealed Na 132 mEq/L, Mg 1.6 mg/dl, lymphopenia (200 k/uL), elevated CRP (0.67 mg/dl), and subnephrotic proteinuria. Negative infectious workup. Further evaluation showed ANA ( > 1:160), Anti Smith ( > 8), anti-dsDNA (4 IU/ml), SSA ( > 8), and low complement levels. CT scan with diffuse thickening and enhancement of the small bowel and entire colon and rectum. IV methylprednisolone and a short course of IV erythromycin was started with significant improvement; later transitioned to hydroxychloroquine, azathioprine, and prednisone with taper dose. Both patients did not present recurrence of symptoms during the next 3 months. DISCUSSION: Lupus enteritis is very rare as an unique feature of SLE flare. Current knowledge is scarce. CT scan is the test of choice. It usually responds to steroids. Steroid-sparing agents are required in severe-relapsing cases. Our cases highlight the difficult diagnosis of this disease. Identifying this condition is crucial to avoid complications as bowel necrosis or perforation.Figure 1.: Contrast enhanced abdomen CT scan coronal axial views revealed “target” sign that represent circumferential thickening of the intestine wall. In this case affecting both small and large intestine.Figure 2.: Contrast enhanced abdomen CT scan showing diffuse thickening of the small and large intestine wall. "Target" sign can also be appreciated here.

S2281 CMV Colitis Mimicking as IBD Flare-Up in Immunocompetent Patient

INTRODUCTION: Although almost 70 % of human beings are likely to be infected with CMV, the majority, being immunocompetent, are unlikely to manifest. Cytomegalovirus (CMV) colitis rarely occurs in immunocompetent patients. Usually, CMV colitis occurs in immunocompromised individuals but there have been reports in immunocompetent individuals as well. Here, we present a case of a 64 year old female initially presenting as IBD flare-up but later getting diagnosed with CMV colitis. CASE DESCRIPTION/METHODS: A 64-year-old woman, with a past medical history of HTN, type II diabetes, and GERD, IBD - Crohn's type on mesalamine, with recently done EGD and colonoscopy, presented to the hospital for abdominal pain and bloody stools for one month. When she came to the hospital, her WBCs were elevated, and she also had elevated lactate, ferritin but the rest of her labs were unremarkable. Subsequently, a CAT scan of Abdomen and Pelvis showed non-specific colitis. Gastroenterology service recommended starting the patient on Solu-Medrol for a possible Crohn’s Disease Flare Up. Other stool studies were negative. Over the course of her hospitalization, the patient underwent colonoscopy which showed severe inflammation and was also started on Infliximab due to unresponsiveness to treatment. Strongyloides serologies were checked and came back negative as well. The pathology results from colonoscopy came back and the findings were consistent with Cytomegalovirus (CMV) colitis. CMV IgG Ab checked came back positive and viral load came back at 7400 U/L. It was decided to treat the patient with Ganciclovir. The patient reported improvement and was able to tolerate her diet. She was subsequently discharged on valganciclovir. On subsequent follow up reported the resolution of her signs and symptoms. DISCUSSION: CMV colitis occurs in immunocompromised individuals but there have been reports in immunocompetent individuals as well. The mechanism is unclear but it has been hypothesized that CMV superinfects already inflamed mucosa. It is also stated that MHC proteins are upregulated leading to an autoimmune response. The treatment of choice for CMV colitis remains ganciclovir. The association between cytomegalovirus infection and inflammatory bowel disease challenges both the clinicians and the pathologists to establish the correct diagnosis and to prescribe the most appropriate form of therapy, therefore a high suspicion should be there for CMV colitis in Immunocompetent IBD patients as well who are not responding to treatment.Figure 1.: CT Scan of Abdomen and Pelvis showing prominent diffuse colonic wall thickening.

