Home / Deep Research / Giant Cell Hepatitis With Autoimmune Hemolytic Anemia

Giant Cell Hepatitis With Autoimmune Hemolytic Anemia

1. Disease Information

2026-05-06
Falcon MONDO:1060166 Model: Edison Scientific Literature 43 citations

1. Disease Information

1.1 Definition / overview

Giant cell hepatitis with autoimmune hemolytic anemia (GCH-AHA/GCH-AIHA) is a rare pediatric syndrome characterized by the association of (i) Coombs-positive autoimmune hemolytic anemia and (ii) biopsy-proven giant cell hepatitis, typically presenting beyond the neonatal period and often progressing with relapses. (maggiore2011giantcellhepatitis pages 1-2, marsalli2016efficacyofintravenous pages 1-2, paganelli2014anticd20treatmentof pages 1-2)

Direct abstract quote (definition framing): In the Pediatrics case series, the abstract begins: “Giant cell hepatitis with autoimmune hemolytic anemia (GCH-AHA) is a rare autoimmune disease of infancy characterized by severe liver disease associated with Coombs-positive hemolytic anemia.” (paganelli2014anticd20treatmentof pages 1-2)

1.2 Synonyms / alternative names used in the literature

1.3 Disease identifiers (OMIM/Orphanet/ICD/MeSH/MONDO)

Within the retrieved full texts, explicit OMIM, Orphanet, ICD-10/ICD-11, MeSH, or MONDO identifiers were not present; therefore, these identifiers cannot be asserted from this evidence set.

1.4 Evidence source type

Evidence is largely derived from case reports and small pediatric series, plus one retrospective multicenter observational study of IVIG and a long-term outcome cohort of 16 children. (maggiore2011giantcellhepatitis pages 1-2, marsalli2016efficacyofintravenous pages 1-2)

2. Etiology

2.1 Primary causes (current understanding)

The etiology is not established as genetic; instead, available evidence supports an immune-mediated (autoimmune) cause, specifically a humoral (B-cell/IgG) and complement-mediated injury mechanism in the liver, alongside antibody/complement-mediated hemolysis. (whitington2014humoralimmunemechanism pages 2-3, marsalli2016efficacyofintravenous pages 1-2)

2.2 Risk factors

Age is the dominant epidemiologic risk factor: most cases occur in infancy/early childhood. (maggiore2011giantcellhepatitis pages 1-2, whitington2014humoralimmunemechanism pages 2-3)

Potential triggers/associations are inconsistently reported. For example, one cohort noted an infectious serology signal (parvovirus) in an individual patient without proving causality (reported in a case series context). (bakula2014giantcellhepatitis pages 1-3)

2.3 Protective factors

No protective genetic or environmental factors were identified in the retrieved disease-specific literature.

2.4 Gene–environment interactions

No gene–environment interaction evidence was identified in the retrieved literature.

3. Phenotypes

3.1 Core clinical phenotypes and suggested HPO terms

Below are recurring phenotypes with suggested HPO mappings based on cohort/case-series descriptions.

Hemolysis/AIHA phenotype complex (often first): * Pallor (HP:0000980) * Jaundice (HP:0000952) * Hemolytic anemia (HP:0001878) * Positive direct antiglobulin test / Coombs positive hemolysis (no single HPO term; can map to laboratory abnormality plus “autoimmune hemolytic anemia” concept) * Splenomegaly (HP:0001744) * Hepatosplenomegaly (HP:0001433) * Fever (HP:0001945)

In a 16-child cohort at diagnosis: jaundice 14/16, hepatomegaly 16/16, splenomegaly 6/16, pallor 9/16, fever 8/16. (maggiore2011giantcellhepatitis pages 1-2)

Liver phenotype complex (often later, relapsing): * Hepatomegaly (HP:0002240) * Hepatitis (HP:0012115) * Cholestasis (HP:0002904) * Hyperbilirubinemia (HP:0002904/HP:0002910 context-dependent) * Elevated transaminases (HP:0002910) * Liver fibrosis / cirrhosis (HP:0001395) * Acute liver failure can occur in some patients (HP:0006557), though not universal (whitington2014humoralimmunemechanism pages 2-3)

