Decompensated Liver Failure Research Articles

S1674 In-Hospital Outcomes in Acute Decompensated Liver Failure Patients With and Without Systemic Lupus Erythematosus: A Three-Year Retrospective Review

S1674 In-Hospital Outcomes in Acute Decompensated Liver Failure Patients With and Without Systemic Lupus Erythematosus: A Three-Year Retrospective Review

Abstract PO5-20-08: A Case of Multifocal Ductal Breast Carcinoma with Extension into Lobules and Concurrent Primary Colon Adenocarcinoma

Abstract Background Multifocal (MF) multicentric breast cancer is a form of breast cancer that consists of disease independently developing at various locations due to a tumor clone spreading within the ductal complex. Multifocal breast cancer is associated with increased local recurrence. Our case highlights an example of multifocal breast cancer and addresses treatment challenges. Case presentation The patient is a 52-year-old African American female with a history of HCV cirrhosis, diabetes mellitus, and hypertension who presented with a palpable 4 cm right breast mass, without adenopathy, clinically Stage II, T2N0. Mammogram revealed a 2.5 cm right breast mass and three right level 1 axillary nodes with biopsy confirming invasive ductal carcinoma with extension into the lobules, ER positive (3%)/PR-/HER2-, Ki-67 95%. Neoadjuvant paclitaxel, carboplatin, and pembrolizumab was initiated but she incurred complications of decompensated liver cirrhosis after the second cycle and treatment was held. After 2 cycles her tumor was not palpable, and surgery was recommended, but due to COVID infection and concurrent decompensated liver failure surgery management was delayed. She underwent staged surgery with partial mastectomy without lymph node exploration. Histopathology showed DCIS grade 3 with extension into lobules and invasive ductal carcinoma with no lymphovascular invasion and all margins were negative, pathological stage ypT3NxM0. Immunohistochemistry demonstrated partial ER+ (50%)/PR-/HER2-, Ki-67 80%. She was given 4 cycles of adjuvant cyclophosphamide, adriamycin, pembrolizumab and continued on maintenance pembrolizumab. The patient was found with anemia out of proportion to chemotherapy and underwent colonoscopy that showed a colonic mass. Biopsy showed a primary moderately differentiated colonic adenocarcinoma. Her re-excision with new margins for partial mastectomy had negative margins, and 2 negative sentinel lymph nodes for ypN0. Genetic testing was negative. She continued on adjuvant immunotherapy with pembrolizumab for breast cancer. She is planned to start on adjuvant anastrozole. Patient has completed adjuvant radiation treatment and has no new complaints. She is pending curative intent completion colectomy for colon cancer. Discussion This case of MF breast cancer is significant, as one foci was ER negative, which responded to neoadjuvant chemoimmunotherapy and other ER positive that did not respond to treatment and was surgically excised. The pathology report from the surgical specimen revealed DCIS with extension into the lobules. Due to her tenuous clinical condition, she had staged surgeries for breast cancer, and now colon cancer. Genetic testing is negative. Currently, there is insufficient data to suggest which surgical approach is preferred in MF breast cancer. Based on the literature, breast conservation therapy (BCT) is a feasible option and is oncologically safe. Due to the patients’ medical condition and infections, it was felt a less invasive surgery could offer cure and minimize complications. Our patient underwent neoadjuvant chemoimmunotherapy, followed by partial mastectomy, adjuvant chemoimmunotherapy, second staged completion breast surgery, radiation therapy, and anti-estrogen therapy. MF breast cancer is associated with increased lymph node involvement. A 2022 meta-analysis found that multifocal and multicentric breast cancer has a slightly increased risk of death as compared to unifocal tumors. Lastly, our patient is African American, and multifocal tumors occur with a higher incidence in African Americans (43.4%) and Asian patients (37%) as compared to whites (28.9%). This case of breast cancer highlights treatment challenges in a case of multifocal multicentric breast cancer occurring concurrently with a secondary primary colonic cancer. Citation Format: Rabab Jafry, Hina Khan, Jessica Jones. A Case of Multifocal Ductal Breast Carcinoma with Extension into Lobules and Concurrent Primary Colon Adenocarcinoma [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-20-08.

