bluuebunny/crossref_metadata_2025_split huggingface dataset:
2338 Drug-Induced Liver Injury From Prolonged Kava Kava and Kratom Use
Authors: Shah Maulik , Ali Hasan , Elgenaidi Hisham 
Published: October 2019

INTRODUCTION:
Several herbal supplements carry the risk of drug-induced liver injury (DILI).Kava Kava is a herbal compound derived from the root of the Piper methysticum plant that is indigenous to the South and Western Pacific. Kratom is a herbal extract derived from the leaves of Mitragyna speciosa, a evergreen tree indigenous to Southeast Asia. Here we report a case of Kava and Kratom induced hepatocellular hepatitis in a male with complex regional pain syndrome (CRPS).

CASE DESCRIPTION/METHODS:
A 48-year-old male with history of CRPS and rheumatoid arthritis presented with a 7-day history of nausea, vomiting, dark urine, and jaundice. He denied alcohol, tobacco, or IV drug abuse. Denied use of medications. On exam, he was jaundiced. His labs on admission were- WBC 10.8, HGB 17.2, INR 1.4, creatinine 0.97, Total Bilirubin 21.8, Conjugated Bilirubin 16.7, ALP 293, ALT 1805, AST 1539. Viral hepatitis, HIV, HSV, EBV, and CMV were ruled out. Autoimmune serologies and ceruloplasmin were negative. Abdominal ultrasound showed a dilated common bile duct measuring 9.6mm. MRCP ruled out biliary ductal abnormality. Patient refused liver biopsy. Further questioning revealed prior use of opioids for pain, but in the last 9 months he had been substituting with a combination of Kava Kava and Kratom tea.

DISCUSSION:
Herbal supplementation use is increasing, and often, not discussed with medical providers. Kava Kava is comprised of kavalactones, which have similar effects to alcohol with regards to relaxation, sociability and euphoria. Kratom is used for its opioid-like ability to increase stamina and treat chronic pain. Its highly potent agonist activity on the mu, kappa and delta opioid-receptors have led to its popularity as a recreational drug. Formulations of Kava Kava and Kratom can be found for sale in herbal supplement stores and on the internet. Although a few case reports exist of these supplements leading to hepatocellular damage, the exact mechanism of injury is still not well understood and more research is necessary. Health care professionals should be aware of the hepatotoxic potential associated with Kratom and Kava Kava use and should be vigilant in identifying patients who would benefit from education regarding supplement use and discontinuation. Although these herbal supplements can cause hepatotoxicity, it’s important to exclude other possible causes of hepatic injury, including infection, vascular, autoimmune, and biliary etiologies.
2345 Do You Wish to Have a Liver Transplant? A Case of Testosterone Booster-Induced Toxic Hepatitis
Authors: Patel Nehal , Choksi Vivek , Rivas John , Yella Prashanth Reddy , Priyadarshni Shivani , Surapaneni Balarama K. , Cantave Rulz T. 
Published: October 2019

INTRODUCTION:
Drug-induced hepatitis is inflammation of the liver that is caused by a toxic amount of certain medicines, vitamins, herbal or food supplements. We present a case of a young adult male with testosterone booster induced acute hepatitis, abnormally high liver enzymes but otherwise relatively asymptomatic presentation.

