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Our patient, Mr. Smith, is a 43 year old caucasian male who came in today with complaints of fatigue, anorexia, malaise, nausea, vomiting, abdominal pain, and low grade fever for the past month, and recently has been alarmed by the discoloration of his skin and sclera turning yellow. He states that his urine has become dark and stool has become clay colored.

Past Medical History:  Blood transfusion in 1992 due to major blood loss in a motor vehicle accident, arthralgia, peripheral neuropathy, hospitalization due to drug overdose in 2010. Patient states that he is fully up to date on vaccination.

Social History : Patient is an injectable drug user for the past 12 years and is currently sexually active with multiple male partners and states he uses protection “sometimes”. His current occupation is a car mechanic.

Family History: Mother: history of hyperlipidemia and diabetes father died of myocardial infarction, no other siblings or family history available .

pictured: jaundice on an individual’s eye; “Jaundice.” Assignment Point , 5 Oct. 2017, www.assignmentpoint.com/science/medical/jaundice.html.

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Case Report: Acute Hepatitis B Infection in a Healthy South Asian Female Following Exposure at an Urban Pedicure Facility

Tummala, Sanjeev MD

Swetha Tummala, Palo Alto Medical Foundation, Mountain View, CA.

Introduction: Acute hepatitis B is caused by infection with hepatitis B virus (HBV). The incubation period from the time of exposure to the onset of symptoms is 6 weeks to 6 months. Most infections in adults are caused by exposure to contaminated blood. Other potential sources are semen, vaginal secretions, and open wound exudate. Acute infection ranges from asymptomatic or mild disease to, rarely, fulminant hepatitis. Disease is more severe among adults aged >60 years. The fatality rate among acute cases reported to Center for Disease Control (CDC) is 0.5-1%.

Case Report: Here, we describe a case of acute hepatitis B infection in a healthy South Asian female from possible exposure at an urban pedicure facility. A 35-year-old, previously healthy but unvaccinated Indian woman was seen in a gastroenterology clinic for acute jaundice. Her initial blood work showed AST 550 U/l, ALT 1745 U/L, total bilirubin 9.3 mg/dL, direct bilirubin 7.3 mg/dL, and ALP 196 U/l. Previous liver function tests were normal. An ultrasound of her abdomen showed normal-appearing liver without gallstones or biliary dilatation. Her serologies showed positive hepatitis A IgG antibody, negative hepatitis A IgM antibody, positive hepatitis B surface antigen, positive hepatitis B core IgM antibody, negative hepatitis C antibody, hepatitis B DNA 81300 IU/mL, and negative hepatitis B surface antibody. Her creatinine was 0.59 mg/dL and prothrombin time/ INR 1.1. She had no features of encephalopathy or hepatic decompensation. Her husband and children were immune for hepatitis B from previous vaccination. She was taking no other medications at the time of her illness. She had no other risk factors except a visit to an urban pedicure facility in downtown San Jose, 2 months prior to her acute illness. She remembered having a cut and a bruise after her nails were done, and her feet were washed in a bowl that was used to wash other customers’ feet. She was managed conservatively with no antiviral medications. Follow-up blood work revealed normalization of liver enzymes in about 3 months with AST 31 U/l, ALT 56 U/l and total bilirubin 0.4 mg/dL. She achieved seroconversion 3 months after presentation with negative hepatitis B surface antigen and reactive hepatitis B surface antibody, and undetectable hepatitis B virus. She remains asymptomatic and clinically well.

Conclusion: Acute hepatitis B infection can be caused from contamination of blood from open cuts/bruise and stains that can happen at a pedicure facility. The Center for Disease Control recommends any blood spills, including dried blood, which can still be infectious for about 7 days, be cleaned using 1:10 dilution of 1 part household bleach to 10 parts of water for disinfecting the area.

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Clinical Cases in Hepatology

• © 2022
• Nora V. Bergasa 0

Department of Medicine, H+H/Metropolitan Physician Affiliate Group of New York, New York, USA

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Features case presentations of how to appropriately approach treating patients with liver disease

Describes the epidemiological characteristics of a variety of liver diseases

Details techniques for interpreting experimental data and techniques for conducting clinical trials

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About this book

This book provides a comprehensive resource for clinical hepatology. It details the systematic approach to patients with liver disease in outpatient and inpatient medical settings. A variety of case studies in hepatology including chronic viral hepatitis, and metabolic, autoimmune, and alcohol related liver disease are presented. The book enables the reader to develop a thorough understanding of the clinical presentation, natural history, epidemiology, genetics, and therapeutic options for the liver diseases that clinicians must recognize and manage from the first encounter with the patient through the years of follow up.

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The Hepatological Curiosities

Diseases of the Liver

• Ischemic hepatitis
• Autoimmune hepatitis
• Fatty liver disease
• Biliary cirrhosis

Table of contents (15 chapters)

Front matter.

Nora V. Bergasa

Approach to the Patient with Liver Disease

Primary biliary cholangitis, autoimmune hepatitis, primary sclerosing cholangitis, chronic hepatitis c, chronic hepatitis b, alcohol induced liver disease, nonalcoholic fatty liver disease, alpha-1-antitrypsin deficiency, hemochromatosis, wilson’s disease, tumors of the liver, drug induced liver injury, complications of liver disease, back matter, editors and affiliations, about the editor.

Dr. Nora V. Bergasa is Professor of Medicine Emerita at New York Medical College and Chairman Emerita of the Department of Medicine at New York City (NYC) Health + Hospitals (H+H)/ Metropolitan and a retired member of the Physician Affiliate Group of New York. She serves as Hepatology Attending at NYC, H+H/Woodhull. She graduated from medical school from the Universidad Central del Este in the Dominican Republic, did her internal medicine residency and gastroenterology fellowship at the State University of New York (SUNY) at Downstate, and completed her clinical and research training in hepatology in the Liver Diseases Section of the National Institutes of Health. She has conducted basic and clinical investigations in several areas of hepatology, including cholestasis. Her major research field has concerned the pruritus of liver disease for which she is internationally recognized.

Bibliographic Information

Book Title : Clinical Cases in Hepatology

Editors : Nora V. Bergasa

DOI : https://doi.org/10.1007/978-1-4471-4715-2

Publisher : Springer London

eBook Packages : Medicine , Medicine (R0)

Copyright Information : Springer-Verlag London Ltd., part of Springer Nature 2022

Hardcover ISBN : 978-1-4471-4714-5 Published: 26 October 2021

eBook ISBN : 978-1-4471-4715-2 Published: 25 October 2021

Edition Number : 1

Number of Pages : XII, 497

Number of Illustrations : 3 b/w illustrations, 34 illustrations in colour

Topics : Hepatology

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CASE REPORT article

Case report: a case of severe acute hepatitis of unknown origin.