Myostatin as a Prognostic Biomarker in Hepatic Cirrhosis Patients with Sarcopenia

Cirrhosis represents the advanced stage of numerous chronic liver conditions. Sarcopenia is a frequently overlooked complication in cirrhotic patients, resulting from factors such as insufficient protein intake, malabsorption, diminished muscle growth, and increased muscle breakdown. Sarcopenia is a multifaceted, chronic condition associated with elevated risks of morbidity and mortality. In the field of hepatology, sarcopenia is typically described as a phenotypic indication of muscle mass loss, affecting approximately 30-70% of liver cirrhosis patients. Sarcopenia has been scientifically linked to an increased risk of falls, reduced quality of life, the emergence of acute decompensated liver failure, and mortality in cirrhotic patients. Myostatin, classified as a cytokine within the transforming growth factor beta (TGF-β) family, is recognized for its role in disrupting protein synthesis. It functions as a negative regulator of muscle growth, inhibiting myogenesisand is linked to the onset of sarcopenia. Extensive literature supports the prognostic importance of sarcopenia in cirrhosis, and serum myostatin levels have the potential to serve as a valuable biomarker. Elevated myostatin concentrations have been linked to the presence of sarcopenia and decreased survival rates in individuals diagnosed with liver cirrhosis.

Viral hepatitis is associated with increased risk of decompensated cirrhosis or liver failure in patients positive for liver cytosol antibody type 1.

Liver cytosol antibody type 1 (anti-LC1) is reported to be a marker of type 2 autoimmune hepatitis (AIH), a type of autoimmune liver disease (AILD). However, anti-LC1 is not entirely disease-specific, and its clinical value in other hepatic diseases has not been well elucidated. Our study aimed to explore the associations between the diagnoses and outcome of decompensated cirrhosis or liver failure (DC/LF) in patients positive for anti-LC1. A total of 157 patients positive for anti-LC1 were included in our final analysis. DC/LF was defined as the outcome of patients positive for anti-LC1. The risk of DC/LF according to diagnosis was estimated using multivariable Cox proportional hazards models, while stratified Cox regression models were used in the subgroup analyses. The diagnoses of patients positive for anti-LC1 were found to be comprised of various liver disorders. Versus other diagnoses, viral hepatitis was associated with a 2.25-fold increased risk of DC/LF in these patients, independent of sex, age, disease course, treatment and drinking history. Additionally, the associations were more significant by subgroup analysis in male patients, younger patients, non-newly diagnosed patients, patients without treatment and patients without drinking history. Anti-LC1 is not a disease-specific antibody, as it was found in multiple types of hepatic disease. Furthermore, viral hepatitis rather than AILD was associated with an increased risk of DC/LF in patients positive for anti-LC1. These findings emphasize the important role of viral hepatitis in the progression of DC/LF in patients positive for anti-LC1.

Risk factors, clinical characteristics, and treatment outcomes for hepatocellular carcinoma in Rwanda.