CASE DESCRIPTION/METHODS:
35 year old man, who presented to the hospital with flu like symptoms for 3 days. Gastroenterology was consulted for urgent evaluation of new onset nausea, vomiting and fatigue, associated with a >60-fold increase in his transaminases and alkaline phosphatase. His liver function was: AST U/L 2450, ALT 3300 U/L, Alkaline Phosphatase 200 U/L, LDH 1660 U/L, GGT 750 U/L, Indirect bilirubinemia, with abnormally high ferritin levels of >6000 ng/ml. His further workup including viral serology of HSV, Hepatitis, EBV, CMV, Influenza; Urine toxicology; ANA; Anti Smooth Muscle Antibody, Ceruloplasmin, Alpha-1 Antitrypsin was negative. Liver function including protein and PT/INR was normal. With an unremarkable spleen and portal vein ultrasound, he also underwent CT abdomen and pelvis without contrast on day 3 of admission which was not rewarding. With uptrending liver enzymes, liver biopsy was done and pathology showed findings consistent with drug-induced hepatitis- collapsed portal tracts with inflammation comprising of histiocytes, lymphocytes, scattered eosinophils with few plasma cells. On detailed questioning, he reported endorsing high dose testosterone booster orally, to improve his muscle mass. The medication was stopped. Liver enzymes started down trending over a period of 1 week. He was eventually discharged on oral steroids. Patient was thereafter lost to follow up outpatient.

DISCUSSION:
Drug induced liver injury (DILI) is mostly a diagnosis of exclusion with supporting liver biopsy findings. DILI has several clinical manifestations ranging from asymptomatic elevations in liver enzymes to fulminant liver failure culminating in death or liver transplantation. DILI may be predictable and dose-dependent, or may be idiosyncratic. Rapid and severe recurrence may occur with re-exposure and stopping the drug or supplement is of utmost importance. Our patient had mixed hepatocellular-cholestatic injury. General guidelines involve giving gluccocorticoids to patients with hypersensitivity reactions who have progressive cholestasis or no significant improvement despite withdrawal of causative agent. Patient counselling for avoidance is of utmost importance.
2355 Rare on Rare: A Simultaneous Presentation of SLE and PBC
Authors: Javed Abid T. , Koch David 
Published: October 2019

INTRODUCTION:
Though autoimmune diseases commonly co-exist, systemic lupus erythematosus and concomitant primary biliary cirrhosis are uncommon. A recent literature review encompassing 34 cases noted that PBC was diagnosed in 69% of cases; in 5/34 cases, SLE and PBC were diagnosed simultaneously.

CASE DESCRIPTION/METHODS:
A 51 year old African American female with chronic kidney disease stage 3, hypertension, vitiligo presented with fatigue, anorexia, and >20 lbs weight loss over 3-4 months. Vitals were notable for blood pressure of 91/47, pulse 62, T 97.3F, and she was breathing room air. On exam, she appeared lethargic and fatigued. Scleral icterus and sublingual jaundice were noted. Discoid rash involving both ears was noted. Vitiligo of lower extremities was noted. Initial labs noted leukocytosis of 13.5 k/cumm, normocytic anemia, BUN 125 mg/dL, K 6.7 mmol/L, Cr 5.5 mg/dL, total bilirubin of 5.0, AST 86 U/L, ALT 218 U/L, ALP 1363 U/LDouble stranded DNA antibody was >13.0 IU/mL. F-actin and anti-smooth muscle antibody were negative. Anti-nuclear antibody was 1:2560. Anti-mitochondrial antibody (IgG) was 3.5. The patient’s hyperkalemia was treated, and after stabilization, patient underwent kidney biopsy and transjugular liver biopsy. These resulted, respectively, nephritis ISN/RPS Class III (C) and a cirrhotic liver severe bile ductular proliferation of the portal triads with absent bile ducts. Diagnoses of SLE with lupus nephritis and AMA negative PBC were made, and the patient was started on plaquenil and ursodiol.

DISCUSSION:
Liver involvement in patients with SLE can include primary liver disease as well as involvement due to SLE itself. Distinguishing between the true etiology of liver damage in these patients can be challenging, often due to confounding serological assays and use of immunosuppressive therapy in SLE. It is currently unknown whether SLE and PBC concurrence shares a common genetic or environmental factor, or if the diseases co-occur by chance. While liver dysfunction is not a diagnostic criteria for SLE, SLE related hepatitis (subclinical hepatopathy) has been described, particularly as a hypertransaminasemia. This is often noted during SLE flares, and improves or resolves with steroid therapy. Unfortunately, steroid therapy independent of other immunosuppressive therapies is associated with worsening outcomes in PBC, as well as development of fatty liver disease. Further exploration regarding co-occurrence and comanagement of SLE and PBC is needed, despite its rare incidence.
2363 Symptomatic Hepatic Sarcoidosis in a Hispanic Patient With Severely Elevated Liver Biochemical Tests
Authors: Harris Michael , Pottebaum Benjamin , Settergren Noah , Ruzkowski Charles 
Published: October 2019

