Stigmata Of Chronic Liver Disease Research Articles

Parkinson’s mimicker in Acute and Chronic Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a neuropsychiatric spectrum mainly caused by cirrhosis, portosystemic shunt, or portal hypertension. It may also mimic the presentation of Parkinson’s disease, which can make clinical diagnosis a challenge. A 42-year-old man with underlying chronic hepatitis C with liver cirrhosis was initially admitted for chronic lower back pain. During admission, he appeared drowsy but was able to answer questions appropriately albeit with delayed and slow speech. He had bradykinesia without stigmata of chronic liver disease. Differentials at the time were hypoactive delirium and Parkinson’s disease. Blood results were normal. Magnetic resonance imaging (MRI) of the brain showed bilateral symmetrical hyperintensities at the inferior temporal lobes, medial thalamus, cingulate gyri, head of caudate nuclei, posterior limbs of internal capsules and insula on fluid-attenuated inversion recovery (FLAIR) sequence. On the T1 weighted imaging (T1WI) sequence, bilateral symmetrical hyperintensities were seen at globus pallidi, cerebral peduncles and periaqueductal regions extending to superior cerebellar peduncles. Based on imaging, a diagnosis of acute chronic hepatic encephalopathy was made. The patient was treated conservatively in the ward and was discharged with persistent Parkinsonism. In patients with neurological abnormalities where hepatic encephalopathy (HE) is least expected due to subtle symptoms, MRI could play an important role in eliciting the underlying cause, and extent of disease and for prognostication.

Relapsed nodular lymphocyte-predominant Hodgkin lymphoma presenting as severe paraneoplastic hepatitis: a case report

BackgroundHematological malignancies are an infrequent but important cause of liver dysfunction. There are several mechanisms by which this can occur, including direct malignant infiltration of the hepatic parenchyma and/or vasculature, vanishing bile duct syndrome, and paraneoplastic hepatitis. Paraneoplastic hepatitis is an extremely rare mechanism by which a hematological malignancy can cause liver dysfunction, and we present the first case, to our knowledge, of paraneoplastic hepatitis caused by nodular lymphocyte-predominant Hodgkin lymphoma in the literature.Case presentationA 28-year-old Caucasian male presented with 3 weeks of fatigue, epigastric pain, and jaundice. His medical history was significant for early stage nodular lymphocyte-predominant Hodgkin lymphoma in the cervical region in remission for 5 years after primary treatment with involved-field radiotherapy. Liver biochemistry was normal at the time of treatment for lymphoma and there was no known liver disease before the current presentation. On physical examination, there was scleral icterus and ecchymoses, but no evidence of hepatic encephalopathy, other stigmata of chronic liver disease, or lymphadenopathy. A computed tomography scan of his neck, chest, abdomen, and pelvis showed heterogeneous enhancement of the liver, multiple enlarged upper abdominal lymph nodes, and an enlarged spleen with multiple rounded lesions. Portal and hepatic veins were patent. Initial workup for viral, autoimmune-, toxin-, and medication-related hepatitis was negative. A transjugular liver biopsy was performed with histology showing a predominantly T-cell mediated hepatitis with very extensive multiacinar hepatic necrosis, but no evidence of lymphoma within the liver. Retroperitoneal lymph node biopsy revealed nodular lymphocyte-predominant Hodgkin lymphoma. The patient’s symptoms, bilirubin, and transaminases improved significantly after treatment with oral prednisolone and a staged introduction of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy.ConclusionsNodular lymphocyte-predominant Hodgkin lymphoma may cause paraneoplastic hepatitis. Physicians should be aware of the possibility of this life-threatening presentation and the importance of early liver biopsy and treatment before acute liver failure occurs. Interestingly, paraneoplastic hepatitis did not occur when nodular lymphocyte-predominant Hodgkin lymphoma was first diagnosed and confined to the cervical region, but was the presenting feature of the recurrence below the diaphragm.