e16339 Background: Hepatocellular carcinoma (HCC) is increasing worldwide with limited treatment options, a poor prognosis, and survival rates of less than 5 years. In Sub-Saharan Africa, over 46,000 new cases are reported every year, and HCC is commonly associated with alcohol consumption, viral hepatitis, especially Hepatitis B (HBV) and C (HCV), aflatoxin exposure, obesity, type II diabetes, and HIV infection. In Rwanda, often young people are diagnosed with HCC in the late stages of the disease, and treatment options are limited. Rwanda has made great achievements in the prevention and treatment of HBV and HCV. However, there is a lack of data on HCC in Rwanda and its associated risk factors. In this study, we report the prevalence of common risk factors, available treatment options, and treatment outcomes among patients with HCC in Rwanda. Methods: This was a retrospective study of patients aged 18 years of age and above diagnosed with HCC from 2016 to 2021 in three tertiary hospitals: University Teaching Hospital of Kigali, King Faisal Hospital, and Rwanda Military Hospitals. Data were abstracted from patients’ paper charts and electronic medical records and recorded in REDCap and analyzed in STATA. Results: Overall, 219 individuals were included in the study. 32.9% were female, the median age was 32 (26–54) years, and 48.4% came from the capital city of Kigali. Only 13.3% of patients had histo-pathological confirmation of HCC, while 86.7 % were diagnosed clinically with radiological images, alpha-fetoprotein, and other clinical findings. The most common risk factors were HCV and HBV infection with a prevalence of 27.4% and 20.1%, respectively. HIV infection and diabetes mellitus were present in 6.9% and 6.2% of patients, respectively. More than 80% of patients had had clinical or ultrasound evidence of cirrhosis, including ascites or hepatic encephalopathy and only 8.9% of patients received Sorafenib, and no patient had surgical resection, ablation, or liver transplant. Only 15.1% of patients received palliative care with opiate therapy. Among all patient diagnosed with HCC, 36% died within 3 months of diagnosis. Conclusions: In this retrospective study of the three largest treatment centers in Rwanda, the majority of HCC cases occurred at a young age with a high rate of mortality. HBV and HCV were the most frequent risk factors, and the majority of patients had clinical characteristics of decompensated liver failure. There is a clear lack of diagnostic tools, most glaringly pathologic diagnosis, and an extreme lack of treatment options. Increased awareness for HBV and HCV prevention and screening as well as further studies on etiology of HCC cases and management are needed.

Living related liver transplantation in the Republic of Uzbekistan: current status and development prospects

To analyze primary results of living related liver transplantation in the Republic of Uzbekistan. There were 44 living related transplantations of the right liver lobe in patients with decompensated liver failure between February 2018 and February 2023. Uneventful postoperative period was observed in 17 (38.6%) recipients. Other 27 patients (61.4%) developed 47 various postoperative complications (1-3 events per a patient). Of these, 8 (18.2%) patients required early postoperative re-laparotomy. Among 44 patients, 9 (20.5%) ones died in early postoperative period, and one patient died in long-term period (3 years after transplantation) from chronic rejection under refusal to take immunosuppressive drugs. Early satisfactory results were obtained in 79.5% of patients, long-term favorable outcomes - in 77.3% of cases. Engraftment rates and survival of recipients to a large extent depend on surgical strategy, baseline disease and clinical severity. The so-called "center effect" is essential at initial stages of implementation of the program.

S3255 A Novel Mutation in ATP7B Gene: A Rare Manifestation of Wilson’s Disease With Liver Failure