INTRODUCTION:
Sarcoidosis is a systemic granulomatous disease of unknown etiology that typically predominates as a respiratory disease process. Hepatic involvement is uncommon and reported in only 11.5% of cases and even rarer is symptomatic hepatic involvement that occurs in approximately 5 to 30% of those cases. Epidemiological studies show substantial variations in extrapulmonary involvement based on race, with few studies on the Hispanic population. This case report presents a Hispanic female who underwent extensive workup and was diagnosed with symptomatic hepatic sarcoidosis.

CASE DESCRIPTION/METHODS:
A 27-year-old Hispanic woman with history of a mediastinal mass presented to the emergency department with an abrupt onset of right upper quadrant (RUQ) abdominal pain and nausea. Liver biochemical tests were severely elevated in a hepatocellular pattern. A RUQ ultrasound showed a dilated common bile duct (CBD) with a questionable stone in the CBD. Next, a magnetic resonance cholangiopancreatography was performed and demonstrated a normal CBD without biliary ductal dilatation or choledocholithiasis. Workup for chronic liver disease was negative, as well as extensive workup for other causes (Table 1). Then a liver biopsy was performed with histology demonstrating scattered non-necrotizing granulomas (Figure 1) with negative stains for mycobacterial and fungal organisms. Review of past medical records revealed a biopsy of her mediastinal mass with histology showing a non-necrotizing granulomas (Figure 2). A diagnosis of sarcoidosis was established and she was started on oral prednisone and referred to pulmonology.

DISCUSSION:
A diagnosis of sarcoidosis involves a suggestive history, granulomas in two organs, negative staining for acid fast bacilli, and a lack of drug-induced disease. The majority of patients with hepatic granulomas have primary biliary cholangitis (PBC). Screening for anti-mitochondrial antibodies and elevated IgM levels is important as these are present in >90% of those with PBC. Infectious diseases should be ruled out including tuberculosis, AIDS-related diseases, Q fever, and Brucellosis. Race is the most important risk factor for developing extrapulmonary sarcoidosis, possibly due to involvement of the reticuloendothelial system. Hispanics account for 18.1% of the U.S population. It is possible that Hispanics are at increased risk for extrapulmonary sarcoidosis compared to whites, but more Hispanic epidemiology studies are warranted.
2367 A Rare Case of Primary Glomus Tumor of Liver
Authors: Sonti Sravanthi , Shreenath Aparna , Parsa Laxmi , Bohman Keith 
Published: October 2019

INTRODUCTION:
Glomus tumors are very rare mesenchymal perivascular tumors arising in glomus body. They are mainly found in skin of extremities but rarely arise in visceral organs like gastrointestinal tract, mediastinum, bladder, and kidney. However, glomus tumors occurring in liver is extremely rare. We found only seven case reports in English literature so far. Our case is incidentally found after imaging was obtained to evaluate significantly elevated inflammatory markers.