A258 SEVERE ACUTE HEPATITIS OF UNKNOWN ORIGIN WITH RAPID PROGRESSION TO PAEDIATRIC ACUTE LIVER FAILURE IN A CHILD

Abstract Background Severe acute hepatitis (SAH) of unknown origin among children has been a major public health concern globally in recent times, with >1010 cases reported to WHO, including 28 in Canada as of July2022. The clinical syndrome in all identified cases (median age 3, IQR 2-5 yrs) was acute hepatitis with progression to paediatric acute liver failure (PALF) and need for liver transplantation (LT) in 5.4-13%. Human adenovirus (HAdV), particularly serotypes 40 and 41, remains the most common pathogen detected around the time of presentation in upto 70%. HAdV hepatitis is a rarity in the immunocompetent. The role of adenovirus in SAH remains unclear and investigations continue Purpose To report the case of a child meeting the WHO case definition of SAH of unknown origin in whom adenovirus was detected with rapid progression to PALF requiring LT Method Case report and literature review Result(s) A previously healthy 4year-old girl presented to us with a 1week history of abdominal pain and vomiting followed by onset of jaundice. 1month prior to presentation, she had an episode of conjunctivitis. Examination revealed a well-appearing girl with icterus, hepatosplenomegaly with no stigmata of chronic liver disease and no features of hepatic encephalopathy. Laboratory results on day of presentation revealed transaminases >10 times upper limit of normal (ALT 4686U/L, AST 5986U/L), total bilirubin-233μmol/L (conjugated bilirubin-153μmol/L) and INR-1.6. Work up for viral hepatitis(A-E), metabolic, autoimmune, genetic or mechanical causes of hepatitis was negative (Table 1). HAdV was detected by PCR in blood (9700 copies/mL), stool and nasopharyngeal swab. Treatment with cidofovir (1mg/kg/dose) was started on day8 after presentation.By day11, laboratory parameters had worsened with ALT 1293U/L, AST 2326U/L, total bilirubin 331μmol/L, INR-9.1 and LT was considered. With failure to improve over the next 48hrs, she received a living donor LT on day13 after presentation and had an uneventful post-transplant course. At the time of writing this report, she was 41 days post-transplant, doing well on immunosuppression with tacrolimus and tapering dose of steroids. Histopathological examination of liver showed extensive hepatocyte loss of upto 80%, replaced by ductules, in a background of mild hepatitis (patchy pan-lobular inflammation with minimal portal inflammation) and no significant fibrosis. Electron microscopy (EM) showed patchy hemophagocytosis. No evidence of HAdV on immunohistochemical stains or EM was identified. These findings are directly in line with what others have reported, namely a lack of direct toxic effect of virus on liver tissue Image Conclusion(s) This case highlights the potential for rapid progression to PALF and need for LT in a child SAH of unknown origin. Early identification and diagnosis of PALF is important and should be followed by transfer to a LT center. As previously described by others, HAdV was detected, but its role in pathogenesis of this clinical syndrome remains elusive Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Prevalence of stigmata of chronic liver disease in patients with decompensated cirrhosis

Prevalence of stigmata of chronic liver disease in patients with decompensated cirrhosis

S3060 Labetalol, a Common Antihypertensive, an Uncommon Cause of Drug-Induced Liver Injury (DILI)

Introduction: Labetalol is an antihypertensive medication (AHM) commonly used as first line agent for non-severe hypertension in pregnancy. We present a case of DILI in a young woman transitioned to labetalol while attempting to conceive. Case Description/Methods: A 35-year-old woman with a h/o hypertension, hashimoto's thyroiditis, anxiety, obesity (BMI 34) was admitted to our hospital for abdominal pain, jaundice, pruritus and aminotransferase (LFT) elevations. She had been admitted previously at an outside facility with nausea, anorexia, and elevated LFTs (ALT 1264, AST 1419, ALP 294, TBili 5) 20 weeks after initiation of labetalol. There were no h/o alcohol abuse or risk factors for hepatitis B/C. Home medications including labetalol were stopped. Imaging studies including MRCP showed no evidence of biliary obstruction. Infectious workup (hepatitis A/B/C/E, CMV, HSV, EBV) and drug/tox screen were negative. A liver biopsy showed acute hepatocellular injury without eosinophils, steatosis, cholestasis or fibrosis; differentials included DILI and infectious hepatitis. LFTs improved, patient was discharged and labetalol restarted. Two weeks later, she presented to our hospital with worsening jaundice. Admission labs: ALT 905, AST 1553, ALP 257, TBili 19.8, INR 1.4 and creatinine 1. On exam, there was no stigmata of chronic liver disease or encephalopathy. Labetalol was discontinued. Infectious, hereditary, metabolic were negative. ANA was positive (1:320) homogenous pattern with mild elevation in IgG. Prednisolone 40 mg daily was started with rapid improvement in LFTs. At 8 week follow up, she was asymptomatic and LFTs were near normal (Tbili 2); prednisolone was tapered. Discussion: Mild to moderate, transient aminotransferase elevations are noted in up to 8% of patients on labetalol. But they are asymptomatic and resolve even with continuation of the medication. Severe liver injury however is rare and rapid resolution typically ensues after cessation of the drug. However acute liver failure, death and OLT have been reported. There are isolated case reports and small case series of labetalol induced DILI, mostly in pregnant women. In a case series, 3 out of 11 patients died and 1 of 5 patients who had liver biopsy had chronic active hepatitis. The mechanism of labetalol hepatic injury is believed to be idiosyncratic. Inadvertent rechallenge has been shown to cause recurrence of DILI. We present this case to increase awareness of labetalol induced DILI as it is the most commonly used AHM in pregnant women.

S1755 Intrahepatic Cholangiocarcinoma in a Patient With Alcoholic Liver Cirrhosis and Markedly Elevated Serum Alpha-Fetoprotein