• 1 The Key Laboratory of Molecular Biology of Infectious Diseases Designated by the Chinese Ministry of Education, Chongqing Medical University, Chongqing, China
• 2 Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Infection and Immunity, Department of Infectious Disease, National Clinical Research Center for Child Health and Disorders, Children’s Hospital of Chongqing Medical University, Chongqing, China
• 3 Department of Endocrine and Breast Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
• 4 Department of Pathology, Children’s Hospital of Chongqing Medical University, Chongqing, China
• 5 Department of Radiology, Children’s Hospital of Chongqing Medical University, Chongqing, China
• 6 Chongqing Municipal Center for Disease Control and Prevention, Chongqing, China
• 7 Key Laboratory of Laboratory Medical Diagnostics, Chinese Ministry of Education, Chongqing Medical University, Chongqing, China

According to analyses of etiology, clinical features, diagnostic methods, and treatment strategies by summarizing a case of unexplained acute hepatitis recently experienced, we are aiming to provide some information to enrich the clinical experience in diagnosis and treatment of severe acute hepatitis of unknown etiology in young children. A boy, aged 10 years and 6 months old, was admitted to the hospital due to acute abdominal pain, jaundice, and exceptionally high levels of ALT and AST. A range of measures, including patient history, physical examination, and routine laboratory testing, were performed. Furthermore, strategies such as trio-based next-generation sequencing (Trio-NGS) and liver biopsy, as well as metagenomic NGS (mNGS) of blood and liver samples were also performed. In summary, this case was an acute severe non-A–E hepatitis that is a probable case with hepatitis of unknown origin. Immunohistochemical analysis showed an immune injury in liver tissues. Torque teno virus (TTV) sequences were detected by mNGS assay. As for treatment strategies, in addition to general treatment, this patient also underwent plasmapheresis and methylprednisolone treatment due to disease deterioration. The patient’s liver function was improved afterward and discharged after one month of treatment. Taken together, this work reported the clinical feature and treatment of severe acute hepatitis with non-A–E hepatitis in detail. The potential mechanism of liver damage might be due to an immune attack in which TTV might play a role as a co-factor.

Introduction

Liver disease of unknown etiology refers to liver diseases that cannot be clearly diagnosed by patient history, physical examination, and routine laboratory testing. Due to differences in race and region, the reported incidence of unexplained liver disease in pediatric patients is variable, ranging from 10 to 50% ( 1 – 4 ). The etiologies of unexplained liver disease can be roughly divided into infectious and non-infectious categories. Although the common viruses (hepatitis viruses A, B, C, D, and E) that cause acute viral hepatitis are undetectable, infectious etiologies, including Epstein–Barr virus (EBV), cytomegalovirus (CMV), herpes simplex viruses (HSV), bacteria, fungi, and parasites, are still common causes of liver injury ( 5 – 9 ). In addition, non-infectious etiologies, such as non-alcoholic fatty liver disease (NAFLD), drug-induced liver injury (DILI), autoimmune hepatitis (AIH), and inherited metabolic liver disease, also account for a relatively large proportion of hepatitis cases ( 10 – 13 ).

Since the first few cases of severe acute hepatitis of unknown origin were reported among young children in Scotland in March ( 14 ), increasing numbers of cases have been reported worldwide. As of 26 May 2022, at least 650 cases of unexplained hepatitis in children ranging from ages 1 month to 16 years have been reported in 33 countries, including England, Spain, Israel, the United States, and Denmark ( 15 ). The clinical manifestation is acute hepatic dysfunction with significantly elevated aminotransferase levels. Most of the affected children have jaundice, abdominal pain, nausea, vomiting, and diarrhea but no fever. Thirty-eight patients had received liver transplantation, and at least nine deaths were reported ( 15 ). According to the World Health Organization (WHO), the case definition of Confirmed is N/A at present. The case definition of Probable is a person presenting with an acute hepatitis (non-hepA–E*) with serum transaminase > 500 IU/L (AST or ALT), who is 16 years and younger, since 1 October 2021 ( 15 ).

The cause of the pediatric liver disease has not been revealed yet. However, a leading hypothesis is that an infectious agent is the underlying cause or a risk factor. Given the presence in about three-fourths of the investigated cases, adenovirus type 41 was initially suspected to be the causative pathogen ( 16 , 17 ). Nevertheless, adenovirus does not fully explain the increased severity of the cases. In addition, adenovirus is a seasonally transmitted virus with a peak period of infection from February to April. It can cause severe infection in multiple organs, including the liver, in immunocompromised children ( 18 ); however, it is rarely able to lead to severe infection in immunocompetent children ( 19 , 20 ). Thus, in the updated technical note released by WHO, adenovirus positivity was considered more likely to be a coincidental factor ( 21 ).

Our team recently experienced a case with severe acute non-A–E hepatitis. Here, we supplement a few noteworthy points based on this case, hoping to provide more information for pediatricians about the current hepatitis of unknown origin in children.

Case description

A boy who was 10 years and 6 months old was admitted to the hospital due to abdominal pain that persisted for 4 days. The patient also vomited three times without concomitant fever or diarrhea. He was found to have jaundice when referred to a local hospital. The biochemical tests showed exceptionally high levels of alanine aminotransferase [(ALT) 2330 U/L], aspartate aminotransferase [(AST) 1326 U/L], and total bilirubin [(TB) 74.2 μmol/L]. The patient received no intervention or treatment before being transferred to our hospital. He was previously in good health, denied taking any medications or having a history of exposure to patients with COVID-19, and received the second dose of inactivated COVID-19 vaccine 3 months before admission. At admission, the physical examination revealed that the child had scleral icterus, jaundice, hepatosplenomegaly, upper abdominal tenderness, and a positive Murphy’s sign.

The patient underwent infectious pathogen screening. Evidence of hepatitis A, B, C, and E viruses, CMV, HSV, and EBV infection is not found by serology (Hepatitis A, B, C, and E virus, CMV, and EBV), immunohistochemical (EBV), and PCR (HSV and EBV) analyses. The autoimmune hepatitis-related antibodies (17 common antibodies including ANA, SSA, AMA M2, and ss-DNA) and metabolism disease-related tests (including blood glucose, blood ammonia, lactate, alpha-fetoprotein, and ceruloplasmin) were also negative. Abdominal ultrasound indicated hepatosplenomegaly, pericholecystic edema, and thickening of the gallbladder wall. Magnetic resonance cholangiopancreatography (MRCP) showed edema of the first porta hepatis, the periportal region, and the gallbladder, as well as stenosis of the choledoch ( Figures 1A–C,G ). To further clarify the potential cause, the patient underwent trio-based next-generation sequencing (Trio-NGS) and liver biopsy. Trio-NGS did not detect any abnormalities, while liver biopsy showed mild interfacial hepatitis and fibrosis of portal area (G1S1) ( Figures 2A,B ), and further classification of the intrahepatic lymphocytes predominantly suggested CD8 + cells ( Figure 2C ). Tests for HBsAg, HBcAg, CMV, IgG4, and EBER in liver tissue remained negative. Although some interlobular bile ducts were very small, the number of intrahepatic bile ducts was normal. Finally, torque teno virus (TTV) sequences were detected by metagenomic NGS (mNGS) in whole blood sample ( Figure 3A ) and liver tissue ( Figure 3B ). The result of electron microscopy ( Figure 2D ) indicated chronic active hepatitis, which was shown as follows: hepatic cells were swollen, rough endoplasmic reticulum and smooth endoplasmic reticulum were slightly expanded, and lipid droplets were observed in hepatocytes (upper image), as well as lymphocytosis were observed in hepatic sinusoidal (lower image). However, no viral inclusions were found.