CASE DESCRIPTION/METHODS:
A 60-Yr-old African American female with medical history of atrial fibrillation, hypertension, rheumatoid arthritis, anxiety, depression, adenomatous polyps was referred for evaluation of an abnormal PET-CT scan. She was seen by her rheumatologist with a complaint of worsening pain in her hips and lower back and 5lbs weight loss over past 3months. Laboratory evaluation showed normal complete blood counts and liver function tests but CRP 14.8mg/L, sedimentation rate 100mm/hr. A PET-CT scan showed an intensely hyper metabolic, peripherally enhancing, 2 cm × 1.8 cm, left hepatic lobe lesion concerning for malignancy. Moderately increased uptake was noted in cecal area suspicious for a primary site. No FDG avid nodal metastases, or vasculitis noted. A colonoscopy showed 1cm adenomatous polyp in cecum but no malignancy seen. A CT guided biopsy of the liver mass was performed which showed sheets of small bland cells with scant to moderate eosinophilic cytoplasm with centrally placed small nuclei.There is prominent vascular network throughout the tumor and the cells are positive for CD34 stain, smooth muscle actin, collagen IV, but negative for glycipan-3, arginase, AE1/3, pCEA, synaptophysin, chromogranin, KIT and DOG1. A diagnosis of glomus tumor was made. She was discussed in hepatobiliary conference and a recommendation was made for a surgical excision. She was seen by a surgeon but she denied surgery.

DISCUSSION:
Glomus tumor in liver is very rare and we report eighth case. Our patient is asymptomatic and immunohistochemical stains confirmed glomus tumor. It is vascular surrounded by epithelioid cells with round to oval nuclei, and eosinophilic cytoplasm. Tumor cells are positive for for markers like SMA, desmin , vimentin; may be positive for CD34/31, but negative for cytokeratins, CD117, neuroendocrine markers like synaptophysin, chromogranin, or protein S-100. The natural course and management options are not clear though surgical resection is recommended. The tumor is benign and has favorable prognosis.
2376 Diffuse Large B-Cell Lymphoma Presenting With Typical Features of HCC on Liver Imaging: A Diagnostic Conundrum
Authors: Liaquat Hammad , Goff Sara , Jhala Nirag , Kiyani Amirali 
Published: October 2019

INTRODUCTION:
Hepatocellular carcinoma (HCC) is the most common primary liver malignancy. HCC can be solely diagnosed on cross-sectional imaging (CT or MRI) if a lesion meets the diagnostic criteria according to the Liver Imaging Reporting and Data System (LI-RADS), which has above 90% specificity. HCC commonly metastasizes to lungs, regional lymph nodes, kidney, bone marrow and adrenals but metastases to the spleen are rare. We present a case of liver masses with typical HCC characteristics on liver MRI which was ultimately proven to be diffuse large B-cell lymphoma (DLBCL) on liver biopsy.

CASE DESCRIPTION/METHODS:
38-year-old Vietnamese male with no past medical history was admitted with significant weight loss, fatigue and abdominal discomfort. He did not have a history of high risk behaviors or recent foreign travel. Physical exam revealed hepatomegaly. On labs, CBC was normal, T-bili 0.7, Alk Phos 147, AST 89, ALT 50, Albumin 3 g/dL, INR 1.1, creatinine 0.7. HBV serology was positive for HBsAg, anti-HBc and anti-HBe and was negative for HBeAg. HBV DNA was 497 IU/ml. HIV, HCV and HDV serology were negative. CT abdomen showed numerous liver lesions, largest of which was 10.4 cm and a single 8.1 cm splenic lesion. MRI showed several large, rounded and well-circumscribed liver lesions demonstrating arterial hyperenhancement, washout and pseudocapsule consistent with diagnosis of HCC (LI-RADS 5). MRI confirmed a single lesion on spleen (Figure 1), suspicious for metastasis. Tumor markers (AFP, CEA, CA 19-9) were within normal range. Lactate dehydrogenase (LDH) was 1200. Given elevated LDH and a spleen lesion, liver biopsy was done which showed high grade DLBCL (Figure 2). Systemic staging tests did not reveal any other tumor sites. Patient was started on tenofovir and chemotherapy with excellent response (Figure 3).