Introduction: Intrahepatic cholangiocarcinoma (ICC) represents 5% of all primary liver malignancies, second only to hepatocellular carcinoma (HCC). Although risk factors such as primary sclerosing cholangitis, hepatolithiasis, and asbestos have been reported, the etiology of ICC is not well understood. An elevated serum AFP accompanied by a space-occupying solid lesion in a cirrhotic patient is typically indicative of HCC. In high-risk patients, such as those with chronic liver disease, AFP > 400 ng/mL has a high positive predictive value for HCC and a specificity of >95%. An elevated serum AFP greater than 20 ng/mL is seen in < 25% of ICC. Case Description/Methods: We present a patient with a past medical history of alcoholic liver cirrhosis Child-Pugh Class C presenting with acute change in mental status. On arrival, he was hemodynamically stable with classic stigmata of chronic liver disease on the exam. Non-contrast CT Head was non-revealing. Laboratory investigations revealed an obstructive pattern of transaminitis with a normal ammonia level, negative hepatitis panel, and serum AFP of 1955.8 ng/mL. EGD demonstrated portal hypertensive gastropathy. CT Abdomen/Pelvis demonstrated a large infiltrative heterogeneous mass involving the entire right hepatic lobe with a non-occlusive thrombus extending to the portal vein. Ultrasound-guided liver biopsy and immunohistochemical analysis demonstrated positive expression for cytokeratin 20, and CA 19-9. Neoplastic cells were negative for Hep-Par1, Glypican 3, and Arginase 1. The histological pattern (Figure) was consistent with poorly differentiated adenocarcinoma, most likely pancreaticobiliary in origin consistent with intrahepatic cholangiocarcinoma (ICC). Discussion: Elevated serum AFP accompanied by a space-occupying solid lesion in a cirrhotic patient is typically indicative of HCC. However, Xiong et al reported an increased risk by 3.92-fold of cholangiocarcinoma in patients with alcoholic liver disease. Even though, an increase in AFP has been reported in patients with ICC, an elevation higher than 20 ng/mL was seen in approximately 20% of the patients according to Wang et al. In our patient, surprisingly, the histopathological report showed findings consistent with ICC and negative hepatic markers, hence a high suspicious index should be held by clinicians for this entity upon approaching a patient with a solid liver mass associated with significantly elevated AFP levels.Figure 1.: On the left, histology of poorly differentiated adenocarcinoma composed of duct-like structures with high pleomorphism. H&E 400X. On the right, immunohistochemical study shows positive CA 19-9 stain of adenocarcinoma.

S3032 Hiding in Plain Sight: An Atypical Presentation of Metastatic Breast Cancer as Acute Decompensated Cirrhosis

Introduction: Liver is a common site of breast cancer metastases, which are typically identified as hypervascular lesions on imaging. We present a rare case of breast cancer leading to diffuse, intra-sinusoidal, radiographically occult metastases in a patient presenting with new hepatic decompensation. Case Description/Methods: A 65-year-old woman with a remote history of grade IIIa invasive ductal carcinoma of the right breast status post lumpectomy, chemotherapy, and local radiation therapy was referred to liver clinic for 1 month of abdominal pain and newly elevated AST 144 U/L, ALT 143 U/L, total bilirubin 5.2 mg/dL, conjugated bilirubin 3.7 mg/dL, and alkaline phosphatase 652 U/L. She denied use of alcohol, substances, new medications, or supplements. Physical exam did not demonstrate stigmata of chronic liver disease. Work up for infectious, autoimmune, and common infiltrative etiologies of liver disease were negative; several tumor markers were elevated (Table 1). A routine surveillance PET-CT and subsequent MRCP demonstrated diffuse heterogeneous liver attenuation with cirrhotic morphology, splenomegaly, trace ascites, and intrabdominal lymphadenopathy. No discrete masses were seen on either study. The following week the patient was admitted for rapidly progressive failure to thrive, worsening ascites, jaundice, and oliguria. Inpatient labs demonstrated worsening hyperbilirubinemia (total bilirubin 14.8 mg/dL, conjugated bilirubin 12.2 mg/dL), hyponatremia, and AKI. Admission MELD-Na score was 31 and CLIF-C ACLF score was 46. Paracentesis demonstrated SAAG 1.6 with ascites protein 1.8 g/dL confirming Child Pugh Class B Cirrhosis. Transjugular liver biopsy measured hepatic venous pressure gradient 12mmHg and pathology demonstrated metastatic breast carcinoma of the sinusoidal and vascular spaces with background steatosis and non-bridging fibrosis. Despite aggressive treatment with fulvestrant and abemaciclib, she had worsening multiorgan failure. Given her overall poor prognosis, the patient elected to transition to hospice. Discussion: Metastatic breast cancer uncommonly presents with diffuse, intra-sinusoidal metastases that are radiographically occult. This case highlights the importance of maintaining a high index of suspicion for metastatic disease in patients with a history of malignancy presenting with new hepatic decompensation even in absence of typical radiographic findings. In such cases, liver biopsy may be required for a definitive diagnosis. (Table) Table 1. - Work up for etiologies of chronic liver disease Autoimmune markers ANA Positive (1:320, speckled) Anti-mitochondrial Ab < 1:20 dsDNA < =200 Smooth muscle Ab < 20 RNP Ab < 20 SSA Ab 68 (Elevated) SSB Ab < 20 Rheumatoid Factor < 10 Thyroid Peroxidase Ab 135 (Elevated) Beta-2-Glycoprotein IgA/IgG/IgM < 10 Cardiolipin IgA/IgG/IgM < 20 C-ANCAMyeloperoxidase AbP-ANCAProteinase-3 Ab < 1:20< 1:20< 1:20< 1:20 Infectious studies Hep A Ab Nonreactive Hep C Ab Nonreactive Hep B surface Ab < 10 Hep B surface Ag Nonreactive Hep B core Ab Nonreactive MTB-Quantiferon-Gold Negative Other causes of Liver Disease Alpha-1-antitrypsin Negative SPEP/UPEP No monoclonal bands observed Ceruloplasmin Elevated Copper Elevated Ferritin Elevated Tumor Markers AFP 4.2 ng/mL, decreased to < 1.82 ng/mL CEA 84 ng/mL, increased to peak 3042 ng/mL (Elevated) CA 125 930 U/mL CA 19-9 1166 U/mL CA 27.29 7450.1 U/mL (Elevated)

An Interesting Case of Hepatomegaly

Question: A 65-year-old man was referred to our center with a 6-month history of progressive shortness of breath, unintentional weight loss (31 kg during the last 6 months), and night sweats. Past medical history included previous alcohol misuse. He was a nonsmoker with no significant family history. Physical examination revealed a cachectic man with hepatomegaly. He had no ascites, no jaundice, and no stigmata of chronic liver disease. Notable laboratory test results included a y-glutamyl transferase 219 IU/L (reference range, 12–68 IU/L) and alkaline phosphatase 194 IU/L (reference range, 30–130 IU/L), with a normal liver profile otherwise.