S2243 Reversal Obstructive Lung Disease in Ulcerative Colitis: A Rare Extraintestinal Manifestation

INTRODUCTION: Ulcerative colitis (UC) is associated with several extraintestinal manifestations that may affect various organ systems, lungs involvement are relatively rare. Our case highlights a patient presenting with symptoms of reversible obstructive airway disease associated with UC disease activity. CASE DESCRIPTION/METHODS: A 23 YO male with history of Ulcerative pancolitis presented to Virginia Commonwealth University (VCU)-IBD Center with unresolving cough, wheezing, diarrhea, fecal urgency and abdominal pain. Physical exam was notable for moderate abdominal tenderness and minimal lung wheeze. Lab data reveled elevated CRP of 14 mg/dL and fecal calprotectin of 1285 µg/gm. CT abdomen/pelvis revealed active inflammation with diffuse colonic wall thickening. UC Treated initially with Mesalamine after diagnosis at age of 22 YO, combination therapy with Adalimumab and Methotrexate started few weeks prior to presentation.Pulmonary symptoms were manifested in cough and wheezing. These symptoms were exacerbated with worsening UC activity and more responsive to steroids courses. CT chest was negative for interstitial lung disease. Prior pulmonary function test (PFT) showed mild obstructive airway disease requiring albuterol and corticosteroids inhalers. He was found to have infectious colitis causing UC flare. GI and pulmonary symptoms improved with therapy optimization, steroids and methotrexate were stopped. Clinical remission were maintained with Adalimumab monotherapy. He remained off respiratory inhalers. Subsequent PFT with improved lung volumes and function. DISCUSSION: The prevalence and pathogenesis of lung involvement in IBD is poorly understood but it may be related to the underlying inflammatory process. Respiratory manifestations of ulcerative colitis are rare, they can be broadly categorized into airway disease and interstitial lung disease. These manifestations usually follow the IBD disease activity and often exacerbate during relapses. Patients with airway disease can have significant airway inflammation, which could potentially lead to airway narrowing. The most common presenting symptoms include cough and wheezing. Chest radiographs are often non-specific and pulmonary function testing may reveal obstruction pattern. CT scan of the chest may not show remarkable findings.This case report highlights that it is imperative to maintain a high index of suspicion for the development of pulmonary disease in the setting of IBD in order to institute appropriate treatment early and avoid complications.

S2926 Isolated Gastritis Secondary to Immune Checkpoint Inhibitors Complicated With Superimposed CMV Infection

INTRODUCTION: This case highlights the clinical manifestations and management of a patient with gastritis that occurred after nivolumab and was complicated by superimposed cytomegalovirus (CMV) infection. CASE DESCRIPTION/METHODS: A 55-year-old male with metastatic renal cell carcinoma on nivolumab, was seen in consultation for epigastric pain, hematemesis, melena, weight loss, nausea, vomiting and food intolerance. He denied diarrhea or hematochezia. Physical exam was notable for ill appearance and epigastric tenderness. Computed tomography showed diffuse gastric wall thickening. EGD revealed diffuse severely erythematous, friable mucosa with mucosal sloughing in the entire examined stomach. Also, a group of nummular lesions were seen in the body (Figure 1). The esophagus and duodenum were normal. Gastric biopsy showed infiltration of the lamina propria with inflammatory cells and erosive mucosa, suggestive of immune checkpoint inhibitor-related gastritis. Helicobactor pylori and CMV immunostain were negative. Nivolumab was discontinued. Prednisone 140 mg and pantoprazole 40 mg oral daily were started; a dose of infliximab 5 mg/kg was administered. His symptoms initially improved but recurred within 3 weeks. A repeat EGD showed diffuse severe inflammation characterized by adherent blood, erosions, erythema, friability, granularity and confluent ulcerations in the entire stomach (Figure 2). Biopsies were notable for severe ulceration and granulation with CMV cytopathic changes, suggestive of superimposed CMV gastritis. Steroids were tapered and intravenous ganciclovir was started, resulting in resolution of hematemesisand melena and partial improvement of other symptoms. EGD was repeated and showed diffuse moderately erythematous, granular and friable mucosa with nodularity and contact oozing in entire stomach (Figure 3). Biopsies showed ulcerative gastric mucosa with dense organized granulation tissue and reactive changes. CMV immunostain was negative. Symptoms gradually improved and at 2 months follow up patient reported near complete resolution of all symptoms. DISCUSSION: Gastritis is a rare complication of nivolumab treatment. The mainstay of treatment is discontinuing nivolumab. Steroids and infliximab have been used for ICI-related colitis. However, data regarding their efficacy in patients with ICI-related gastritis is sparse. Superimposed CMV made the management of this case more challenging. Further studies are needed to better characterize the natural history and outcome of ICI-related gastritis.Figure 1Figure 2Figure 3