Temporal phenotype relationship: hemolytic anemia may precede hepatitis by weeks to months; one review-level synthesis described hepatitis appearing 1 week to 15 months after hemolysis onset (often 1–2 months). (raj2011giantcellhepatitis pages 1-2, kim2020successfultreatmentof pages 2-4)

3.2 Laboratory phenotypes and suggested HPO terms

From cohort/case evidence: * Low hemoglobin (HP:0001903): median Hb 6.7 g/dL in the 16-child cohort (maggiore2011giantcellhepatitis pages 1-2) * High reticulocyte count (HP:0001898): median reticulocytes 207,000/mL in the 16-child cohort (maggiore2011giantcellhepatitis pages 1-2) * Hyperbilirubinemia (HP:0002904): median total bilirubin 13.5 mg/dL, direct 11 mg/dL in the 16-child cohort (maggiore2011giantcellhepatitis pages 1-2) * Markedly elevated ALT/AST (HP:0002910): ALT reported as 45× ULN median in the 16-child cohort; extreme values reported in case reports (maggiore2011giantcellhepatitis pages 1-2, raj2011giantcellhepatitis pages 1-2)

3.3 Quality of life impact

Disease is described as severe, requiring prolonged immunosuppression and repeated hospitalization for relapses and infections; formal QoL instruments (e.g., PedsQL) were not reported in the retrieved texts. (maggiore2011giantcellhepatitis pages 1-2, marsalli2016efficacyofintravenous pages 1-2)

4. Genetic / Molecular Information

4.1 Causal genes

No causal genes or recurrent pathogenic variants were identified in the retrieved disease-specific literature; current evidence supports an immune-mediated syndrome rather than a monogenic disorder.

4.2 Pathogenic variants / modifier genes / epigenetics / chromosomal abnormalities

No disease-specific evidence was found in the retrieved texts.

5. Environmental Information

5.1 Environmental/lifestyle factors

No environmental or lifestyle risk factors were established in the retrieved texts.

5.2 Infectious agents

Infectious workups are often described as negative in pediatric reports; occasional associations (e.g., parvovirus serology in an individual) do not establish causality. (bakula2014giantcellhepatitis pages 1-3, cho2016giantcellhepatitis pages 1-2)

6. Mechanism / Pathophysiology

6.1 Key mechanistic concept

A central, disease-defining mechanistic insight is that liver injury in GCH-AIHA appears to be antibody/complement (humoral) mediated, differing from classic T-cell–predominant autoimmune hepatitis (AIH). This is supported by: * Pan-lobular hepatocyte C5b-9 (membrane attack complex) deposition in GCH-AHA biopsies (high-grade in all cases in one mechanistic series) (whitington2014humoralimmunemechanism pages 2-3, whitington2014humoralimmunemechanism pages 1-1) * A lobular inflammatory pattern enriched for macrophages/neutrophils rather than portal/periportal lymphocyte–rich inflammation typical of AIH (whitington2014humoralimmunemechanism pages 3-6) * Clinical refractoriness to “standard” AIH regimens in many patients and strong responses to B-cell depletion (rituximab) (whitington2014humoralimmunemechanism pages 2-3, paganelli2014anticd20treatmentof pages 1-2)

6.2 Causal chain (upstream → downstream)

Proposed causal chain (human biopsy and clinical-response supported): 1) B-cell–derived IgG binds an (unknown) hepatocyte target antigen (upstream trigger not yet defined). (whitington2014humoralimmunemechanism pages 6-6, whitington2014humoralimmunemechanism pages 1-1) 2) IgG triggers classical complement pathway activation on hepatocytes, leading to deposition of C5b-9; Whitington et al. note the staining intensity is a marker of complement-mediated injury (“The degree of C5b-9 staining…is indicative of the degree of complement-mediated cell injury”). (whitington2014humoralimmunemechanism pages 2-3) 3) Complement split products (e.g., C3a/C5a) recruit/activate innate immune cells, producing lobular inflammation dominated by macrophages and neutrophils and hepatocyte necroinflammation. (whitington2014humoralimmunemechanism pages 3-6, whitington2014humoralimmunemechanism pages 6-6) 4) Injured hepatocytes undergo giant cell transformation (multinucleation/fusion), a histologic hallmark. (perezatayde1994coombspositiveautoimmunehemolytic pages 1-4, whitington2014humoralimmunemechanism pages 3-6) 5) In parallel, antibody/complement activity produces Coombs-positive hemolytic anemia, sometimes preceding the hepatitis, reinforcing a systemic humoral immune disorder phenotype. (marsalli2016efficacyofintravenous pages 1-2, maggiore2011giantcellhepatitis pages 1-2)