DISCUSSION:
Liver biopsy is rarely required to diagnose HCC if certain diagnostic criteria are met on cross sectional imaging, even without significantly elevated AFP. Extranodal lymphoma with liver and spleen involvement can present with lab and imaging abnormalities which can mimic HCC, as in our case. Markedly elevated LDH and spleen lesion raised suspicion for a different diagnosis. Undiagnosed or untreated advanced DLBCL can limit survival to a few months while hepatic involvement can also cause liver failure. In conclusion, a biopsy should be considered for liver lesions diagnosed as HCC on cross sectional imaging when atypical features, in our case elevated LDH and spleen lesion, are present.
2399 West Nile Encephalitis in a Post-Liver Transplant Patient
Authors: Yang Grace H. , Apfel Tehilla , Shah Mehul , Krawitz Steven 
Published: October 2019

INTRODUCTION:
West Nile Virus (WNV) is a neurotropic flavivirus that is transmitted from animals to humans by the bite of the Aedes, Anaphales, or Culex mosquito, with disease incidence peaking in the late summer and early fall. It is the leading cause of arboviral illness in the U.S. While many infected with WNV are asymptomatic, 25% of patients develop fever, and less than 1% of patients will develop neurologic symptoms. Age over 75-years old and immunosuppressed state are risk factors for developing neuroinvasive disease.

CASE DESCRIPTION/METHODS:
A 65-year old woman with a history of HCV cirrhosis complicated by HCC status post successful orthotopic liver transplantation (OLT) in 2016 compliant with tacrolimus and everolimus immunosuppression (ISP) presented with painless jaundice and acute transaminemia. Liver biopsy revealed severe acute cellular rejection (ACR), so steroids and thymoglobulin were started. Tacrolimus was increased and everolimus was changed to mycophenolate mofetil. Clinically, she appeared well and her LFTs responded to treatment. Suddenly, she developed fever to 103º associated with bilateral hand tremors. Infectious workup was obtained, and she was started on broad-spectrum antibiotics. Initially, symptoms were attributed to changes in ISP and treatment of ACR. However, she developed progressively worsening dyskinesia and encephalopathy eventually requiring intubation. Given initial negative infectious workup, lumbar puncture was obtained; see Table 1. HSV, VZV, and Lyme PCR as well as VDRL in the CSF were negative. Given clinical symptoms, positive WNV IgM in the CSF, and MRI Brain concerning for WNV neuroinvasive disease, patient was treated with IVIG for 5 days. WNV IgG became positive as well on repeat lumbar puncture 2 weeks later. Patient’s encephalopathy improved, and she was able to be extubated.

DISCUSSION:
There may be a delay in diagnosis and treatment of WNV encephalitis in post-liver transplant patients as neurologic symptoms may be attributed to ISP or as in this patient, to the treatment of acute cellular rejection. West Nile encephalitis must remain on the differential diagnosis when neurologic symptoms are present in a post-liver transplant patient, especially in endemic areas during the summer and fall months. A change in this patient’s ISP for the treatment of ACR may have caused the development of a more severe, neuroinvasive response to WNV infection and ISP management in such patients should be studied further.
2400 An Unusual Case of Spontaneous Reactivation of Hepatitis B in Adult T-Cell Lymphoma/Leukemia
Authors: Alexandre Cassidy , Batool Asra 
Published: October 2019

INTRODUCTION:
Reactivation of hepatitis B (HBV) is typically triggered by immunosuppressive therapy of cancer, autoimmune disease, or organ transplantation. Here we report a rare case of spontaneous reactivation of hepatitis B in a patient newly diagnosed with adult T-cell lymphoma/leukemia without any exposure to immunosuppressive therapy of cancer.