S1620 A Case of Cocaine-Induced Ischemic Colitis With Increased Fecal Calprotectin

INTRODUCTION: Ischemic colitis can be caused by a wide variety of factors and is most often seen as an atherosclerotic event in the elderly. We report a case of a healthy young male who presented with multiple episodes of hematochezia and was found to have ischemic colitis due to cocaine use. CASE DESCRIPTION/METHODS: A healthy 27 year old male presented to the emergency department with one day history of left lower quadrant abdominal pain and over 10 episodes of hematochezia. He denied recent travel, sick contacts or family history of inflammatory bowel disease. His exam revealed diffuse abdominal tenderness. Laboratory data was significant for hemoglobin of 16 g/dL on arrival, which decreased to 12.7 g/dL after ongoing hematochezia. A CT of his abdomen/pelvis revealed diffuse circumferential wall thickening of sigmoid and descending colon with adjacent pericolonic fat stranding, suggestive of colitis. A GI PCR for infectious diarrhea was negative. Fecal calprotectin was greater than 1,250 μg/g. A colonoscopy demonstrated diffuse, erythematous and friable mucosa in the sigmoid and transverse colon with discontinuous areas of nonbleeding ulcerated mucosa. Biopsies showed surface ulceration, regenerative epithelial changes and superficially injured and withered crypts as seen with ischemia. Once pathology results returned, the patient disclosed using intranasal cocaine prior to the onset of the abdominal pain and his hematochezia was the result of cocaine induced ischemic colitis. DISCUSSION: Our patient was a young male presenting with hematochezia, diffuse abdominal pain, signs of colitis on imaging and had an elevated fecal calprotectin. Because of this, inflammatory bowel disease was high on the differential diagnosis. However his biopsies revealed pathology consistent with ischemia. A study by Hsieh et al, evaluated ten patients with ischemic colitis and found that each of them had an elevated fecal calprotectin. The levels were not indicative of severity or prognosis. Cocaine induced ischemic colitis is well described, especially in young patients with severe abdominal pain and hematochezia, as in our patient. Early suspicion and a careful history are essential to avoid significant morbidity and mortality. This case highlights the importance of maintaining high suspicion of cocaine abuse in young patients with ischemic colitis despite an elevation in fecal calprotectin levels.Figure 1.: Visualized splenic flexure ulcerated mucosa, erythematous (hyperemic mucousa), friable mucosa.Figure 2.: Visualized descending Colon with ulcerated mucosa, erythematous (hyperemic mucousa), friable mucosa.Figure 3.: Visualized descending colon with ulcerated mucosa, erythematous (hyperemic mucousa), friable mucosa.

S1417 Painless Jaundice: A Case of Primary Pure Squamous Cell Carcinoma of the Gallbladder