6.3 Suggested ontology mappings

GO biological process terms (suggested): * complement activation, classical pathway * regulation of complement activation * B cell mediated immunity * antibody-mediated immune response * inflammatory response * macrophage activation * neutrophil chemotaxis * liver regeneration * hepatic fibrosis

Cell Ontology (CL) terms (suggested): * hepatocyte * B cell (CD20+) * macrophage (CD68+) * neutrophil * Kupffer cell (liver macrophage; if specifically described)

UBERON anatomy (suggested): * liver * hepatic lobule * spleen * bone marrow * blood

7. Anatomical Structures Affected

7.1 Organ level

Primary: liver (giant cell hepatitis, cholestasis, fibrosis/cirrhosis risk). (perezatayde1994coombspositiveautoimmunehemolytic pages 1-4, maggiore2011giantcellhepatitis pages 1-2)

Secondary/related: hematologic system (autoimmune hemolytic anemia; often hepatosplenomegaly). (maggiore2011giantcellhepatitis pages 1-2, whitington2014humoralimmunemechanism pages 2-3)

7.2 Tissue and cell level

8. Temporal Development

8.1 Onset

Typically infancy/early childhood. Median age 6 months in a 16-child cohort; mechanistic series range 4–52 months. (maggiore2011giantcellhepatitis pages 1-2, whitington2014humoralimmunemechanism pages 2-3)

8.2 Progression and course

Course is often relapsing and may require years of immunosuppression. In the 16-child cohort, relapses occurred in 11/16 (hepatitis) and 10/16 (anemia); treatment could eventually be stopped after a mean 6 years in some patients with sustained remission. (maggiore2011giantcellhepatitis pages 1-2)

9. Inheritance and Population

9.1 Epidemiology

Population-level prevalence/incidence estimates were not available in the retrieved texts; the syndrome is repeatedly described as very rare, with literature case counts increasing over time (e.g., 18 cases reported before 2011 cohort; approximately 50 cases by 2015; “<100 reported cases” by 2020). (maggiore2011giantcellhepatitis pages 1-2, cho2016giantcellhepatitis pages 1-2, kim2020successfultreatmentof pages 2-4)

9.2 Inheritance

No inherited pattern is established from available evidence.

10. Diagnostics

10.1 Core diagnostic components

A. Hematology: direct antiglobulin (Coombs/DAT) positivity demonstrating autoimmune hemolysis (commonly IgG±complement). (maggiore2011giantcellhepatitis pages 1-2, marsalli2016efficacyofintravenous pages 1-2)

B. Hepatology: liver biochemistry consistent with hepatitis/cholestasis plus liver biopsy showing diffuse giant cell transformation and associated injury/fibrosis patterns. (perezatayde1994coombspositiveautoimmunehemolytic pages 1-4, maggiore2011giantcellhepatitis pages 1-2)

C. Exclusion of other causes: cohorts describe exclusion of viral, metabolic, toxic, and cholestatic etiologies as part of case definition/selection. (maggiore2011giantcellhepatitis pages 1-2)

10.2 Key histopathology

A classic early report describes: “loss of lobular architecture with diffuse giant cell transformation of hepatocytes and portal and pericellular fibrosis.” (perezatayde1994coombspositiveautoimmunehemolytic pages 1-4)

Mechanistic work emphasizes complement immunostaining: high-grade hepatocyte C5b-9 deposition as evidence for complement-mediated injury and potential stratification for B-cell–targeted therapy. (whitington2014humoralimmunemechanism pages 2-3, whitington2014humoralimmunemechanism pages 6-6)

10.3 Differential diagnosis (from available evidence)

The literature emphasizes distinguishing GCH-AHA from classic pediatric autoimmune hepatitis (different autoantibody patterns, different histology/immune infiltrates, different treatment responsiveness). (whitington2014humoralimmunemechanism pages 2-3, whitington2014humoralimmunemechanism pages 1-1)