Clinical Characteristics and Etiology of Chronic Liver Disease among Egyptian Patients in Nile Delta: A Clinical Study

Background: Chronic liver disease (CLD) is an extremely common clinical condition that causes significant morbidity and mortality and was responsible for 1.3 million deaths worldwide. There had been a 46% increase in CLD mortality in the world between 1980 and 2013 and most of this increase has been reported in low-income countries in Asia and Africa including Egypt. These countries are experiencing a demographic and epidemiologic transition in disease burden and Egypt is one of the epicenters of this change. Previously, CLD in Egypt was traditionally attributed to schistosomiasis mainly in the region of the Nile Delta until the mid-1980s.&#x0D; Aims: To capture the modes of clinical presentation and at which stage CLD patients seek clinical care, as well as the dramatic change in the etiological profile of CLD in this area of the Nile Delta&#x0D; Methods: 1013 newly diagnosed CLD patients were selected and identified from the Tanta Liver Center (TLC) across the middle of the Nile Delta. After informed or written consent, all consecutive patients (18 years and above) referred to TLC with suspected or overt chronic liver disease were subjected to full history taking, clinical examination searching for stigmata of chronic liver disease, and laboratory studies including urine, blood sugar, liver biochemical tests (bilirubin, ALT, AST&amp; serum albumin), prothrombin, viral markers (HCV Ab &amp; HBS Ag) and AFP. Imaging studies including the abdominal US for all patients and triphasic CT and liver biopsy in selected patients.&#x0D; Results: About 50% of our CLD patients present at a relatively advanced stage of decompensated cirrhosis (ascites in 39.2%, bleeding in 22.8%, and HCC in 9.3%).&#x0D; CLD patients of schistosomal etiology presented mainly with manifestations of portal hypertension (splenomegaly, UGI Bleed &amp; thrombocytopenia) that was significantly higher than the other 2 groups.&#x0D; The vast majority of our CLD patients (83.5%) have viral etiology, while only 11.1% have schistosomal etiology and the remaining 5.4% have non-identified etiology.&#x0D; Conclusion: based on the results of the present study, it is evident that HCV had replaced schistosomiasis as the predominant cause of CLD in Egypt particularly in the region of the Nile Delta. The late presentation of a good percentage of our CLD patients raises the importance of screening programs for CLD in this endemic area of the Nile Delta.

Child-Pugh Score of Decompensated Chronic Liver Disease Patient as a Predictor of Short-Term Prognosis

Objective: The study was carried out to produce the short-term prognosis of decompensated Liver Disease through the Child-Pugh scoring system and as the complications of cirrhosis and to find out the eligible Percentage of patients for liver transplantation suffering from advanced liver disease. Methodology: This cross-sectional prospective shady was conducted in two best institutes of Bangladesh (DMCH and RSMMU) from January to June 2010. The target population for this study was patients with chronic liver disease in the decompensated state. The patient was selected by meticulous history and clinical examination, including stigmata of chronic liver disease and decompensation, especially ascites, edema, hematemesis melaena, and hepatic encephalopathy. The ultrasonography evidence of coarse echogenicity and Albumin: Globulin ratio alteration was recorded as chronic liver disease evidence. Investigation such as serum bilirubin serum albumin, prothrombin time, ultrasonography of the whole abdomen, the viral market was done in all cases. If the patients are compensated states or decompensated signs explained by any other illness were excluded from the enrollment, 50 patients were randomly selected, and the child Pugh scoring was done within 24 hours of hospitalization. The study physician followed the patients daily up to discharge or death, whichever comes first. Result: In this study, the maximum age incidence among the decompensated CLD patients was between 46-55 years (36%), and the male-female ratio was 4.55:1. Among 50 patients, 64% of patients fall in the Child-Pugh class C group, 28% fall in the class B group, and only 8% fall in the class A group. In the first three months of the study period, death occurred in 37.5% in class C₂ 14.28% in class B and 0% in class A. Overall, death occurred in 14 patients out of 50 patients (28%). In total, 46 patients out of 50 have Esophageal varix. The most frequent presenting symptoms in different Child-Pugh classes are .....

Congenital intrahepatic portosystemic shunt with invasive hepatocellular carcinoma.

A 60-year-old man with a history of congenital intrahepatic portosystemic shunt (CIPS) presented with acute bilateral lower-extremity edema. There were no stigmata of chronic liver disease. However, mildly abnormal liver function tests and α-fetoprotein 79.1 ng/mL were noted. Subsequent imaging revealed a 8 cm right lobe liver mass, extending into the right hepatic vein into the IVC and right atrium (A,B). An 8 mm side-to-side intrahepatic shunt between the right portal vein and the IVC (C,D – CT; E - US) was confirmed.