INTRODUCTION: Gallbladder cancer is the most common malignant tumor of the biliary tract with the majority of cases are adenocarcinoma (AC). Pure squamous cell carcinoma (SCC) of the gallbladder (GB) is extremely rare and accounts for only around 0.5 - 3% of all GB cancers. The initial presentation of these cases varies significantly due to its rarity. We, therefore, present a case of painless jaundice due to SCC of the gallbladder. CASE DESCRIPTION/METHODS: The patient is a 78-year-old man who presented with a 3-day history of painless jaundice. Accompanied by dark urine and clay-colored stools. He denied notable weight loss, night sweats, nausea, or vomiting. Hepatic function panel was significant for ALT 686, AST 483, Alkaline Phosphatase 1183, total bilirubin 25.6, and direct bilirubin 20.6. MRCP revealed intrahepatic biliary dilatation, a 7 mm cystic structure at the level of the head of the pancreas, and diffuse gallbladder thickening. ERCP was attempted, however, aborted due to distorted anatomy secondary to distorted anatomy. Endoscopic ultrasound demonstrated an irregular hypoechoic mass of 45 mm × 40 mm at the level of the gallbladder. Fine needle aspiration was consistent with squamous cell carcinoma. On further evaluation by multidisciplinary committee, it demonstrated invasion into the duodenum therefore surgical resection was not feasible decided to proceed with palliative radiation. DISCUSSION: Most of the published literature on pure SCC of the gallbladder is based on case reports and case series. SCC of the GB is thought to be due to keratinization of the columnar lining of the GB due to chronic repeated irritants, like cholelithiasis. Therefore, populations more prone to developing stones are thought to be higher in incidence, with a known female predominance. We described the rare presentation of painless jaundice in an elderly male with locally invasive SCC of the GB. The survival rates of SCC of the GB are significantly lower (mean: 5 months) compared to AC of the GB (mean survival: 11.4 months). As most of these lesions are advanced at presentation, rendering them unresectable (70–90%), resulting in poor prognoses. A standard regimen of chemotherapy for squamous-cell gallbladder cancer does not exist and, the only definite curative measure is resection. Therefore, while encountering painless jaundice it is important to consider carcinomas of the GB, as earlier detection of these cancers can open greater opportunities for curative resection.Figure 1.: Irregular malignant cells with hyperchromatic nuclei and glassy keratinizing cytoplasm positive for p63 consistent with Squamous cell carcinoma.Figure 2.: Irregular malignant cells with hyperchromatic nuclei and glassy keratinizing cytoplasm positive for p63 consistent with Squamous cell carcinoma.Figure 3.: Endoscopic Ultrasound: 45 mm × 40 mm irregular mass with poorly defined borders at the level of the gallbladder.

S2316 Evaluating Bloody Diarrhea During the COVID-19 Pandemic in a 20-Year-Old Patient

INTRODUCTION: During the COVID-19 pandemic, differentiating between acute infectious diarrhea versus a chronic inflammatory bowel disease (IBD) presents a new challenge altering the way we approach the diagnosis and treatment of IBD. CASE DESCRIPTION/METHODS: A 20-year-old gentleman with no known past medical history presented to his PCP with 14 bloody bowel movements daily. He was started on a 5-day course of Azithromycin. Stool studies were sent and his C. Difficile stool antigen turned positive. He was switched to oral Vancomycin. He presented to the hospital 3 days later after no improvement. On presentation, patient was febrile with diffuse abdominal and rectal pain. Initial lab results revealed leukocytosis (29.5K) with elevated bands (35), CRP 127.3, Albumin 3.0, Ferritin 236, Procalcitonin 1.13, Fibrinogen 698, and D-Dimer 1.57. Repeat stool studies were negative. His SARS CoV-2 PCR was positive. Chest X-ray was unremarkable. CT abdomen revealed diffuse colonic wall thickening and peri-colonic inflammation consistent with pancolitis without intra-abdominal or pelvic abscess. Symptoms improved with antibiotics. Flexible sigmoidoscopy revealed diffuse, severely edematous and erythematous mucosa with granularity and discontinuous areas of ulcers of varying size and depth seen in descending colon. Ulcerations were superficial and circumferential. Due to severity of disease and contact bleeding, scope was not advanced beyond this point. The lumen became narrowed due to inflammation without overt stricture or obstructing lesions. The sigmoid colon and rectum, ulcerations became mixed with exudates and the area was generally less effected. Numerous biopsies were taken. Pathology showed severe chronic active colitis with ulceration. Histology showed frequent crypt abscesses, cystic crypt changes and basal lympho-plasmacytosis. There is no definite Paneth cell metaplasia, pseudomembranous or viral cytopathic changes. After multidisciplinary discussion, he was started on IV Solumedrol. 72 hours later patient reported near resolution in symptoms and was transitioned to oral Prednisone taper. He was started on Infliximab 10 mg/kg prior to discharge after a repeat COVID test was negative. Outpatient follow up was arranged for repeat testing and interval colonoscopy. DISCUSSION: The documentation of collective experiences with newly diagnosed IBD patients during the COVID pandemic presents a diagnostic and therapeutic dilemma possibly altering our decisions moving into a new era.Figure 1.: Descending colon images.Figure 2.: Sigmoid colon images.Figure 3.: Rectal images.