Introduction: Wilson’s disease (WD) is a rare genetic condition characterized by excess copper build. Due to the presence of several genotypic and phenotypic variances; diagnosis can be challenging. We report a case of acute liver failure due to a novel ATP7B gene mutation, which has never been reported before. Case Description/Methods: A 16-year-old previously healthy male presented to the hospital with abdominal pain, nausea and vomiting for 3 days. Family history was significant for a sister who passed away due to “hepatitis”, he denied using alcohol or Tylenol; of note, parents immigrated from Honduras. On examination he was hemodynamically stable, jaundiced with marked scleral icterus, furthermore he was also lethargic and somnolent. His labs showed acute liver failure and acute kidney injury. Further workup included genetic testing with, alpha 1-antitrypsin, copper, ceruloplasmin and iron studies. Serum toxicology was negative. Infectious and autoimmune work-up was performed including ANA, anti-smooth muscle antibody; EBV, HSV, CMV, Hepatitis panel, VZV serologies; total IgG and subclasses, IgA, IgM, soluble IL-2, and Treponema Cruzi, which all came back negative other than low ceruloplasmin 6.0 mg/dL, and high 24hr urine copper excretion. Patient was diagnosed with decompensated liver failure due to Wilson’s disease and thus was listed for liver transplant at MELD-Na of 41. He later underwent orthotopic liver transplant. Of note, his detailed genetic studies with whole exome sequencing (WES) identified, two likely pathogenic ATP7B variants (c.3446G >C & c.2355G >A) (see Table-1). Postoperatively, he improved considerably. Moreover, patient and his entire family were also seen by genetic counselor once he was discharged home. Discussion: Wilson's disease is an autosomal recessive disease involving ATP7B gene, responsible for copper metabolism. Around 1019 mutations for ATP7B gene have been reported in literature. In our patient, p.(G1149A) variant was inherited from his father and has been reported before, however p.(K785=) variant has been unreported. This mutation alters the last nucleotide of the exon and causes aberrant splicing (see Figure-1). The fact that our patient exclusively had liver failure without any other organ system involvement in the setting of a novel mutation makes it a unique case for gastroenterologists for timely diagnosis and management of WD. Early treatment with copper chelators and zinc salts can not only halt the disease progression but may also prevent end organ damage.Figure 1.: A diagrammatic representation of mutated splicing site. Splicing is a process whereby introns (non-coding part) of mRNA are removed allowing for joining of exons (coding part of mRNA) resulting in mature mRNA which is then used for protein synthesis. The p.(K785=) mutation in ATP7B gene destroys the splicing donor site affecting downstream protein production leading to a dysfunctional copper metabolism. Table 1. - Causative Variant(s) in Disease Genes Associated with Reported Phenotype Gene Disease Mode of Inheritance Variant Zygosity Inherited Form Classification ATP7B ATP7B-related Wilson disease Autosomal c.3446 G >C Heterozygous Father Likely Pathogenic Recessive p.(G1149A) Variant ATP7B ATP7B-related Wilson disease Autosomal c.2355 G >A Heterozygous Unknown Likely Pathogenic Recessive p.(K785=) Variant

Dysregulation of S-adenosylmethionine Metabolism in Nonalcoholic Steatohepatitis Leads to Polyamine Flux and Oxidative Stress.

Nonalcoholic fatty liver disease (NAFLD) is the number one cause of chronic liver disease worldwide, with 25% of these patients developing nonalcoholic steatohepatitis (NASH). NASH significantly increases the risk of cirrhosis and decompensated liver failure. Past studies in rodent models have shown that glycine-N-methyltransferase (GNMT) knockout results in rapid steatosis, fibrosis, and hepatocellular carcinoma progression. However, the attenuation of GNMT in subjects with NASH and the molecular basis for its impact on the disease process is still unclear. To address this knowledge gap, we show the reduction of GNMT protein levels in the liver of NASH subjects compared to healthy controls. To gain insight into the impact of decreased GNMT in the disease process, we performed global label-free proteome studies on the livers from a murine modified amylin diet-based model of NASH. Histological and molecular characterization of the animal model demonstrate a high resemblance to human disease. We found that a reduction of GNMT leads to a significant increase in S-adenosylmethionine (AdoMet), an essential metabolite for transmethylation reactions and a substrate for polyamine synthesis. Further targeted proteomic and metabolomic studies demonstrated a decrease in GNMT transmethylation, increased flux through the polyamine pathway, and increased oxidative stress production contributing to NASH pathogenesis.

Liver Transplantation in Malaysia: Needs, Obstacles, and Opportunities.

Liver Transplantation in Malaysia: Needs, Obstacles, and Opportunities.

S3659 Elevated Bilirubin Levels in Decompensated Liver Failure Causing a Confounding Effect on Acetaminophen Level