Figure 1. Magnetic resonance cholangiopancreatography (MRCP) results of the patient. MRCP showed edema of the first porta hepatis and the periportal region (A,B) and thickness of the gallbladder wall (C) at the beginning of treatment (thick arrow), and they were resolved after treatment (D–F) . However, MRCP showed a narrow bile duct that was not relieved during hospitalization (G,H) .

Figure 2. Results of liver histology of the patient. (A–C) Liver biopsy results. H&E staining of liver tissue showed swollen hepatocytes and inflammatory cells infiltrating into portal duct areas, and there was mild interfacial inflammation (A) . Masson staining indicated mild hepatic fibrosis in the portal area (B) . Immunohistochemical staining of CD8 + T-lymphocytes (C) . (D) The result of electron microscopy showed chronic active hepatitis. No viral inclusions were found.

Figure 3. Results of metagenomic sequencing. (A) Sequencing results of whole blood. (B) Sequencing results of liver tissue.

After hospitalization, the patient received ceftazidime (based on cholecystitis), lipid-soluble vitamins, and reduced glutathione treatment. Unfortunately, the patient’s situation deteriorated with rapid progressive jaundice (peak TB: 173 μmol/L), underwent plasmapheresis once, and was administered methylprednisolone. The patient’s liver function was improved after the administration of steroids ( Figures 4A–C ). MRCP tests showed that the narrow bile duct was not relieved, but the hepatosplenomegaly and gallbladder edema had disappeared ( Figures 1D–F,H ). The patient was discharged after one month of treatment. Two weeks post-discharge, he revisited the hospital. He was clinically stable without any adverse and unanticipated events. The biochemical tests showed that ALT was 163 U/L, AST was 60 U/L, and TB was 11.6 μmol/L.

Figure 4. Schematic diagram of the transaminase and bilirubin fluctuations during treatment. The alanine aminotransferase (A) , aspartate aminotransferase (B) , and total bilirubin (C) levels were tested every 3–5 days during treatment. Ceftazidime was used for the first two weeks followed by methylprednisolone treatment. The patient also received plasma exchange once due to rapid aggravation of jaundice.

As a whole, this case report follows the CARE Case Report Guidelines. Our adherence to these reporting guidelines has been listed in the Supplementary material .

Patient in this case report presented with gastrointestinal symptoms of abdominal pain and vomiting, elevated transaminases, and jaundice at the onset. He was healthy before disease onset and had no history of taking certain drugs or exposure to poisons. The results of viral hepatitis serology screen were negative, indicating that this case was consistent with the definition of a Probable case by the WHO ( 15 ).

Viral hepatitis due to hepatitis viruses or to occasionally hepatotropic viruses is one of the main etiological groups of acute or chronic hepatitis in children ( 22 ). Recently, with the popularity of hepatitis virus vaccines and the improved detection methods, non-hepatotropic virus (including CMV, EBV, and coxsackievirus) infection-induced acute hepatitis in young children has gained increased attention ( 23 ). In the recent outbreak of acute and severe hepatitis of unknown etiology in children, some clues suggested that adenovirus and SARS-CoV-2 might be the etiologies ( 24 ). However, until now, there is still a lack of definite evidence on associated mechanisms or causative relationships. As for this case we reported, evidence of adenovirus and SARS-CoV-2 infection was negative, indicating that such two virus infections are unlikely. However, both blood sample and liver tissues were tested positive for torque teno virus (TTV) according to mNGS analysis. TTV is a small single-stranded DNA virus that was discovered in the late 20th century. TTV has an extremely high prevalence worldwide, which is frequently detectable in healthy infants, healthy adults, patients with HBV/HCV, and cases of hepatitis without an obvious viral agent ( 25 – 27 ). Previous studies indicate that TTV is hepatotropic, and TTV infection-induced liver damage could present a diverse spectrum of pathological damage, including ballooning, acidophilia degeneration, formation of apoptosis bodies and focus of necrosis, and mild inflammation in the lobule and portal area ( 28 ). Nevertheless, there was no significant difference of TTV DNA positivity in patients with hepatitis when compared to that in healthy controls ( 28 ). Moreover, due to the lack of reliable cell culture and animal models, the pathogenicity of TTV remains controversial ( 27 ). Notably, most studies assumed that TTV is non-pathogenic. A published article by Okamura et al. reported that genotype 1a of TTV might play a role in the pathogenesis of fulminate hepatitis and chronic liver disease in children liver disease of unknown etiology ( 29 ), indicating that some specific genotype of TTV may be pathogenic in children. In the current case, TTV was monitored by mNGS, and its expression level is not high enough to identify the genotype. In addition, no TTV virus particles were observed in liver tissues by electron microscopy. Therefore, before well-grounded evidence emerges, we cannot determine the pathogenicity of TTV. On the contrary, the immunohistochemical analysis showed that IgG4 staining was negative, but the majority of infiltrating inflammatory cells were CD8 + lymphocytes. More importantly, the response of this patient to hormones treatment was good, implying that it is more likely to be an immune injury. Given the uncertainty about the pathogenicity of TTV, we consider that TTV is more likely a co-factor responsible for the inappropriate immune response.

Besides infectious factors, given the immune-mediated hepatic damage, as well as the well-response to methylprednisolone treatment, AIH could not be ruled out yet in this case report. Even though majority of common autoimmune hepatitis-related antibodies were negative, we might also have to consider the possibility of autoantibody-negative autoimmune hepatitis. It has been suggested that seronegative AIH accounts for less than 5% of all adult patients with AIH ( 30 ). However, little information is available in children. A retrospective study conducted by Islek et al. found that seven of 54 patients with AIH under 18 years of age were seronegativity persisted during treatment ( 31 ), indicating that seronegative AIH could not be ignored in clinical practice. As for this child in our report, he has no documented history of other autoimmune diseases and no typical histologic features of AIH. We considered that the mild interfacial hepatitis is not enough to explain his severe liver damage. Thus, before more substantial evidence emerges, seronegative autoimmune hepatitis cannot be determined.

There were some limitations in the exploration of etiologies in this study. First, the depth and breadth of laboratory testing are not comprehensive enough. Some investigations such as multiplex PCR for respiratory viruses, multiplex PCR gastrointestinal viruses panel, and stool culture for common bacterial enteropathogens are not performed, which might cause the loss of some clinical data. Second, the detection of pathogens and histology was performed after the condition was stable, which is not conducive to the search for etiology. Similarly, no typical manifestations of the acute phase were observed in liver biopsy, which might influence the clinical assessment. Third, this case is a single case report. Continuous follow-up is required to further clarify the clinical characteristics and etiology of such liver diseases in young children.

Collectively, we report a case with severe acute hepatitis of unknown origin. Based on laboratory examinations and treatment response, we suspect the etiology of this case may be due to an immune injury in which TTV might play a role as a co-factor. We suggest liver biopsy for patients with severe acute hepatitis of unknown origin and trial steroid therapy when the liver damage is similar to autoimmune hepatitis. By reporting this case, we expect to add further support to the notion that immune dysfunction might be the main cause of liver damage in children with acute hepatitis of unknown origin.

Data availability statement

The datasets for this article are not publicly available due to concerns regarding participant/patient anonymity. Requests to access the datasets should be directed to the corresponding authors.