S3021 Checkpoint Inhibitor-Induced Gastritis

INTRODUCTION: Nivolumab, a novel chemotherapy drug, is a monoclonal antibody immune checkpoint inhibitor that is commonly used in the treatment of many different malignancies. Immune checkpoint pathways are important for immune response regulation, and their inhibition has been associated with autoimmune reactions affecting several different organ systems. While multiple GI side effects have been documented, gastritis appears to be rare. As the use of these agents becomes more frequent, so too will their side effects. Clinicians should familiarize themselves with the potential adverse effects of these medications. CASE DESCRIPTION/METHODS: A 61 year old man with a PMH of HTN, Type 2 DM, and Stage III malignant melanoma of the plantar surface of his right foot, now on Nivolumab, presented to clinic with intermittent mid-epigastric abdominal pain, nausea/vomiting, and decreased PO intake. Recent abdominal CT imaging showed diffuse gastric wall thickening. EGD was performed showing severe, diffuse, hemorrhagic gastric inflammation characterized by adherent blood, edema, erythema, friability and shallow ulcerations concerning for drug induced injury vs malignancy. Biopsies were obtained and showed severe chronic active gastritis with extensive ulceration, inflammatory granulation tissue formation, focal complete-type intestinal metaplasia, and bacterial colonies. Nivolumab was discontinued, and the patient was started on pantoprazole, prednisone and sucralfate. His symptoms resolved, and a repeat upper endoscopy showed marked improvement in the gastric mucosa. DISCUSSION: Indications for checkpoint inhibitor use continue to increase, and their side effects will likely become more frequent. Lower GI involvement is well described but gastritis is rare. PD-1 induced autoimmunity should be considered in patients presenting with gastritis and recent use of Immune checkpoint inhibitor therapy. EGD with gastric biopsies is required to confirm the diagnosis. PD-1 inhibitor associated gastritis histopathology findings are non-specific, but common findings include epithelial lymphocyte and neutrophil infiltration, lamina propria expansion and crypt gland abscesses. Treatment consists of discontinuing the offending agent and corticosteroids. If the side effects are mild, clinicians can attempt to restart the medication or use alternative checkpoint inhibitors. Given that the presentations of checkpoint inhibitor gastritis appears to be variable and non-specific, clinicians should have a high suspicion for this complication.Figure 1.: gastric fundus, severe hemorrhagic gastritis.Figure 2.: pre-pyloric stomach, inflammation and ulceration.Figure 3.: gastric body nodularity.

S1834 A Case of Neutropenic Enterocolitis With a Hyperinflammatory Twist

INTRODUCTION: Neutropenic enterocolitis is a life-threatening diagnosis of exclusion commonly presenting with fever, abdominal pain, and radiographic evidence a thickened bowel wall (1). Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening immune-mediated disorder characterized by systemic inflammation, severe cytokine storms, and organ damage (2). HLH is commonly triggered by viral infection or malignancy and is associated with significant in-hospital mortality (3). It is not commonly triggered by bacterial infection and does not typically present as neutropenic enterocolitis. We present a case of a patient who presented with neutropenic enterocolitis, which may have been a cause or consequence of HLH. CASE DESCRIPTION/METHODS: A 56-year old African American male with hypertension, type 2 diabetes mellitus, end-stage renal disease on hemodialysis, cardiomyopathy, and recurrent left-sided pleural effusions, presented with sudden-onset diffuse abdominal pain associated with nausea, vomiting, and non-bloody diarrhea. On admission, he was febrile and tachypneic. On exam, he appeared to be in pain. His abdomen was nondistended with hypoactive bowel sounds. He exhibited guarding, and there was tenderness to palpation, however there was no rebound tenderness. His labs were significant for bicytopenia (leukopenia and anemia), and a lactate of 9.42 mmol/L. CT scan of the abdomen and pelvis was consistent with enterocolitis (Figure 1). Despite supportive measures with broad spectrum antibiotics and fluids, his mental status and respiratory status declined, eventually requiring an ICU level of care. Although no specific pathogen was identified, workup revealed a likely diagnosis of HLH. Patient was treated with intravenous steroids, followed by a steroid taper. Treatment with etoposide was postponed due to the patient’s renal dysfunction, rapid deterioration and death. DISCUSSION: Neutropenic enterocolitis has yet to be documented as the initial presentation of HLH. We present a case of a patient who presented with severe neutropenic enterocolitis, who met diagnostic criteria for HLH. The overlap between diagnostic features of severe sepsis and HLH made the diagnosis of HLH challenging. Continued rapid decline and persistent leukocyte dysfunction prompted further investigation, which led to his diagnosis. Early identification of HLH in the setting of neutropenic enterocolitis may expand therapeutic possibilities and help improve outcomes for patients with this life-threatening condition.Figure 1.: Radiographic image revealing diffuse large bowel wall thickening.