N-Acetyl Cysteine to Treat &amp;lt;i&amp;gt;Polygonum multiflorum&amp;lt;/i&amp;gt; Hepatotoxicity: A Case Report

Background: Polygonum multiflorum (brand name Fo-ti) is a Chinese herb used as an antioxidant, antiaging agent, and liver and kidney health. It can cause acute hepatotoxicity and even death. There is no published data on the effectiveness of N-Acetyl cysteine (NAC) as a sole effective therapy. Case: A 23-year-old, healthy male, presented with jaundice and malaise of one-month duration. He had been taking a Chinese herb named Fo-Ti for 2 months. Physical examination revealed jaundice, with no stigmata of chronic liver disease. His laboratory results showed transaminitis with markedly elevated transaminases. Testings for infectious and autoimmune causes were unremarkable. The patient was admitted to the hospital. Fo-Ti was stopped and he was started on oral NAC as peroral protocol. He was discharged home on esomeprazole and oral NAC. He returned on the second day with worsening jaundice. He was readmitted and esomeprazole was discontinued. NAC was continued and his liver enzymes eventually improved. The supplement was tested by gas-chromatography mass spectrometry and measured the presence of emodin. Discussion: This case highlights the potential benefit of NAC as treatment of Polygonum multiflorum induced hepatotoxicity. The proposed mechanism of emodin induced liver injury is through disturbing glutathione metabolism in liver cells. This could explain the favorable response as NAC has the ability to replenish intracellular glutathione. Conclusion: Polygonum multiflorum use has been associated with severe and prolonged hepatotoxicity. Oral NAC should be considered in the treatment of these patients due to the favorable risk-benefit ratio.

S2481 A Case of Sertraline-Induced Hepatotoxicity Correlated With Pharmacogenomic Testing

INTRODUCTION: Sertraline is a commonly used medication for depression and anxiety and is a type of selective serotonin reuptake inhibitor (SSRI). SSRIs are generally well tolerated, but there have been a few reports of drug induced liver injury (DILI) from this exposure. There is no reliable mechanism to predict the risk of DILI from SSRIs. Pharmacogenomic (PGx) testing is a form of genetic testing analyzing alleles of enzymes involved in metabolism. This is a case of Sertraline-induced DILI further correlated by PGx testing. CASE DESCRIPTION/METHODS: A 73 year old woman with fibromyalgia and anxiety presented for evaluation of cholestatic hepatitis. 2 months prior to presentation, she was started on sertraline 75 mg daily for chronic anxiety. 4 weeks after starting the medication, she noticed pruritus and dark urine. The SSRI was discontinued, but she continued to have symptoms. Her physical exam was notable for normal vital signs with a BMI of 20.90 kg/m2, scleral icterus and excoriations but no hepatospenomegaly or stigmata of chronic liver disease. Prior to presentation, she had normal liver function testing. Her labs were notable for total bilirubin 4.7 mg/dL, direct bilirubin 3.1 mg/dL, ALP 509 U/L, AST 280 U/L, ALT 468 U/L, INR 0.9. Viral hepatitis serologies, ANA, ASMA, ceruloplasmin, liver kidney microsomal antibody, SPEP were all unremarkable. MRCP showed no biliary ductal dilation. A liver biopsy was done showing resolving cholestatic hepatitis with no evidence of autoimmune liver disease or fibrosis. Given the slow improvement in enzymes, she was referred for PGx testing. Testing revealed that the patient was an intermediate metabolizer of serotonin with an allelic variation of the SLC6A4 as well as the HTR2A gene. Eventually, her liver enzymes normalized, and she was recommended to avoid SSRIs. DISCUSSION: Sertraline is a rare yet known culprit of DILI. There is no current reliable way of predicting one’s risk of developing DILI from SSRIs. PGx testing showed that she two polymorphisms in sertraline metabolism. SLC6A4 encodes a serotonin transporter and augments the synaptic concentration of the drug. HTR2A changes also are associated with an increase in antidepressant response of higher serotonin levels. This possibly led to increased drug levels and side effects from poor metabolism of SSRIs. With further affordability, PGx testing can be considered prior to starting medications associated with DILI to avoid prescribing it to those who may be higher risk of developing it.

S2718 Harmful Gains: Drug-Induced Liver Injury From Selective Androgen Receptor Modulators