11. Outcome / Prognosis

11.1 Mortality, transplant, long-term outcomes

Outcomes can be severe: * In the 16-child long-term cohort: 4/16 died (sepsis or multiple organ failure) and 1/16 survived after liver transplantation (alive 9 years post-transplant). (maggiore2011giantcellhepatitis pages 1-2) * Earlier literature summarized within that cohort reported mortality or need for liver transplantation of 39% in reported cases at that time. (maggiore2011giantcellhepatitis pages 1-2) * In a 6-case mechanistic series: only 1/6 achieved remission with standard therapy; 1 died and 1 underwent transplantation; 3/3 rituximab-treated patients achieved remission. (whitington2014humoralimmunemechanism pages 2-3)

11.2 Prognostic factors

A small 3-infant report concluded: “We conclude that serum ferritin at diagnosis may be used for prediction of the outcome.” However, thresholds and validation were not available in the extracted evidence. (marsalli2016efficacyofintravenous pages 2-3)

A dominant practical prognostic concern across cohorts is infection risk during prolonged immunosuppression (death from sepsis reported). (maggiore2011giantcellhepatitis pages 1-2)

12. Treatment

12.1 Immunosuppression (historical backbone): corticosteroids + azathioprine

In the 16-child cohort, prednisone + azathioprine (± cyclosporine) led to complete remission in 8/16, partial remission in 6/16, and failure in 2/16, but relapses were common (11/16 hepatitis; 10/16 anemia). (maggiore2011giantcellhepatitis pages 1-2)

Suggested MAXO terms (examples): immunosuppressive therapy; glucocorticoid therapy; azathioprine therapy.

12.2 IVIG (immunomodulatory) as adjunct / steroid-sparing

In a multicenter retrospective series of 7 children, IVIG (0.5–2 g/kg; sequential monthly dosing in 5/7) significantly reduced aminotransferases (P=0.04) and showed steroid-sparing benefit, but relapse occurred in all patients over follow-up (hemolysis and/or liver disease). (marsalli2016efficacyofintravenous pages 1-2, marsalli2016efficacyofintravenous pages 6-7)

Suggested MAXO terms: intravenous immunoglobulin therapy.

12.3 Rituximab (anti-CD20) B-cell depletion: targeted therapy with strong signal

Multiple series report strong responses: * Whitington et al.: rituximab induced remission in 3/3 refractory patients. (whitington2014humoralimmunemechanism pages 2-3) * Paganelli et al. (Pediatrics): “complete response” in 4 children, with steroid weaning in all; several doses and 5–11 maintenance injections in severe cases; no infections/side effects reported in that series. (paganelli2014anticd20treatmentof pages 1-2)

Suggested MAXO terms: anti-CD20 monoclonal antibody therapy; B-cell depletion therapy.

12.4 Other immunomodulatory/second-line approaches

Reports include cyclosporine, tacrolimus, mycophenolate, cyclophosphamide, plasmapheresis, splenectomy, and (rarely) stem-cell transplantation in complex immune-dysregulation scenarios; evidence is limited and heterogeneous. (bakula2014giantcellhepatitis pages 1-3, kim2020successfultreatmentof pages 5-6, raj2011giantcellhepatitis pages 1-2)

12.5 Liver transplantation

Transplantation has been used for end-stage liver disease, but recurrence/relapse concerns exist. One child in the 16-patient cohort was alive 9 years post-transplant. (maggiore2011giantcellhepatitis pages 1-2)

A later case review table notes that transplantation has been complicated by relapse/rejection and “is no longer recommended presently” (as a routine strategy), emphasizing immune control instead where possible. (kim2020successfultreatmentof pages 5-6)

12.6 Clinical trials

ClinicalTrials.gov searches in this environment did not yield clear, disease-specific interventional trials for GCH-AIHA.

13. Prevention

No primary prevention strategies are established due to unclear triggers and extreme rarity. Secondary/tertiary prevention in practice focuses on relapse monitoring and infection prevention during immunosuppression (not quantified in retrieved sources). (maggiore2011giantcellhepatitis pages 1-2)

14. Other Species / Natural Disease

No naturally occurring animal disease analogs were identified in the retrieved texts.