S2909 Granulomatous Appendicitis: Idiopathic or Prospective Crohn’s Disease?

INTRODUCTION: Isolated granulomatous inflammation of the appendix is a rare entity, identified histologically in < 2% of specimens, and typed into idiopathic granulomatous appendicitis (GA) and appendiceal Crohn’s disease (CD). Less than 10% of GA cases develop CD. CASE DESCRIPTION/METHODS: A healthy 26-year-old male was advised to seek care for computed tomography (CT) suggesting acute appendicitis, ordered to assess dysuria and right testicular and abdominal pain of 1-month duration. CT measured a dilated appendix extending to the seminal vesicle, with fecolith and fat stranding. Vitals were stable, abdomen benign, and labs normal. During appendectomy, an inflamed appendix was seen adherent to the bladder. An uneventful post-op period was followed by discharge home. Despite interval recovery, readmission for pain, vomiting, and diarrhea occurred on POD 10. Tachycardia was noted without fever. Abdomen was distended and generally tender. There was leukocytosis. CT found thickened jejunum with proximal dilation and air-fluid-levels. Jejunitis and obstruction resolved with conservative care, but evidence of GA (granuloma with giant cell, negative AFB and GMS stains) on recent pathology prompted testing for a broadened differential. There was denial of travel, ill contacts, personal and family history of CD, but admittance to colonoscopy a decade prior with findings of proctitis. Blood, urine, and stool cultures, as well as C. difficile and O&P were negative. CD, tuberculosis, fungal, and Coccidioides serologies were negative. Ileocolonoscopy found post-op cecal changes. Random ileocolonic biopsies resulted normal mucosa. With clinical stabilization, discharge home was planned. During follow-up visit, the patient declared return to normalcy, and thus declined investigations for CD. DISCUSSION: Causes of GA include infectious, systemic, and local reactions, but often remains elusive, as does a uniform approach to diagnosis and management. Omitted tests limit confidence in diagnosing idiopathic GA, and uncertainty in proper follow-up delays diagnosis of related conditions. Despite idiopathic labeling, we remain vigilant to alternate causes. The patient at first lacked acute infectious features, but as Yersenia is linked to ¼ of cases, serologic testing would be ideal to exclude infection and support idiopathic nature. Sub-acuity lends support to interval appendectomy as a cause. Lastly, a remote history of proctitis, in concert with enteritis on readmit, may hint at chronicity, and begs close follow-up for CD.Figure 1.: Histology showing presence of non-caseating granulomas in a background of lymphocytic inflammation in the appendiceal wall (x10).Figure 2.: Histology showing a giant cell in a granuloma in the appendiceal wall (x10).Figure 3.: Computed tomography of the abdomen and pelvis with IV contrast showing diffuse circumferential thickening of multiple distal jejunal loops.