INTRODUCTION: Hepatotoxicity associated with androgenic anabolic steroids (AASs) is well-recognized. Selective androgen receptor modulators (SARMs) such as RAD-140 (Testolone) are a novel class of agents being marketed by some supplement manufacturers as “legal steroids” that carry the advantage of androgen receptor specificity, tissue selectivity and lack of undesired AAS side effects. Data on the association of SARMs with drug-induced liver injury (DILI) is limited. Here, we present a rare case of drug-induced liver due to SARM use. CASE DESCRIPTION/METHODS: A 31-year-old male with asthma presented with 3 days of epigastric pain, jaundice and pruritis. He reported using a SARM supplement (RAD-140) for 12 weeks prior to admission. He denied alcohol use. Vital signs were normal. Physical exam was notable for scleral icterus and jaundice without other stigmata of chronic liver disease. Admission labs showed total bilirubin 8.4 mg/dL (unconjugated 2.1,conjugated), alkaline phosphatase 122 mg/dL, ALT 293 mg/dL, AST 145 mg/dL. Work-up for causes of liver injury including viral hepatitis, Wilson’s disease, hemochromatosis, autoimmune hepatitis and alpha-1-antitrypsin was unremarkable. MRI abdomen showed normal liver parenchyma, patent portal and splenic vasculature, no ductal dilatation or cholelithiasis. The cause of liver injury was thought to be SARM use. His pruritis was treated with cholestyramine. The bilirubin peaked at 20.3 mg/dL on day 15 and trended down on repeat labs 1 month after admission to 15.1 mg/dL. DISCUSSION: Despite FDA-issued public advisories regarding safety concerns associated with SARMs, they continue to be promoted for use particularly as a body building supplement. While the reported tissue selectivity of SARMs can be promising for therapeutic use in hormonal and age-related disorders, this case among others brings the aspect of tissue selectivity into question. Cases of SARM-related DILI are likely underreported and underrecognized. SARMs are thought to activate the intracellular androgen receptor that influences transcription of genes that result in androgen-stimulated cell growth. As such, they are thought to have similar consequences as AAS, which results in three types of liver injury related to augmented cell growth: peliosis hepatis, hepatic tumors and nodular regenerative hyperplasia. As SARM use becomes more prevalent, it is crucial to report these cases for earlier identification and offending agent cessation and for a better understanding of long-term consequences.

S2745 Thinking Outside the Box: Is This Really NASH?

INTRODUCTION: Nonalcoholic steatohepatitis (NASH) is a diagnosis of exclusion and an alternative diagnosis should always be sought. We present a patient with features of portal hypertension and possible sepsis, concerning for decompensated NASH cirrhosis. He was eventually diagnosed with a hemophagocytic syndrome-associated variant of intravascular large B-cell lymphoma on autopsy. CASE DESCRIPTION/METHODS: A 64-year-old Caucasian male with metabolic syndrome presented with a 2-month history of fatigue, fevers, and 20-pound weight loss. Initial work-up was notable for an elevated AST (65 IU/L) and high total bilirubin (2 mg/mL; direct 1.3 mg/mL). Albumin was 3.2 g/dL, INR was 1.0 and platelets were 48,000 cells/mL. CT imaging showed mild hepatosplenomegaly with no ascites. He had no known history of liver disease or alcohol use. He was referred to the liver clinic for possible chronic liver disease and portal hypertension, thought to be from NASH. At the time of presentation, he was febrile (101.8 °F), tachycardic (105 bpm), and hypotensive. Besides hepatosplenomegaly, there were no other stigmata of chronic liver disease on exam. Admission labs were unchanged except an increase in total bilirubin (4 mg/mL) and a high ferritin (2400 ng/ml). Work-up for infectious etiologies, autoimmune liver serologies and drug toxin screen were unrevealing. He met 5 out of 8 criteria to diagnose hemophagocytic lymphohistiocytosis (HLH) including fever, splenomegaly, cytopenia, increased ferritin, and absent NK cell function. A PET scan showed uptake in the bone marrow, liver, spleen and lymph nodes. The patient rapidly declined clinically and died from respiratory failure. Autopsy showed diffuse involvement of the liver, spleen, bone marrow, lymph nodes and several other organs by intravascular large B-cell lymphoma (IVBCL). DISCUSSION: Our case emphasizes the importance of considering a broad differential in patients with thrombocytopenia and hepatosplenomegaly, even if typical risk factors for liver cirrhosis are present. Hematological malignancies should be strongly considered in the differential especially if patients present with B symptoms. Hemophagocytic syndrome-associated variant of IVBCL, the so-called ‘Asian variant’, is a rare and aggressive form of diffuse large B cell lymphoma. A prompt diagnosis is crucial, given its life-threatening potential and possibility of recovery with institution of therapy early in the course of the disease.Figure 1.: The cut sections of the liver looked relatively normal and did not show any gross evidence of cirrhosis.Figure 2.: Histology of the liver, which shows intravascular infiltration of tumor cells.

S3449 OVESCO Clip Can Save Lives - A Success Story of Non-Variceal Upper GI Bleed From a Large Vessel