Ethics statement

The studies involving human participants were reviewed and approved by the Institutional Review Board of Children’s Hospital of Chongqing Medical University (2022-177). Written informed consent to participate in this study was provided by the participants’ legal guardian/next of kin.

Author contributions

JC and Z-ZZ were involved in the interpretation of the data, conceptualized the manuscript, and participated in the revisions. JC, Z-ZZ, and FL provided the financial support. JZ, TA, and KZ were involved in the acquisition of all the clinical data. Y-JZ, H-YG, and Q-QT were involved in the drafting of the manuscript and analyzed the data. B-YX, QW, and A-LH participated to the revisions. All authors approved the final version of the manuscript.

This study was supported by the Program for Youth Innovation in Future Medicine, Chongqing Medical University (Z-ZZ); Chongqing Natural Science Foundation (Grant no. cstc2021jcyj-msxmX0139 to Z-ZZ); and the Medical Scientific Research Project of Chongqing (Grant no. 2021MSXM067 to FL).

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Supplementary material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fped.2022.975628/full#supplementary-material

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29. Okamura A, Yoshioka M, Kikuta H, Kubota M, Ma X, Hayashi A, et al. Detection of TT virus sequences in children with liver disease of unknown etiology. J Med Virol. (2000) 62:104–8. doi: 10.1002/1096-9071(200009)62:1<104::AID-JMV16>3.0.CO;2-P

30. Mieli-Vergani G, Vergani D, Baumann U, Czubkowski P, Debray D, Dezsofi A, et al. Diagnosis and management of pediatric autoimmune liver disease: ESPGHAN hepatology committee position statement. J Pediatr Gastroenterol Nutr. (2018) 66:345–60. doi: 10.1097/MPG.0000000000001801

31. Islek A, Keskin H. Seronegative autoimmune hepatitis in children: a single-center experience. Acta Gastroenterol Belg. (2021) 84:305–10. doi: 10.51821/84.2.305

Keywords : case report, unexplained acute hepatitis, torque teno virus, immune injury, methylprednisolone

Citation: Zhou Y-J, Gu H-Y, Tang Q-Q, Li F, Zhu J, Ai T, Zhu K, Xu B-Y, Wang Q, Huang A-L, Chen J and Zhang Z-Z (2022) Case report: A case of severe acute hepatitis of unknown origin. Front. Pediatr. 10:975628. doi: 10.3389/fped.2022.975628

Received: 22 June 2022; Accepted: 12 September 2022; Published: 05 October 2022.

Reviewed by:

Copyright © 2022 Zhou, Gu, Tang, Li, Zhu, Ai, Zhu, Xu, Wang, Huang, Chen and Zhang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Juan Chen, [email protected] ; Zhen-Zhen Zhang, [email protected]

† These authors have contributed equally to this work

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Hepatitis A Clinical Presentation

• Author: Richard K Gilroy, MD, FRACP; Chief Editor: BS Anand, MD  more...
• Sections Hepatitis A
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Approach Considerations
• Complete Blood Count and Coagulation Study
• Liver Function Tests
• Serologic Tests
• Ultrasonography
• Histologic Findings
• Supportive Care
• Liver Transplantation
• Postexposure Prophylaxis
• Immunization
• Diet and Activity
• Medication Summary
• Analgesic agents
• Antiemetics
• Vaccines, viral, prevention
• Immune globulins
• Questions & Answers
• Media Gallery

Along with outlining the presenting complaint and its severity and sequelae, the history should also initiate a search for the source of exposure (eg, overseas travel, lack of immunization, intravenous [IV] drug use) and attempt to exclude other possible causes of acute hepatitis (eg, accidental acetaminophen overdose). The incubation period is 2-6 weeks (mean, 4 wk). Shorter incubation periods may result from higher total dose of the viral inoculum.

Discussion focusing on excluding other potential causes should be undertaken early in order to guide further investigation. Not every patient with fever, hepatomegaly, and jaundice has hepatitis A virus (HAV) infection. Some of the important differential diagnoses for acute hepatitis warrant early and specific management.

In the prodrome, patients may have mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise, low-grade fever (usually < 39.5°C), myalgia, and mild headache. Smokers often lose their taste for tobacco, like persons presenting with appendicitis.

Icteric phase

In the icteric phase, dark urine appears first (bilirubinuria). Pale stool soon follows, although this is not universal. Jaundice occurs in most (70%-85%) adults with acute HAV infection; it is less likely in children and is uncommon in infants. The degree of icterus also increases with age. Abdominal pain occurs in approximately 40% of patients. Itching (pruritus), although less common than jaundice, is generally accompanied by jaundice.

Arthralgias and skin rash, although also associated with acute HAV infection, are less frequent than the above symptoms. Rash more often occurs on the lower limbs and may have a vasculitic appearance.

Relapsing hepatitis A

Relapsing hepatitis A is an uncommon sequela of acute infection, is more common in elderly persons, and is characterized by a protracted course of symptoms of the disease and a relapse of symptoms and signs following apparent resolution (see Complications ).

The physical examination focuses on detecting features that support a diagnosis of acute hepatitis and should include an assessment of features of chronic liver disease and, similarly, assessment of any evidence of decompensation.

Hepatomegaly is common. Jaundice or scleral icterus may occur. Patients may have a fever with temperatures of up to 40°C.

Longatti A. The dual role of exosomes in hepatitis A and C virus transmission and viral immune activation. Viruses . 2015 Dec 17. 7(12):6707-15. [QxMD MEDLINE Link] .

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Wasley A, Grytdal S, Gallagher K, Centers for Disease Control and Prevention (CDC). Surveillance for acute viral hepatitis--United States, 2006. MMWR Surveill Summ . 2008 Mar 21. 57(2):1-24. [QxMD MEDLINE Link] .

Ansaldi F, Bruzzone B, Rota MC, et al. Hepatitis A incidence and hospital-based seroprevalence in Italy: a nation-wide study. Eur J Epidemiol . 2008. 23(1):45-53. [QxMD MEDLINE Link] .

Dominguez A, Bruguera M, Plans P, et al. Declining hepatitis A seroprevalence in adults in Catalonia (Spain): a population-based study. BMC Infect Dis . 2007. 7:73. [QxMD MEDLINE Link] .

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Kanyenda TJ, Abdullahi LH, Hussey GD, Kagina BM. Epidemiology of hepatitis A virus in Africa among persons aged 1-10 years: a systematic review protocol. Syst Rev . 2015 Sep 26. 4:129. [QxMD MEDLINE Link] .

Chobe LP, Arankalle VA. Investigation of a hepatitis A outbreak from Shimla Himachal Pradesh. Indian J Med Res . 2009 Aug. 130(2):179-84. [QxMD MEDLINE Link] .

Cao J, Wang Y, Song H, et al. Hepatitis A outbreaks in China during 2006: application of molecular epidemiology. Hepatol Int . 2009 Jun. 3(2):356-63. [QxMD MEDLINE Link] . [Full Text] .

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Fischer GE, Thompson N, Chaves SS, et al. The epidemiology of hepatitis A virus infections in four Pacific Island nations, 1995-2008. Trans R Soc Trop Med Hyg . 2009 Sep. 103(9):906-10. [QxMD MEDLINE Link] .