S1764 Three Undiagnosed Primary Malignancies Presenting as Chronic Diarrhea

INTRODUCTION: Clinicians are taught to differentiate the symptoms of unintentional weight loss, decreased appetite and night sweats to include malignancies in their differentials. When these clues are absent or replaced with seemingly unrelated symptoms, the diagnosis of malignancy is often delayed. We present a case of chronic diarrhea, neurologic symptoms and urinary retention found to be secondary to three undiagnosed primary malignancies. CASE DESCRIPTION/METHODS: A 68 year old man with unremarkable past medical history transferred to Honolulu from the Philippines after extended hospitalization. He presented with 3 months of chronic watery diarrhea, 30 lbs weight loss, progressive weakness of all extremities, peripheral neuropathy, and unexplained urinary retention. While hospitalized in the Philippines a Foley catheter was placed. He was also informed that his bladder wall was thickened. Arriving at Tripler Army Medical Center, preliminary tests evaluating chronic diarrhea were unremarkable. CT abdomen and pelvis was significant for diffuse bladder wall thickening and previously unknown abdominal mass in the lesser sac. Bladder biopsy showed papillary bladder tumor which was transitional cell carcinoma. Investigation of the abdominal mass via endoscopy revealed moderately differentiated gastric adenocarcinoma (HER2neu+). Given his persistent extremity weakness and muscle wasting, MRI of the spine and brain was obtained which demonstrated diffuse signal abnormalities in the thoracic and lumbar spine. PET scan revealed 5.2 cm hypermetabolic pararectal mass and transrectal ultrasound biopsy diagnosed a gastrointestinal stromal tumor (GIST). Initial treatment plan included trastuzumab and surgery, therefore screening echocardiogram was obtained. Unfortunately, this revealed significant infiltrative cardiomyopathy with severely reduced ejection fraction. Thus, the patient was no longer deemed a good treatment candidate. Given poor prognosis, he declined further diagnostic workup and transitioned to comfort care. DISCUSSION: This case is the first instance in literature of these three primary cancers presenting in one patient. Tumors in the pararectal area account for only 5% of all GIST presentations, and presence of two additional primary cancers makes this rare presentation even more unique. Diffuse signal abnormalities in spine along with his infiltrative cardiomyopathy also raised suspicion for multiple myeloma, however as the patient transitioned to comfort care, any further investigation was precluded.Figure 1.: Gastric Adenocarcinoma: Dysplastic glands overlying invasive moderately differentiated adenocarcinoma.Figure 2.: Pararectal Gastrointestinal Stromal Tumor: Cell block section showing clusters of atypical cells with abundant delicate eosinophilic cytoplasm. Nuclei are enlarged, appear round to oval with smooth nuclear contours, and display a mild to moderate degree of pleomorphism 40x.Figure 3.: Pararectal Gastrointestinal Stromal Tumor: Positive Immunohistochemical Staining DOG-1 (20x) (Specific for GIST).

S2959 Eosinophilic Gastritis: An Imposter of Gastric Malignancy

INTRODUCTION: Eosinophilic gastroenteritis (EGE) is an uncommon condition characterized by eosinophilic infiltration into the lining of the GI tract with a predilection for the stomach and proximal small bowel. Symptoms are non-specific, and the disease is known to take a chronic, relapsing/remitting course. To date, approximately 300 cases are described in literature. Here, we present a case of EGE closely mimicking gastric malignancy. CASE DESCRIPTION/METHODS: A 57-year-old male with a past medical history of DM II, HTN, GERD, and ESRD was admitted to the hospital with 30 lbs weight loss, postprandial fullness, and intractable vomiting. Physical examination showed moderate tenderness to deep palpation in the upper abdomen. CT scan revealed gastric outlet obstruction from an incidental finding of gastric antrum mass. An EGD was performed and revealed a malignant appearing mass in the pre-pyloric region of the stomach. Biopsies showed peptic duodenitis without any evidence of malignancy or H. Pylori infection. Given high suspicion for malignancy, an endoscopic ultrasound was performed to evaluate the deeper layers and obtain snare mucosal biopsies. EUS showed a 12mm diffuse wall thickening of the pylorus with distortion of the gastric wall layer architecture. FNA of the deep gastric layers was performed using a 22G needle. FNA and repeat mucosal biopsies were negative for malignancy and showed reactive epithelial cells and non-specific inflammation. After a multi-disciplinary discussion, the decision was made to perform diagnostic laparoscopy, followed by gastro-jejunostomy, for the gastric outlet obstruction. Intra-operative findings did not show any evidence of peritoneal disease or lymphadenopathy. Pathology showed diffuse eosinophilic infiltration of the mucosa and muscularis propria, consistent with eosinophilic gastritis. He recovered well from his surgery and tolerated solid food prior to discharge. DISCUSSION: The pathogenesis of EGE is not well understood. Available evidence suggests that it is a hypersensitivity reaction. Histopathological analysis can confirm the diagnosis. Eosinophilic infiltration can involve any layer of the stomach (mucosa, muscularis propria, or serosa), which impacts clinical presentation. The treatment is primarily based on dietary modifications and systemic steroids. In conclusion, eosinophilic gastroenteritis should remain on the differential diagnosis in appropriate clinical cases where the diagnosis of cancer is unclear.Figure 1.: Endoscopic visualization of mass in the gastric antrum. The mass extended into the pylorus.Figure 2.: Hematoxylin and eosin stain of superficial pylorus biopsy taken during EGD. This largely shows inflammation, with mildly increased eosinophils. This image was taken at 20x magnificationFigure 3.: Hematoxylin and eosin stain of full-thickness antral tissue taken during exploratory laparotomy. This shows focally increased mucosal eosinophils. This image was taken at 40x magnification.