Introduction: Decompensated liver cirrhosis is a common reason for admission to the hospital that is associated with a high risk for mortality. Common causes of decompensated liver disease are hepatic infections, toxin-induced hepatotoxicity (ie, acetaminophen), or alcohol-related hepatitis. Here, we describe a young patient with acute decompensated liver failure secondary to alcohol abuse that presented with ascites, elevated bilirubin levels, ammonia levels, and hepatic coagulopathy. Case Description/Methods: A 32-year-old female with an extensive history of alcohol abuse and alcoholic liver cirrhosis presented to the emergency department with a three-week history of intermittent fevers, abdominal pain and abdominal distension. The patient stated that she drank nips of vodka 1-2/week. The patient had been diagnosed with liver cirrhosis by biopsy in January 2020. Upon admission, the patient was alert and oriented with stable vitals and significantly jaundiced. Labs were sent which were consistent with decompensated liver failure. The patient was found to have a bilirubin of 41. Alkaline phosphate of 285, and alcoholic transaminitis. Coagulation studies showed increased bleeding risk. Ammonia levels during admission were elevated and trended up. Hepatitis panel was sent which was negative. Acetaminophen levels were sent for which showed elevation to 16.7. Patient was started on NAC protocol for acetaminophen toxicity. Poison control was consulted and stated that elevated bilirubin levels may confound acetaminophen levels, creating a false positive. During her hospital course, the patient was started on lactulose for elevated ammonia levels, which down trended. She was placed on ceftriaxone for spontaneous bacterial peritonitis prophylaxis and was transferred to a larger center for further evaluation. Discussion: In patients who present with liver failure, a cause must be determined. Some potential etiologies of liver failure include alcohol, drug-toxicity including acetaminophen, toxins, or viral hepatitis. Panels and toxin levels are sent to direct the type of care. Due to acetaminophen toxicity being one of the most common cause of acute liver failure, empiric therapy with NAC is often started with elevated levels which has been shown to improve outcomes. In this case, the patient had known liver cirrhosis secondary to alcohol abuse, but NAC therapy was initiated due to elevated acetaminophen levels. It is important to keep in mind that levels can be erroneously elevated due to confounding factors.

S3303 Outcomes of Gastrointestinal Bleeding During the COVID-19 Pandemic

Introduction: The novel circumstances during the pandemic have led to many challenges for clinicians and patients, including cancellation of procedures, policy regulations and the reluctance of patients to seek medical attention, potentially leading to adverse outcomes. Patients with gastrointestinal bleeding (GIB) require early resuscitation and possible intervention. The aim of this study was to investigate differences in the outcomes of hospitalized patients who encountered GIB during the initial peak of Coronavirus 2019 (COVID-19) pandemic in March 2020, compared to the year prior. Methods: In this retrospective cohort study, patients with GIB who presented to our institution during the first two weeks of March 2019 and 2020 were identified using ICD-10 codes for GIB. The diagnosis of GIB was confirmed based on assessment of hemoglobin (Hb), diagnostic imaging, endoscopy or clinical evidence of gross hemorrhage. Analysis was conducted with the Welch T-test and Pearson's chi-square test utilizing R 4.1.0. Results: We identified 89 patients with GIB in 2019 and 76 in 2020. Of the 2020 cohort, 88.2% tested positive for COVID-19. Compared with 2019, patients in 2020 were significantly older (years) (62.1 vs 68.3, P < 0.01), required longer hospital length of stay (days) (11.3 vs 20.9, P < 0.01), had higher rate of mortality (12.5% vs 36%, P < 0.01), were less likely to have history of cirrhosis (25.8% vs 6.6%, P < 0.01), presented with a higher Hb (mL/dL) (9.9 vs 11.9, P < 0.001), were less likely to undergo EGD (58.4% vs 13.2%, P < 0.001), or colonoscopy (21.6% vs 4 %, P < 0.01). There was no significant difference between baseline Hb or nadir Hb, P >0.05. The most common primary causes of death in 2019 were decompensated liver failure (27.3%), followed by septic shock (18%) and cardiogenic shock (18%), compared to 2020 deaths, which were COVID-19 respiratory failure (67.9%), hemorrhagic shock (11.1%) and cardiogenic shock (7%). Conclusion: Despite presenting with higher Hb on admission, patients during the COVID-19 pandemic had a higher rate of mortality. The most common cause of death was respiratory failure secondary to COVID-19. Our results also suggested patients with GIB were less likely to undergo endoscopic evaluation during the pandemic. Given the limitations of our study, it’s difficult to say whether this was due to strict COVID-19 isolation precautions, cardiopulmonary instability making endoscopy high risk, or clinical assessment suggesting GIB was not the primary cause of patient decline.Table 1.: Primary causes of death in year 2019 and 2020.