INTRODUCTION: The most common causes of upper GI bleed are non-variceal. Despite major advances in medical and endoscopic therapies, mortality rate and cost of hospitalization from upper GI bleed are still significant. We report successful use of Over-the-scope clip (OVESCO) in an elderly patient with cardiovascular and other comorbidities presenting with hemodynamically significant upper GI bleed. CASE DESCRIPTION/METHODS: A 79-year-old man with past medical history of CAD s/p CABG, AFib on eliquis, HTN, DM type 2 and CKD stage 3, presented to the ER with black tarry stool for one day and dizziness for one week. Vitals on admission were significant for BP 50/30mmHg and HR 110/min. Abdominal exam was negative for tenderness or stigmata of chronic liver disease. Rectal exam showed black stool. Laboratory findings were significant for Hct 26.2%, Hb 7.4g/dL (baseline ∼ 10), BUN 83mg/dL (baseline ∼ 17), Cr 1.3mg/dL (baseline ∼0.5), platelets 183K and INR 2.5. Elevated INR was attributed to eliquis. Patient was admitted to ICU. Resuscitation was initiated with IV fluids and PRBC transfusions to maintain SBP > 100 and Hb > 8 respectively. Prothrombin complex concentrate was given to normalize INR. Urgent upper endoscopy was done after resuscitation within 24 hours. This showed 5-6mm gastric antral ulcer with a large non-bleeding vessel about 3mm and blood. It was controlled by epinephrine injection around the vessel and OVESCO clip application to completely occlude the vessel and ulcer. Repeat upper endoscopy within 72 hours revealed atrophy of the vessel and absence of rebleed. Patient was restarted on anticoagulant after 72 hours and was discharged home. DISCUSSION: Peptic ulcer disease is the most common cause of NVUGIB. The timing of endoscopy is guided by overall clinical status and type of intervention depends on endoscopic findings. Our patient had high Glasgow Blatchford Score which placed him at high risk for mortality. Urgent upper endoscopy showed a large vessel within an antral ulcer, most likely a branch of the left gastric artery. We thought conventional endoscopic therapy like thermal or standard clips would be insufficient to achieve complete hemostasis and would carry risk of rebleed. Patient was high risk for surgery, therefore epinephrine injection followed by OVESCO clip was chosen to control the bleeding and was successful. To conclude, OVESCO clip should be a part of GI bleed kits in every endoscopy unit. It can be life-saving and spare repeat interventions such as IR therapy or surgery.Figure 1.: Upper endoscopy within 24 hours showing gastric antral ulcer 5–6mm with a large non-bleeding vessel about 3mm and blood.Figure 2.: Upper endoscopy within 24 hours showing OVESCO clip application.Figure 3.: Repeat upper endoscopy within 72 hours showing atrophy of the vessel and absence of rebleed.

S2387 A Case of Terbinafine-Induced Hepatotoxicity: Is There a Role for Routine Monitoring of Liver Enzymes?

INTRODUCTION: Terbinafine (Lamisil), a common treatment for onychomycosis, is infrequently associated with hepatotoxicity. Asymptomatic transaminase elevations occur in < 1% of users with normalization typically occurring after Terbinafine discontinuation. Rare cases of severe hepatic injury requiring transplantation have been reported. While most studies recommend against routine lab monitoring with Terbinafine, the potential seriousness of hepatotoxicity may warrant specific guidelines for testing of liver enzymes during treatment. We report an unusual case of Terbinafine-induced liver injury. CASE DESCRIPTION/METHODS: A 28-year-old male without previously diagnosed medical conditions presented with jaundice, dark colored urine, and itching of his abdomen, back, palms, and soles. He had been on Terbinafine 250 mg once a day for onychomycosis for 45 days. His pre-treatment liver function tests were normal. He occasionally used Ibuprofen. He denied other medications, herbal products and health supplements. He denied alcohol, tobacco and recreational drug use. His exam was notable for jaundice with no stigmata of chronic liver disease. Labs included a normal CBC, elevated liver enzymes [AST 189 U/L, ALT 526 U/L, bilirubin 4.7 mg/dL (direct 1.8), alkaline phosphatase 238 U/L]. Viral serologies were negative for HAV IgM, HBsAg, HBV DNA, HCV Ab, HCV RNA and HEV IgM. Anti-nuclear antibody, anti-smooth muscle antibody, and anti-mitochondrial antibody were also negative. Ceruloplasmin and ferritin were normal. An abdominal ultrasound was negative for biliary obstruction. After exclusion of other causes of liver injury, a diagnosis of drug-induced liver injury due to Terbinafine was made. Terbinafine was stopped and his liver function tests have persistently improved. DISCUSSION: Hepatic injury from Terbinafine can be hepatocellular, cholestatic, or both. While abnormalities are generally reversible upon discontinuation, prolonged cholestasis and hepatic failure requiring transplantation have been reported. The mechanism causing injury, while incompletely understood, has been hypothesized to result from binding of an allylic aldehyde metabolite to hepatobiliary proteins causing direct toxicity or altering canalicular proteins leading to immune-mediated cholestasis. It is necessary that all clinicians are aware of the potential for severe hepatic injury from Terbinafine. Further studies are needed to determine when monitoring of liver enzymes should be performed during Terbinafine treatment.