Amin J, Gilbert GL, Escott RG, et al. Hepatitis A epidemiology in Australia: national seroprevalence and notifications. Med J Aust . 2001 Apr 2. 174(7):338-41. [QxMD MEDLINE Link] .

Cooksley WG. What did we learn from the Shanghai hepatitis A epidemic?. J Viral Hepat . 2000 May. 7 Suppl 1:1-3. [QxMD MEDLINE Link] .

[Guideline] Mofenson LM, Brady MT, Danner SP, et al. Guidelines for the prevention and treatment of opportunistic infections among HIV-exposed and HIV-infected children: recommendations from CDC, the National Institutes of Health, the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics. MMWR Recomm Rep . 2009 Sep 4. 58:1-166. [QxMD MEDLINE Link] . [Full Text] .

Kodani M, Mixson-Hayden T, Drobeniuc J, Kamili S. Rapid and sensitive approach to simultaneous detection of genomes of hepatitis A, B, C, D and E viruses. J Clin Virol . 2014 Oct. 61(2):260-4. [QxMD MEDLINE Link] .

Worns MA, Teufel A, Kanzler S, et al. Incidence of HAV and HBV infections and vaccination rates in patients with autoimmune liver diseases. Am J Gastroenterol . 2008 Jan. 103(1):138-46. [QxMD MEDLINE Link] .

Kanda T, Nakamoto S, Wu S, et al. Direct-acting antivirals and host-targeting agents against the hepatitis A virus. J Clin Transl Hepatol . 2015 Sep 28. 3(3):205-10. [QxMD MEDLINE Link] .

Jacobsen K, Wierman S. Hepatitis A virus seroprevalence by age and world region. 1990-2005. Vaccine . 2010. 28(41):6653-6657.

Jacobsen KH, Koopman JS. Declining hepatitis A seroprevalence: a global review and analysis. Epidemiol Infect . 2004 Dec. 132(6):1005-22. [QxMD MEDLINE Link] . [Full Text] .

Klevens RM, Miller JT, Iqbal K, et al. The evolving epidemiology of hepatitis a in the United States: incidence and molecular epidemiology from population-based surveillance, 2005-2007. Arch Intern Med . 2010 Nov 8. 170(20):1811-8. [QxMD MEDLINE Link] .

Costas L, Vilella A, Trilla A, et al. Vaccination strategies against hepatitis A in travelers older than 40 years: an economic evaluation. J Travel Med . 2009 Sep-Oct. 16(5):344-8. [QxMD MEDLINE Link] .

Marano C, Freedman DO. Global health surveillance and travelers' health. Curr Opin Infect Dis . 2009 Oct. 22(5):423-9. [QxMD MEDLINE Link] .

Askling HH, Rombo L, Andersson Y, Martin S, Ekdahl K. Hepatitis A risk in travelers. J Travel Med . 2009 Jul-Aug. 16(4):233-8. [QxMD MEDLINE Link] .

Centers for Disease Control and Prevention (CDC). National, state, and local area vaccination coverage among children aged 19-35 months - United States, 2008. MMWR Morb Mortal Wkly Rep . 2009 Aug 28. 58(33):921-6. [QxMD MEDLINE Link] .

Centers for Disease Control and Prevention (CDC). Hepatitis a vaccination coverage among children aged 24-35 months - United States, 2006 and 2007. MMWR Morb Mortal Wkly Rep . 2009 Jul 3. 58(25):689-94. [QxMD MEDLINE Link] .

Irving GJ, Holden J, Yang R, Pope D. Hepatitis A immunisation in persons not previously exposed to hepatitis A. Cochrane Database Syst Rev . 2012 Jul 11. 7:CD009051. [QxMD MEDLINE Link] .

Petrignani M, Verhoef L, Vennema H, et al. Underdiagnosis of foodborne hepatitis A, The Netherlands, 2008-2010(1.). Emerg Infect Dis . 2014 Apr. 20(4):596-602. [QxMD MEDLINE Link] .

Parron I, Planas C, Godoy P, et al, for the Working Group for the Study of Hepatitis A in Catalonia. Effectiveness of hepatitis A vaccination as post-exposure prophylaxis. Hum Vaccin Immunother . 2017 Feb. 13(2):423-7. [QxMD MEDLINE Link] . [Full Text] .

Tejada-Strop A, Zafrullah M, Kamili S, Stramer SL, Purdy MA. Distribution of hepatitis A antibodies in US blood donors. Transfusion . 2018 Dec. 58(12):2761-5. [QxMD MEDLINE Link] .

Summers A, Hu J, Berger L. Important role of family physicians in reporting communicable diseases: Outbreak of hepatitis A in a kindergarten class. Can Fam Physician . 2018 Oct. 64(10):742-3. [QxMD MEDLINE Link] . [Full Text] .

Brennan J, Moore K, Sizemore L, et al. Notes from the field: acute hepatitis A virus infection among previously vaccinated persons with HIV infection - Tennessee, 2018. MMWR Morb Mortal Wkly Rep . 2019 Apr 12. 68(14):328-9. [QxMD MEDLINE Link] . [Full Text] .

Linder KA, Malani PN. Hepatitis A. JAMA . 2017 Dec 19. 318(23):2393. [QxMD MEDLINE Link] . [Full Text] .

• Hepatitis A virus as viewed through electron microscopy.
• Hepatitis A. Time course of infection.
• Hepatitis A.

Contributor Information and Disclosures

Richard K Gilroy, MD, FRACP Gastroenterologist, Intermountain Healthcare Disclosure: Received salary from gilead, NPS pharmaceuticals, salix pharmaceuticals, AbbVie for speaking and teaching.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape.

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases , American College of Gastroenterology , American Gastroenterological Association , American Society for Gastrointestinal Endoscopy Disclosure: Nothing to disclose.

George Y Wu, MD, PhD Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases , American Gastroenterological Association , American Medical Association , American Society for Clinical Investigation , Association of American Physicians Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

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• v.14(9); 2022 Sep

Rare Diagnostic and Clinical Manifestations in an Acute Hepatitis A Infection: A Case Report

Wesley d figg.

1 Department of Medicine, Baylor College of Medicine, Houston, USA

David L Crawford

Tristen n taylor, mayar al mohajer.

The hepatitis A virus (HAV) is a common cause of infectious hepatitis worldwide. In adults, clinical manifestations typically involve fever, nausea/vomiting, fatigue, abdominal pain, and jaundice, although rarer manifestations may be observed. Acute hepatitis A infection is detected via anti-HAV IgM antibodies, which are present in almost all patients at symptom onset. In this case, we present a patient who not only tested negative for acute HAV infection at symptom onset, but also presented with uncommon, extrahepatic manifestations including maculopapular skin rash and polyarthralgia. Wariness of such a presentation can facilitate the timely diagnosis of atypical cases of HAV infection.

We report the case of a 51-year-old man who presented with fever, abdominal pain, headaches, and diarrhea for one week with elevated liver enzymes and leukocytosis. Workup consisting of viral hepatitis panels, various infectious studies, and rheumatologic antibody titers did not initially reveal an etiology for the patient’s presentation. Computed tomography (CT) abdomen and pelvis, abdominal ultrasound, magnetic resonance cholangiopancreatography (MRCP), and hepatobiliary iminodiacetic acid (HIDA) scan did not reveal acute pathology. The patient’s symptoms worsened over the following days, and he additionally developed bilateral wrist pain, digital arthralgias, paraspinal back pain, diffuse muscular weakness, and a pruritic maculopapular rash affecting the flanks and extremities. Eventually, viral hepatitis studies were repeated which revealed elevated levels of anti-HAV IgM antibodies, indicating acute hepatitis A infection. The patient was treated supportively while hospitalized with subsequent improvement of symptoms and lab abnormalities. Since discharge, the patient had not experienced persistent sequelae of the disease.