S2740 A Rare Case of Acute Decompensated Liver Failure in a Patient With Marchiafava Bignami Disease Associated With Poor Outcome

S2740 A Rare Case of Acute Decompensated Liver Failure in a Patient With Marchiafava Bignami Disease Associated With Poor Outcome

The Use of Extracorporeal Liver Support Systems In Acute Decompensated Liver Failure

The aim of the study: to evaluate the efficacy of extracorporeal liver support systems in patients with acute liver failure of various etiologies.Material and methods. The study included 117 patients with acute liver failure of various etiologies. The main group consisted of 71 patients who received complex intensive therapy, including MARS-therapy and hemodiafiltration. The comparison group included 46 patients who received albumin dialysis (24 patients) and hemodiafiltration (22 patients) alone. The mean age of the patients was 34±5.6 years, the majority (56.4%) were men. Dynamic assessment of patients' severity was performed using Sequential Organ Failure Assessment (SOFA) and Model for End-Stage Liver Disease (MELD) scales.Results. A more significant reduction of SOFA and MELD scores was noted as early as by day 10 of intensive therapy in the main group with sequential use of extracorporeal liver detoxification methods — to 2.7±0.2 vs. 8.3±0.5 points (P=0.021) on SOFA and to 16.7±0.4 vs. 23.4±1.4 points (P=0.023) MELD scales. The use of a comprehensive approach to extracorporeal detoxification in acute decompensated liver failure increased the regression rate of multiple organ failure from 51.2 to 74.6% and reduced mortality from 47.8 to 25.4% (χ2=6.266; df=1; P=0.013). At the same time, the cumulative proportion of survivors depending on the type of complication within 30 days was 88.4% in the main group and 69.0% in the comparison group (χ2=4.164; df=1; P=0.042).Conclusion. A comprehensive approach to extracorporeal detoxification is highly effective, providing a more significant reduction of SOFA and MELD scores, increasing the proportion of regression of multiple organ dysfunction and reducing mortality.

Hepatocyte Nuclear Factor 4 alpha 2 Messenger RNA Reprograms Liver-Enriched Transcription Factors and Functional Proteins in End-Stage Cirrhotic Human Hepatocytes.

The only definitive therapy for end‐stage liver disease is whole‐organ transplantation. The success of this intervention is severely limited by the complexity of the surgery, the cost of patient care, the need for long‐term immunosuppression, and the shortage of donor organs. In rodents and humans, end‐stage degeneration of hepatocyte function is associated with disruption of the liver‐specific transcriptional network and a nearly complete loss of promoter P1‐driven hepatocyte nuclear factor 4‐alpha (P1‐HNF4α) activity. Re‐expression of HNF4α2, the predominant P1‐HNF4α, reinstates the transcriptional network, normalizes the genes important for hepatocyte function, and reverses liver failure in rodents. In this study, we tested the effectiveness of supplementary expression of human HNF4α2 messenger RNA (mRNA) in primary human hepatocytes isolated from explanted livers of patients who underwent transplant for end‐stage irreversibly decompensated liver failure (Child‐Pugh B, C) resulting from alcohol‐mediated cirrhosis and nonalcoholic steatohepatitis. Re‐expression of HNF4α2 in decompensated cirrhotic human hepatocytes corrects the disrupted transcriptional network and normalizes the expression of genes important for hepatocyte function, improving liver‐specific protein expression. End‐stage liver disease in humans is associated with both loss of P1‐HNF4α expression and failure of its localization to the nucleus. We found that while HNF4α2 re‐expression increased the amount of P1‐HNF4α protein in hepatocytes, it did not alter the ability of hepatocytes to localize P1‐HNF4α to their nuclei. Conclusion: Re‐expression of HNF4α2 mRNA in livers of patients with end‐stage disease may be an effective therapy for terminal liver failure that would circumvent the need for organ transplantation. The efficacy of this strategy may be enhanced by discovering the cause for loss of nuclear P1‐HNF4α localization in end‐stage cirrhosis, a process not found in rodent studies.