CASE DESCRIPTION/METHODS:
A 34-year-old African American male was transferred from an outside institution for further management of probable T-cell lymphoma/leukemia as severe lymphocytosis was initially noted. Presenting symptoms included weakness and fatigue as well as bilateral conjunctival redness. His abdomen was mildly distended, and hepatomegaly was noted. Of interest, he was found to have elevated liver function tests (LFTs) and hepatitis panel showed acute hepatitis B with bloodwork significant for positive hepatitis B surface antigen, negative hepatitis B surface antibody, negative hepatitis B core IgM, positive hepatitis B core antibody and hepatitis B viral load of 16,954. Labs for hepatitis A and C were negative. He denied any known risk factors for hepatitis. Abdominal imaging showed peripancreatic concern of mass or swelling, mild hepatomegaly, splenomegaly and marked lymphadenopathy in the celiac, perigastric, pancreatic and aortocaval regions. Of note, he has not been on any immunosuppressive therapy or steroids prior to hospital admission. On hospitalization day #5, he was started on tenofovir and subsequently liver function tests continued to improve. He was also started on IV Solu-Medrol 1 g per day for 3 days with IV hydration and oral allopurinol. He continued to undergo diagnostic work-up as per hematology and Oncology prior to starting chemotherapy. On the day of discharge (day #17), remarkable improvement in his LFTs was noted. He was seen in GI clinic about 3 weeks later and his hepatitis B viral load was 760 and ALT was within normal limits.

DISCUSSION:
HBV reactivation is common following chemotherapy and is associated with a high mortality, however spontaneous HBV reactivation in the absence of cancer chemotherapy or transplantation is a rare clinical entity. Adult T-cell lymphoma/leukemia likely contributes to immune suppression or alteration in immune function causing spontaneous HBV reactivation. This case highlights the importance of screening all patients who are to undergo cancer chemotherapy, marked immunosuppressive treatments or solid organ or bone marrow transplantation for evidence of ongoing or previous hepatitis B.
2406 Cinnamon-Induced Acute Hepatitis
Authors: Odish Fadi , Karmo Dillon , Imam Zaid , Hanna Angy , Aneese Andrew 
Published: October 2019

INTRODUCTION:
There is no denying the increasing interest in alternative medical practices in the United States, especially in regards to supplement use. According to a recent survey, 33.2% of adults in the US used complementary health approaches, and 17.7% reported using a supplement. As the use of supplements rises, it is imperative that physicians recognize the potential adverse effects. One example of this is the popular practice of using cinnamon supplementation to improve glycemic control in Diabetes. However, less attention has been given to a potential adverse effect of cinnamon use. Coumarin is a compound found in cinnamon and its metabolite are hepatotoxic. Our patient presented with hepatitis triggered by the use of a seemingly innocent supplement.

CASE DESCRIPTION/METHODS:
A 51 year old male with a past medical history of hyperlipidemia presented with 10 days of right upper quadrant abdominal pain, jaundice and dark urine. He denies tobacco, alcohol, or illicit drug use. Home medications are aspirin and atorvastatin. Only new medication is cassia cinnamon supplements for the past month. Physical exam was significant for scleral icterus, jaundice, abdominal distention, and tenderness to palpation in the RUQ. Lab work revealed a CBC within normal limits, and elevated LFTs. Acute hepatitis panel, ANA, anti-smooth muscle antibody, anti-mitochondrial antibody, ferritin, HIV, HSV, EBV, and CMV were negative. An ultrasound of the abdomen was unremarkable. His atorvastatin and cinnamon supplements were held. An MRCP was obtained and was unremarkable. His symptoms and LFTs improved and he was discharged home after two days of hospitalization with instructions to hold the atorvastatin until his liver function tests normalized, and to discontinue the cassia cinnamon. The acute hepatitis was determined to be due to the cassia cinnamon supplementation with concomitant statin use.

DISCUSSION:
This case illustrates the importance of a thorough history when evaluating a patient. Special attention must be paid to over the-counter medications, herbs, and supplements. Often times patients will not volunteer this information when asked about what medications they take, so they must be specifically prompted. Given the increasing popularity of alternative and “natural” medical practices, it is also imperative that physicians stay up to date on the potential adverse effects. Emphasis needs to be placed on scientific investigation into potential risks and benefits of popular alternative medical practices.