This case of acute viral hepatitis A infection is notable for two reasons: (1) the patient experienced uncommon, delayed, extrahepatic manifestations of disease, and (2) the initial viral hepatitis studies revealed undetectable anti-HAV IgM levels despite having experienced symptoms of illness for several days. This case suggests that repeat viral hepatitis testing may be warranted in patients who continue to experience manifestations of the infection after initially testing negative. It also emphasizes the importance of recognizing potential atypical manifestations of acute hepatitis A infection.

Introduction

Hepatitis A virus (HAV), a nonenveloped, single-stranded RNA virus of the Picornaviridae family, is a virus that causes acute infectious hepatitis [ 1 ]. Hepatitis A, which is typically spread via the fecal-oral route, is endemic in developing countries due to factors such as poor sanitation or contamination of food or water. In contrast, since the implementation of the hepatitis A vaccine and improved sanitation, infection rates in developed countries have substantially declined making acute hepatitis A infection relatively uncommon [ 1 ]. The average incubation period of hepatitis A is roughly 30 days, and the manifestations of acute infection are age-dependent [ 2 ].

The typical clinical manifestations of acute hepatitis A virus infection vary depending on age. In children under the age of 6 years old, roughly 70% of acute infections are asymptomatic, whereas about 70% of adult patients experience jaundice and markedly elevated aminotransferases [ 3 ]. Adult hepatitis A infection most commonly presents with abrupt onset of fever, malaise, nausea or vomiting, abdominal pain, dark-colored urine, and jaundice [ 4 ]. Atypical manifestations of acute HAV infection that have been reported primarily include cholestasis, relapsing and remitting infection, and autoimmune phenomena such as chronic autoimmune hepatitis [ 5 ]. However, symptoms such as a pruritic skin rash, diarrhea, and arthralgia have seldom been reported in the literature [ 4 , 6 ]. In one such case, a biopsy of the patient’s skin rash revealed leukocytoclastic vasculitis with direct immunofluorescence studies showing vascular deposition of IgM and C3 complement [ 7 ]. Recognition of such variable manifestations of HAV infection in adults is critical for the timely and accurate diagnosis of HAV infection.

The symptoms of acute hepatitis A infection in adults are nonspecific, vary widely, and may include fever, nausea/vomiting, fatigue, abdominal pain, and/or jaundice [ 8 ]. IgM antibodies are present in almost all patients at the time of their initial presentation and detection of these antibodies is the gold-standard method for diagnosis [ 9 ]. The methods for detecting these antibodies are highly sensitive and specific, thus the probability of obtaining a falsely negative test result at the onset of clinical symptoms is exceedingly low.

In this case, however, we report a patient who presented several days after the onset of symptoms and initially tested negative for acute hepatitis A infection, but eventually tested positive 16 days later. Additionally, this patient exhibited a widespread, maculopapular rash and polyarthralgia - symptoms that are rarely associated with acute hepatitis A infection. The uncommon diagnostic course and atypical manifestations presented in this case exemplify a unique presentation of acute hepatitis A infection.

This article was previously presented as a poster at the 2022 Baylor College of Medicine Department of Medicine Housestaff Research Symposium on April 11-15, 2022.

Case presentation

A 51-year-old Caucasian man with hypertension living in the United States presented with fever, abdominal pain, headaches, and diarrhea for seven days. Initial laboratory tests revealed leukocytosis and mildly elevated liver enzymes. Computed tomography (CT) of the abdomen, magnetic resonance cholangiopancreatography (MRCP), abdominal ultrasound, and hepatobiliary iminodiacetic acid (HIDA) scan were performed and did not reveal acute pathology. Further workup included a viral hepatitis panel (eight days from symptom onset), autoimmune antibody titers, and anti-cytomegalovirus (CMV) IgG levels, all of which returned negative. Notably, the viral hepatitis panel did not reveal acute hepatitis B or C infection, and anti-HAV IgM and IgG antibodies were not detected. The patient was given empiric treatment with ceftriaxone for suspected cholangitis and was discharged home on hospital day 10.

For two days after discharge, the patient continued to experience daily fevers and developed new bilateral wrist pain and interphalangeal arthralgias, bilateral paraspinal back pain, and diffuse muscular weakness. His diarrhea and vomiting had resolved. The patient then presented to a different hospital (our facility) for re-evaluation at this time. The patient was febrile to 38.3°C (101.0°F) and a physical exam on this admission notably revealed proximal and distal interphalangeal arthralgias with active and passive range of motion on the third and fourth digits of both hands. The abdominal exam demonstrated a non-distended abdomen without hepatosplenomegaly, a lack of tenderness to palpation of all four abdominal quadrants, and normal bowel sounds. There was no evidence of jaundice or scleral icterus. The patient works as a salesman and reports no recent sexual activity, travel, drug use, seafood consumption, exposure to unclean water, or contacts with a known hepatitis A diagnosis. Notably, the patient reported not previously receiving vaccination against hepatitis A, serving as his only apparent risk factor for acquiring acute hepatitis A infection. Extensive infectious and rheumatologic workup ensued (Table ​ (Table1) 1 ) with all results returning negative and unrevealing for an etiology of the patient’s symptoms and lab abnormalities. Additionally, his liver function tests and alkaline phosphatase levels continued to rise throughout admission.

CMV: Cytomegalovirus

Twenty-three days after the onset of symptoms (five days after presenting to our facility), the patient developed new-onset diffuse, pruritic maculopapular rash involving his bilateral flanks (Figure ​ (Figure1) 1 ) and proximal upper and lower extremities. Additionally, the patient’s aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase levels peaked at this time as well at 128 U/L, 154 U/L, and 159 U/L, respectively. He continued to experience polyarthralgia with a similar distribution as previously mentioned.

Given the lack of an explanation for the patient’s presentation, the decision to retest for viral hepatitis A, B, and C was made (24 days after symptom onset) which consequently revealed a positive anti-HAV IgM serology, indicating acute hepatitis A viral infection and providing a plausible unifying diagnosis (Table ​ (Table2). 2 ). The patient continued to receive supportive treatment and was given instructions to follow up with infectious disease specialists upon discharge. His symptoms improved over the course of one week and no persistent complications from the infection had become apparent since discharge.