Fatal acute hepatic failure secondary to thrombotic portal venopathy after commencing abemaciclib and fulvestrant treatment for advanced breast carcinoma: a unique autopsy finding.

We present an autopsy case of hepatic thrombotic portal venopathy resulting in decompensated liver failure and death which occurred rapidly after commencing abemaciclib and fulvestrant chemotherapy for advanced invasive lobular carcinoma of the breast. The diagnosis was confirmed histologically. This is the first reported case of such a finding. We suggest that further cases displaying this previously unpublished pattern are collated in order that we may begin to investigate the underlying etiological mediators.

Progress in basic and clinical and clinical research of a cell therapy for end-stage liver disease

Clinically, the incidence of end-stage liver disease including decompensated cirrhosis and liver failure is high, which seriously threatens people's health. The existing comprehensive internal medicine treatment is ineffective, and liver transplantation is still the most effective treatment method. However, the shortage of matching liver donors and other reasons constrain the development of liver transplantation, thus limiting the treatment of patients with end-stage liver disease. In recent years, domestic and foreign scholars have conducted many pre-clinical and clinical trials using a variety of cells, and have achieved certain results, providing a new method for the treatment of end-stage liver disease. This article reviews and discusses the existing problems, research status and application progress of varieties of cell therapy for end-stage liver diseases.

Acute exacerbation of hepatitis B with hepatic failure during the first trimester of pregnancy: Delivery of a healthy term baby after liver transplantation

The severe form of acute exacerbation of hepatitis B during pregnancy is a rare but life-threatening condition for both the mother and the fetus. A 32-year-old pregnant woman at 10weeks of gestation was diagnosed with acute decompensated liver failure due to acute exacerbation of hepatitis B. The Model for End-stage Liver Disease score was up to 37. The patient was managed carefully with antiviral treatment, fluid resuscitation, correction of coagulopathy, close monitoring of hepatic function, and regular assessment of the fetus. She was transplanted with a deceased liver at 14weeks and 1day of gestation. With careful post-transplant care and avoidance of medication with risk of miscarriage and teratogenicity, a healthy baby was delivered at 39weeks and 1day of gestation. Herein, we report this critical condition of pregnancy that was complicated with liver failure due to acute exacerbation of hepatitis B, but had favorable outcomes for both the mother and the baby after liver transplantation.

Spontaneous Spinal Epidural Hematoma due to Anticoagulant Therapy: A Case Report and Literature Review

Aims: We report a case of spontaneous spinal epidural hematoma (SSEH) that occurred in a patient on life-long warfarin following liver transplant due to decompensated liver failure secondary to primary Budd-Chiari syndrome. Patients and Methods: Our patient presented with acute central back pain with bilateral lower limb paralysis and incontinence with neurological level of T8 American Spinal Injury Association Impairment Scale (AIS) A. There were no history of fever, trauma or straining. MRI revealed a hyper-intense lesion at level of T8 till T10 and patient underwent an urgent laminectomy which revealed an epidural hematoma at that level. Result: Post-operatively, patient gradually improved with final neurology level at level of T9 AIS D prior to discharge. Conclusion: A prompt diagnosis and intervention are needed in cases of SSEH to achieve a favourable outcome.