ACTINOMYCOSIS MIMICKING LUNG CANCER: A CASE REPORT

SESSION TITLE: Medical Student/Resident Chest Infections Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Pulmonary actinomycosis is a rare disease that can be challenging to diagnose and is associated with multiple risk factors such as poor oral hygiene, alcoholism, and chronic underlying lung diseases. Actinomycosis can often be misdiagnosed as lung abscess, tuberculosis, or malignancy with radiologic findings that might be misleading. Here we present a case with initial chest CT finding concerning neoplasm but diagnosed as pulmonary actinomycosis on further evaluation. CASE PRESENTATION: 55-year-old male with past medical history of HTN presented with right sided upper back pain and 6 pounds of unintentional weight for 4 weeks. He did not report any symptoms of cough, hemoptysis, shortness of breath, or chest pain. He was a heavy smoker with 45 pack years of smoking and a history of chronic alcoholism with 30 ml of 3-4 vodka shots twice a week for the last 30 years. Patient’s laboratory studies were pertinent for WBC count of 19.6 X 10 3. CT of the chest showed 4.6 x 3.4 cm thick-walled cavitary mass in the right lower lobe concerning for neoplasm with the extension of mass to the right paravertebral region and diffuse right pleural metastases, pathologic lymphadenopathy, and trace right pleural effusion. He underwent BAL with bronchial brushing which showed significant endobronchial inflammation. Microbiological examination of samples obtained from BAL showed Gram-positive filamentous bacteria. Treatment was given with IV clindamycin and he was discharged home on PO Clindamycin for 4 weeks with a repeat chest X-ray in 2 weeks. He was readmitted after 2 weeks with worsening shortness of breath, was found to be hypoxic with SpO2 of 65% on RA and RR of 40/min, he was intubated. Repeat CT chest showed diffuse right pleural thickening and ground-glass opacity of the right upper and middle lung. He was started on broad-spectrum antibiotics with IV vancomycin, IV Zosyn and IV Penicillin but he remained critically ill and a decision was made by the family to withdraw care. The patient was terminally extubated. DISCUSSION: Actinomycosis is a chronic, granulomatous disease mostly caused by A. israelii which is a normal commensal of human oropharynx, GI tract, and female genitalia. Pulmonary actinomycosis accounts for 15% of total disease burden and is usually caused by aspiration of the oropharyngeal or gastrointestinal secretion especially in patients with chronic alcoholism and poor dentition, facial or dental trauma1. CONCLUSIONS: Diagnosis of actinomycosis can be challenging given that presentation and radiologic findings might resemble various other conditions. Pulmonary actinomycosis if diagnosed and treated early has an excellent prognosis, the clinician should have high levels of suspicion in patients with risk factors such as chronic alcoholism, poor dental hygiene, prompting further evaluation with radiology and confirmation of diagnosis with histology and microbiology. Reference #1: 1. Mabeza GF, Macfarlane J. Pulmonary actinomycosis. Eur Respir J. 2003;21(3):545-551. doi:10.1183/09031936.03.00089103 DISCLOSURES: No relevant relationships by Sotirios Doukas, source=Web Response No relevant relationships by Leena Kavali, source=Web Response No relevant relationships by Shashank Nuguru, source=Web Response