AST: Aspartate aminotransferase; ALT: Alanine aminotransferase

This case proved diagnostically challenging for several reasons. The patient initially tested negative for HAV after the onset of symptoms, he presented with symptoms that are uncommon for acute HAV infection, and since the development of the HAV vaccine, rates of infection have declined significantly in developed countries making HAV an often-overlooked disease. Interestingly, however, reported cases of hepatitis A infection in the United States have increased considerably since 2016 due to the occurrence of large person-to-person outbreaks [ 10 ]. Since the beginning of said outbreaks, 43,705 cases of acute hepatitis A infection have been reported across 37 states (as of February 11, 2022), resulting in 26,659 hospitalizations and 420 deaths [ 11 ]. The present case occurred in Texas and, according to the Texas Department of State Health Services, there has been a recent rise in the number of reported cases of hepatitis A infection [ 12 ]. Eighty-eight cases were reported in 2018, 160 cases reported in 2019, and 223 cases reported in 2020 [ 12 ]. This sudden change in the epidemiology of HAV infection highlights the importance of recognizing potential signs and symptoms of HAV infection, as well as understanding instances where retesting for HAV infection may be warranted.

Following exposure, the incubation period of HAV ranges from 20 to 45 days, and peak viremia is achieved near the time of onset of abnormal liver function tests [ 13 ]. Anti-HAV antibodies are almost uniformly present at the time of onset of clinical symptoms, and acute infection is diagnosed via the detection of anti-HAV IgM antibodies in the patient’s serum by highly sensitive and specific commercially available immunoassays [ 14 ]. In a study performed by Lee et al., 10.9% of patients that were later confirmed on repeat testing to have acute hepatitis A infection initially lacked anti-HAV IgM antibodies, as seen in the present case [ 15 ]. This study revealed that the patients who initially tested negative for anti-HAV IgM antibodies shared certain characteristics, such as higher rate of fever and lower aminotransferase and bilirubin levels compared to patients with an initially positive anti-HAV IgM serology, similar to our observations of the present case. Therefore, in the setting of clinical manifestations concerning for infectious hepatitis in which an alternative explanation has not been discovered, it is important to consider retesting for HAV after an initially negative test.

Risk factors for HAV infection include travel to endemic regions, intravenous drug use, multiple blood transfusions, male homosexual activity, and occupations such as childcare, sanitation, and healthcare [ 16 , 17 ]. Primary prevention of HAV includes avoidance of risk factors, active immunization, and passive immunization. In areas with high rates of hepatitis A, nearly all inhabitants have previously acquired asymptomatic HAV infection in childhood, providing future protection against clinical hepatitis A and negating the need for vaccination [ 16 ]. When HAV vaccination is indicated, such as when residing in regions with intermediate endemicity or when traveling to countries with a high incidence of hepatitis A, it is typically offered as a two-dose series beginning after 12 months of age [ 16 , 18 ]. Older children, teens, and adults who were not previously immunized may also receive the HAV vaccine [ 18 ]. People with preexisting chronic liver disease have a higher risk of developing fulminant hepatitis when infected with hepatitis A and thus should be routinely vaccinated for HAV [ 16 ]. Following exposure to HAV, vaccination is indicated in all individuals aged one year and older within two weeks of exposure. In addition, hepatitis A immune globulin (IG) may be co-administered based on age, immune status, comorbidities, or in place of vaccination in those for whom vaccines are contraindicated [ 19 ].

Currently, there are no drugs targeted for the treatment of acute hepatitis A infection; thus, individuals confirmed to have an infection are managed supportively and treated symptomatically with the use of antiemetics, intravenous fluids, and antipyretics as indicated [ 3 , 20 ]. Given that the identified risk factors for acquiring acute HAV infection in the present case were lack of prior vaccination and a potential state-wide outbreak, our patient was treated supportively with antipyretics and antihistamines for his pruritic rash. He was additionally counseled on potential risk factors for acquiring hepatitis A infection and was recommended to follow up with his primary care physician to receive routine age-appropriate vaccinations.

Conclusions

In a patient presenting with symptoms of an atypical viral syndrome, such as rash and arthralgias as in the presented case, acquiring further history of recent gastrointestinal symptoms or recent exposures can lead to a timely diagnosis. Diligent history-taking can prevent prolonged hospital admission and avoid the financial costs of an extensive medical workup and therapeutic trials, as experienced in this case. This unusual case of hepatitis A, as well as the recent epidemiologic changes of HAV, demonstrates the importance of including hepatitis A infection on a differential diagnosis in patients presenting with a seemingly non-specific viral illness. Furthermore, if hepatitis A virus is included on the differential, it may be prudent to consider retesting for anti-HAV antibody titers if initial titers were negative in patients lacking a unifying diagnosis.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study

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Concordant fatal congenital anomaly in twin pregnancy: a case report and review of the literature

• Amenu Diriba 1 ,
• Temesgen Tilahun   ORCID: orcid.org/0000-0003-4138-4066 1 ,
• Lammii Gonfaa 1 ,
• Jemal Gebi 1 ,
• Bikila Lemi 1 ,
• Jiregna Fyera 1 ,
• Suleiman Mazeng 1 ,
• Aschalew Legesse 1 &
• Dinaol Alemu 1  

Journal of Medical Case Reports volume  18 , Article number:  406 ( 2024 ) Cite this article

Metrics details

When a pregnant mother finds out she has a fetus with a congenital defect, the parents feel profound worry, anxiety, and melancholy. Anomalies can happen in singleton or twin pregnancies, though they are more common in twin pregnancies. In twins, several congenital defects are typically discordant.

Case summary

We present a rare case of concordant fatal anomaly in twin pregnancy in a 22-year-old African patient primigravida mother from Western Ethiopia who presented for routine antenatal care. An obstetric ultrasound scan showed anencephaly, meningomyelocele, and severe ventriculomegaly. After receiving the counseling, the patient was admitted to the ward, and the pregnancy was terminated with the medical option. Following a successful in-patient stay, she was given folic acid supplements and instructed to get preconception counseling before getting pregnant again.

The case demonstrates the importance of early obstetric ultrasound examination and detailed anatomic scanning, in twin pregnancies in particular. This case also calls for routine preconceptional care.

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Introduction

A “congenital anomaly” is defined as any abnormal deviation from the expected structure, form, or function. “Malformations” are morphological abnormalities of organs or regions of the body resulting from an intrinsically abnormal developmental process, whereas “disruptions” are defects from interference with an initially normal developmental process [ 1 , 2 ].

Congenital anomalies present in twins also include any anomaly that may occur in singletons, including primary structural malformations, chromosomal defects, and genetic syndromes [ 1 , 2 ]. The anomalies may involve one or both twins [ 2 , 3 ]. The former is called discordant, while the latter is termed concordant [ 1 , 2 , 3 ]. Due to the anomaly’s multifactorial inheritance pattern, which is influenced by both genetic and environmental factors, twins are usually discordant for this anomaly, with only one co-twin affected [ 1 , 3 ].

However, some research has shown that identical twins have concordant anomalies such as neural tube defects [ 3 , 4 ]. Here we present a rare case of concordant congenital anomaly in twin pregnancy.

Case presentation

This 22-year-old African patient primigravida from western Ethiopia came to Wallaga University Referral Hospital for her second appointment as part of her routine prenatal care schedule. She said she had been amenorrheic for the past 4 months, but she could not recall the last time she had had a regular menstrual cycle. She received folic acid 5 mg (orally daily and iron sulphate 325 mg orally three times daily for 3 months, and two doses of tetanus–diphtheria vaccine during her prenatal care. However, she had no preconceptional care.

In the course of the index pregnancy, she had never experienced headaches, vaginal bleeding, blurred vision, or epigastric pain. In addition, she had no history of smoking tobacco, chewing khat, drinking alcohol, or using other forms of medication. She had never had bronchial asthma, hypertension, diabetes mellitus, or heart disease.