P230 Pulmonary embolism due to hepatocellular carcinoma: A rare presentation

Abstract Introduction Hepatocellular carcinoma (HCC) is one of the most common malignant tumors and the second leading cause of cancer-related deaths. HCC is a highly progressive cancer with a high rate of metastasis. Intra-cardiac involvement with HCC is quite rare with a very poor prognosis. Acute pulmonary embolism is a very rare presentation of hepatocellular carcinoma (HCC) complicated with tumor thrombi into the inferior vena cava (IVC), right atrium (RA) and right ventricle (RV) with very poor reported prognosis. Case presentation A 72-years old hepatitis C virus (HCV) positive male patient for 20 years but he didn’t receive any treatment. He was admitted at our medical faculty with decompensated liver failure and resolved hepatic encephalopathy. He started complaining of acute onset of dyspnea. On clinical examination, he was tachypneic, tachycardic with thready pulse, distressed with deep icteric tinge. He had a massive ascites and bilateral lower limb pitting oedema. His electrocardiogram (ECG) showed sinus tachycardia. Urgent transthoracic echocardiography (TTE) revealed a large solid mass extending through the IVC to RA (Figure 1 Panel A) with another highly mobile cauliflower mass at the RV apex occupying the RV cavity, protruding into RA through TV and nearly obliterating RVOT into pulmonary artery. (Figure 1 Panel B, C, D). Due to patient’s frailty and hazards of contrast medium in an already impaired renal status of him, no further contrast study was performed. Only conservative and supportive measures were initiated for the management of his deteriorated general condition but unfortunately, he passed away shortly after. Conclusion Cardiac involvement in HCC rarely occurs and usually develops in advanced stages of HCC. The main mechanism of metastasis into the cardiac cavity is through a direct vascular extension of the tumor to the right side via hepatic vein and IVC. Acute pulmonary embolism in the setting of HCC is a quite rare manifestation of HCC that usually occur due to tumor thrombi in the IVC, RA and RV. The reported prognosis of HCC with intra-cardiac involvement is very poor, with a mean survival of 1 to 4 months at the time of diagnosis. Abstract P230 Figure. TTE of HCC invading RVOT

2480 Nivolumab-Induced Hepatitis and Vesiculopustular Skin Rash in a Patient With Metastatic Melanoma

INTRODUCTION: The advent of immunotherapy has been hailed as a breakthrough in cancer treatment. However, it comes with a multitude of immune mediated adverse effects. Gastrointestinal adverse effects include hepatitis and colitis. Immunotherapy related hepatitis can range from asymptomatic elevation of liver enzymes (grade 1) to decompensated liver failure (grade 4). CASE DESCRIPTION/METHODS: 82 years old male with stage IIC Malignant Melanoma of right posterior diagnosed in 2014, treated with wide excision. In December 2016, PET scan revealed right chest wall lesion, treated with re-excision. c-kit and BRAF were negative. In June 2017, PET scan showed metastatic disease involving lung, pancreas, gluteus maximus and left flank. The patient was started on Nivolumab. After 7 cycles, the PET scan became negative for any metastatic lesions. After 8 cycles, he had a severe morbilliform, vesiculopustular rash secondary to Nivolumab. Skin Biopsy showed a lymphocytic infiltrate with scattered eosinophils and numerous neutrophils. High dose prednisone was started with tapering for 3 months. Nivolumab was temporarily held and resumed after a good response to steroids. After 14 cycles, the patient developed malaise, fatigue, nausea and mild abdominal pain. ALT was 393, AST 302, ALK 164. Bilirubin was 1.1. Hepatitis A, B, and C testing were negative, anti-liver kidney microsomal antibody and anti-mitochondrial antibody was negative, acetaminophen level was normal, CT and Ultrasound of the liver were negative for metastatic lesions or other hepatic pathology. No recent change in medication or alcohol use was reported. As per ASCO guidelines, hepatitis was classified as Grade III (ALT and AST &gt;5-20 times the upper limit of normal). The patient was started on 100 mg prednisone daily with tapering for 2 months. Liver enzymes normalized and symptoms resolved. Nivolumab was discontinued. PET scan 6 months from the last cycle showed disease in remission. DISCUSSION: Treatment of immunotherapy induced hepatitis depends on severity. Immunotherapy can be continued in grade 1, temporarily held in grade 2, and permanently discontinued in grade 3 and 4 as per guidelines. High dose steroids (prednisone 1-2 mg/kg) with tapering serve as the mainstay of treatment. Mycophenolate or azathioprine can be considered in refractory cases. However, it needs further research whether immunotherapy can be re-trialed in patients with grade 3 toxicity, who have responded well to the steroids, and would potentially benefit from a repeat trial.