A STICKY SITUATION

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Patients with cirrhosis regularly undergo endoscopy for management of portal hypertensive complications. Little is known about the pulmonary complications of such procedures. Here, we present an acute pulmonary complication post gastric variceal gluing. CASE PRESENTATION: A 61-year-old female with type 2 diabetes, hypertension, and Child Pugh A cirrhosis secondary to non-alcoholic steatohepatitis presented with a two-day history of right-sided shoulder and sub-diaphragmatic pain, 3 days after elective injection of a gastric varix with Glubran and Lipidol. She described the pain as being sharp and pleuritic. She denied shortness of breath, hemoptysis, or constitutional symptoms. She had a temperature of 36.7 degrees Celsius, heart rate of 83 beats/min, blood pressure of 136/81, respiratory rate of 18/min, and an oxygen saturation of 91% on room air. Her physical exam was unremarkable. She was tender to palpation of the right sub-diaphragmatic area. Stigmata of chronic liver disease were not noted. Her investigations revealed normal electrolytes, creatinine, hemoglobin and white blood cell count. Her platelets were 111, INR 1.2, ALT 27 U/L, Bilirubin 38 umol/L, GGT 43 U/L, and the D-dimer was 1.82 mg/L. Her chest x-ray showed several new nodular densities in both lungs. Computed tomography pulmonary angiogram reported diffuse pulmonary arterial calcification; it was later addended to reveal a large caliber variceal gastrorenal shunt and high density filling defects consistent with severe burden of embolized glue throughout the segmental and subsegmental pulmonary vasculature bilaterally. DISCUSSION: The use of glue is commonly used in endoscopic therapeutics to prevent and treat gastrointestinal bleeding [1,2]. It has an associated 0.5%-4.3% risk of embolization [1], which can result in cardiopulmonary collapse [2]. Embolization is believed to occur through travel through gastrorenal and splenorenal veins into the inferior vena cava, with eventual deposition into the pulmonary circulation [2]. Large, high-flow portosystemic shunts and glue injections of more than 1 mL are predicted risk factors for pulmonary embolization [3]. The differential diagnosis for our patient included septic emboli, pulmonary embolus, malignancy, or pulmonary hypertension associated with vessel calcification. Initial management included administration of Cefazolin for a possible infection, followed by watchful waiting as the patient was hemodynamically stable. A secondary review of her imaging by Radiology further confirmed the findings of embolized glue. CONCLUSIONS: Pulmonary embolization of glue is an uncommon endoscopic complication of variceal treatment that has been linked to complications such as cardiopulmonary collapse and septic emboli [2]. It is important that clinicians keep this on the differential diagnosis when evaluating patients with chest pain or hemodynamic instability after gluing of varices. Reference #1: Al-Hillawi L, Wong T, Tritto G, Berry PA. Pitfalls in histoacryl glue injection therapy for oesophageal, gastric and ectopic varices: A review. World J Gastrointest Surg. 2016;8(11):729–734. doi:10.4240/wjgs.v8.i11.729 Reference #2: Hameed F, Pepperell J, Sidney J. A rare complication of endoscopic intervention. Breathe. 2018;14(2):e40-e42. doi:10.1183/20734735.019017 Reference #3: Jindal A, Philips CA. Pulmonary Glue Embolization after Endoscopic Treatment of Bleeding Sigmoid Colon Varices. ACG Case Rep J. 2017;4:e52. Published 2017 Apr 12. doi:10.14309/crj.2017.52 DISCLOSURES: No relevant relationships by Jennifer Landry, source=Web Response No relevant relationships by Dana Saleh, source=Web Response

A 14-year-old boy presenting with gradual abdominal distension and occasional abdominal pain for 2 years

This article has no abstract. The first 100 words appear below:&#x0D; A 14-year-old boy, 4th issue of his non-consanguineous parents got admitted in the Department with the complaints of gradual abdominal distension and occasional abdominal pain since two years of his age. There was no history of jaundice, upper gastrointestinal bleeding, fever, contact with a known case of tuberculosis patient or family history of such type of illness. On examination, he was alert, anicteric, no facial dysmorphism, vitally stable, no stigmata of chronic liver disease and anthropometrically well thrived.

Evaluation of the Sabadell noninvasive hepatitis C-related cirrhosis early detection index and right lobe diameter to albumin ratio in the prediction of presence of varices in Egyptian cirrhotic patients

IntroductionPortal hypertension in cirrhosis results from progressive fibrotic remodeling of the liver, which increases the resistance to hepatic sinusoidal blood flow. Increased portal venous pressure causes esophageal and gastric varices, which contribute substantially to cirrhosis-related morbidity and mortality. The gold standard in the diagnosis of varices is esophagogastroduodenoscopy, but identification of noninvasive predictors of esophageal varices (OVs) will allow upper gastrointestinal tract endoscopy to be carried out only in a selected group of patients. Different noninvasive parameters including clinical, laboratory, and sonographic predictors are an alternative approach to perform selective screening endoscopy only in patients at high risk.ObjectiveOur objective is to evaluate whether the noninvasive hepatitis C-related cirrhosis early detection (NIHCED) score and the right lobe diameter to albumin ratio can predict the presence of OVs in a group of Egyptian cirrhotic patients.Patients and methodsSeventy-five patients with liver cirrhosis were enrolled in the study depending on the clinical evidence of stigmata of chronic liver disease (e.g. jaundice, ascites, palmar erythema, spider naevi, etc.) and ultrasonographic features of liver cirrhosis (e.g. coarse echo texture, shrunken liver, etc.).ResultsAccording to the esophagogastroduodenoscopy results, the patients were categorized into two groups: those with OVs (47 patients, 63%) and those without OVs (28 patients, 37%).Receiver operating characteristic curve analysis of the NIHCED score was applied to both groups with a cutoff score of more than 45. The estimation cohort study had a sensitivity of 70%, specificity of 78%, and diagnostic accuracy of 74% with an area under the receiver operating characteristic curve of 0.77 (95% confidence interval, 0.66–0.86).Receiver operating characteristic curve analysis of the right lobe diameter to albumin ratio was applied to both groups with a cutoff score of more than 2.80. The estimation cohort study had a sensitivity of 80%, specificity of 53%, and diagnostic accuracy of 67% with an area under the receiver operating characteristic curve of 0.67 (95% confidence interval, 0.55–0.77).ConclusionThe NIHCED score and right lobe diameter to albumin ratio are simple noninvasive predictors of the presence of varices in Egyptian patients with liver cirrhosis.