There was no history of twin pregnancies in her family. This patient was diagnosed with hyperemesis gravidarum and hospitalized to the gynecology ward a month prior to the current presentation. She was released from the hospital after 2 days, having improved. It proved that the pregnancy was twins at 11 weeks appropriate for gestational age (AGA). However, no fetal anomaly was detected.

On examination, she was healthy-looking. Her vital signs were blood pressure (BP) = 120/70 mmHg, pulse rate (PR) = 84 beats per minute, respiratory rate (RR) = 20 breaths per minute, and a temperature of 37.6 °C. She had slightly pale conjunctiva. An abdominal exam showed a 20-week-sized gravid uterus. The lymph glandular system, respiratory system, cardiovascular system, and genitalia were normal. On neurologic examination, reflexes were intact, and meningeal signs were negative.

Urinalysis; complete blood count; random blood sugar (RBS); serology for syphilis, hepatitis, and human immunodeficiency virus (HIV); obstetrics ultrasound; and blood group were done. Obstetrics ultrasound showed a twin intrauterine pregnancy with an anencephalic twin A and severe ventriculomegaly and lumbar myelo-meningocele in twin B (Table  1 ).

With the final diagnosis of a second-trimester twin pregnancy with a concordant fatal anomaly, the patient was admitted to the gynecology ward. In the ward, the patient was given mifepristone 200 mg orally. After 24 hours, 400 µg of misoprostol was inserted vaginally. A total of 8 hours later, she expelled twin A, weighing 120 g of anencephalic abortus with cervical, thoracic, and lumbar vertebral defect, and twin B, weighing 150 g of hydrocephalic abortus with a thoracic and lumbar vertebral defect, and protrusion of the intestine via the right side para umbilical area without the covering membrane (Fig.  1 A, B). The placenta was monochorionic.

A Twin abortuses with neural tube defects at Wallaga University Referral Hospital, Western Ethiopia, 2023. B Twin abortuses with neural tube defects and gastroschisis at Wallaga University Referral Hospital, Western Ethiopia, 2023

When compared with singleton pregnancies, the rates of congenital anomalies are higher with multiple pregnancies [ 5 , 6 ]. In fetuses in multiple gestations, these anatomic abnormalities are more commonly linked to monozygotic (MZ) twining than dizygotic (DZ) twining [ 2 , 7 ].

Anomalies may affect all organ systems, but the commonest involve cardiovascular and central nervous systems, followed by ophthalmic and gastrointestinal abnormalities [ 1 , 4 , 7 , 8 ]. The concordance rate of major congenital malformations is around 20% for monozygotic twins, with most dizygotic twin pairs being discordant [ 1 ]. Only in certain organ systems do monozygotic twins exhibit higher concordance rates than DZ twins [ 4 , 7 ]. Our case is MZ twins. In both twins, the neural nervous system was affected. The twin pairs had neural tube defects. One twin had gastroschisis.

Anomalies in singleton and twin pregnancies are associated with maternal exposure to various factors such as diazepam use, cigarette smoking, maternal obesity, and nutritional deficiencies [ 9 ]. Our case was complicated by hyperemesis gravidarum. Because of repeated vomiting, it could result in nutritional deficiency, which could in turn result in neural tube defects and other anomalies.

There is limited published evidence about screening for structural abnormalities in twin or higher order pregnancies [ 10 ]. Careful sonographic surveys of fetal anatomy are indicated in multifetal pregnancies because the risk for congenital anomalies is increased [ 11 ]. A complete fetal anatomic survey is therefore recommended for all twin gestations at 18–22 weeks’ gestational age [ 12 ]. The accuracy of ultrasonography for detecting congenital fetal anomalies in multiple gestations has not been adequately studied in large series [ 11 ].

Following diagnosis of an anomaly affecting only one fetus, practitioners may face the dilemma of expectant management versus selective termination. If the option of selective fetocide is considered, the main variable determining the technique to achieve this aim is chorionicity [ 13 , 14 , 15 ]. In a dichorionic pregnancy, passage of fetocidal agents from one twin into the circulation of the co-twin is unlikely due to the lack of placental anastomoses [ 13 , 14 ]. When monochorionic (MC) twins are complicated with discordant fetal anomalies, the management scheme will be much more complex [ 13 , 14 ]. In this case, selective termination needs to be performed by ensuring complete and permanent occlusion of both the arterial and venous flows in the umbilical cord of the affected twin. Bipolar cord coagulation under ultrasound guidance is associated with approximately 70–80% survival rates [ 14 , 15 ]. However, management of concordant fatal anomaly in twin pregnancy is not controversial [ 3 ]. In our case, both twins had fatal congenital anomalies, which required immediate termination of the pregnancy using misoprostol.

Availability of data and materials

The datasets used during the current study are available from the corresponding author on reasonable request.

Abbreviations

Hepatitis B surface antigen

Human immunodeficiency virus

Monozygotic

Rhesus factor

Venereal disease research laboratory

White blood count

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We thank the patient for allowing the publication of this case report.

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Department of Obstetrics and Gynecology, School of Medicine, Wollega University, Nekemte, Ethiopia

Amenu Diriba, Temesgen Tilahun, Lammii Gonfaa, Jemal Gebi, Bikila Lemi, Jiregna Fyera,  Suleiman Mazeng, Aschalew Legesse & Dinaol Alemu

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All authors made a significant contribution to the work reported, whether that was in the conception, study design, execution, acquisition of data, analysis, and interpretation, or in all these areas; they took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted, and agree to be accountable for all aspects of the work.

AD is an assistant professor in the Department of Obstetrics and Gynecology, Institute of Health Sciences, Wollega University; TT is an associate professor of Obstetrics & Gynecology, Institute of Health Sciences, Wollega University; LG is an assistant professor in the Department of Obstetrics and gynecology, Institute of Health Sciences, Wollega University; JG is an assistant professor in the Department of Obstetrics and Gynecology, Institute of Health Sciences, Wollega University; JF is an assistant professor in the Department of Obstetrics and Gynecology, Institute of Health Sciences, Wollega University; BL is an assistant professor in the Department of Obstetrics and Gynecology, Institute of Health Sciences, Wollega University; S is an obstetrics and gynecology resident at the Institute of Health Sciences, Wollega University; AL is an obstetrics and gynecology resident at the Institute of Health Sciences, Wollega University; and DA is an obstetrics and gynecology resident at the Institute of Health Sciences, Wollega University.

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Correspondence to Temesgen Tilahun .

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Ethical clearance was obtained from the Research Ethics Review Committee of Wallaga University Referral Hospital. The study protocol is performed per the relevant guidelines.

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Diriba, A., Tilahun, T., Gonfaa, L. et al. Concordant fatal congenital anomaly in twin pregnancy: a case report and review of the literature. J Med Case Reports 18 , 406 (2024). https://doi.org/10.1186/s13256-024-04732-8

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Received : 05 February 2024

Accepted : 28 June 2024

Published : 28 August 2024

DOI : https://doi.org/10.1186/s13256-024-04732-8

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• Twin pregnancy
• Anencephaly
• Meningomyelocele
• Ventriculomegaly
• Gastroschisis

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