15. Model Organisms

No dedicated model organism systems for this syndrome were described in the retrieved texts. Mechanistic reasoning references complement biology and includes supportive statements from experimental complement-depletion contexts, but disease-specific engineered models were not presented in the available extracts. (whitington2014humoralimmunemechanism pages 6-6)

Current applications and real-world implementation (clinical practice implications)

1) Diagnosis in real-world settings relies on recognizing the syndrome pattern (DAT-positive hemolysis plus progressive cholestatic hepatitis) and confirming with liver biopsy and exclusion of other causes. (maggiore2011giantcellhepatitis pages 1-2) 2) Treatment implementation is increasingly aligned with the mechanistic model: conventional immunosuppression may induce remission but relapse is common, while B-cell depletion (rituximab) has repeatedly induced remission in refractory disease and is supported by complement-pathology findings. (whitington2014humoralimmunemechanism pages 2-3, paganelli2014anticd20treatmentof pages 1-2)

Limitations of this report (evidence availability)

  • Disease-specific 2023–2024 primary studies were not accessible via the current retrieval tools; thus, up-to-date (2023–2024) GCH-AIHA-specific statistics (e.g., contemporary response rates to rituximab regimens) could not be extracted here.
  • Standard ontology identifiers (MONDO/OMIM/Orphanet/MeSH/ICD) were not present in the retrieved full texts; they should be sourced from dedicated ontology databases in a separate curation step.
  • Image extraction from key papers failed in this environment, so no histology figure panels could be provided.

Key referenced sources (publication date, URL)

References

  1. (maggiore2011giantcellhepatitis pages 1-2): Giuseppe Maggiore, Marco Sciveres, Monique Fabre, Laura Gori, Lucia Pacifico, Massimo Resti, Jean-Jacques Choulot, Emmanuel Jacquemin, and Olivier Bernard. Giant cell hepatitis with autoimmune hemolytic anemia in early childhood: long-term outcome in 16 children. The Journal of pediatrics, 159 1:127-132.e1, Jul 2011. URL: https://doi.org/10.1016/j.jpeds.2010.12.050, doi:10.1016/j.jpeds.2010.12.050. This article has 72 citations.

  2. (whitington2014humoralimmunemechanism pages 2-3): Peter F. Whitington, Miriam B. Vos, Lee M. Bass, Hector Melin‐Aldana, Rene Romero, Claude C. Roy, and Fernando Alvarez. Humoral immune mechanism of liver injury in giant cell hepatitis with autoimmune hemolytic anemia. Journal of Pediatric Gastroenterology and Nutrition, 58:74–80, Jan 2014. URL: https://doi.org/10.1097/mpg.0b013e3182a98dbe, doi:10.1097/mpg.0b013e3182a98dbe. This article has 39 citations and is from a peer-reviewed journal.

  3. (marsalli2016efficacyofintravenous pages 1-2): Giulia Marsalli, Silvia Nastasio, Marco Sciveres, Pier Luigi Calvo, Ugo Ramenghi, Simona Gatti, Veronica Albano, Sara Lega, Alessandro Ventura, and Giuseppe Maggiore. Efficacy of intravenous immunoglobulin therapy in giant cell hepatitis with autoimmune hemolytic anemia: a multicenter study. Clinics and research in hepatology and gastroenterology, 40 1:83-9, Feb 2016. URL: https://doi.org/10.1016/j.clinre.2015.03.009, doi:10.1016/j.clinre.2015.03.009. This article has 24 citations and is from a peer-reviewed journal.

  4. (raj2011giantcellhepatitis pages 1-2): Shashi Raj, Thomas Stephen, and Robert F. Debski. Giant cell hepatitis with autoimmune hemolytic anemia: a case report and review of pediatric literature. Clinical Pediatrics, 50:357-359, Mar 2011. URL: https://doi.org/10.1177/0009922810379501, doi:10.1177/0009922810379501. This article has 18 citations and is from a peer-reviewed journal.

  5. (kim2020successfultreatmentof pages 2-4): Young Ho Kim, Ju Whi Kim, Eun Joo Lee, Gyeong Hoon Kang, Hyoung Jin Kang, Jin Soo Moon, and Jae Sung Ko. Successful treatment of a korean infant with giant cell hepatitis with autoimmune hemolytic anemia using rituximab. Pediatric Gastroenterology, Hepatology & Nutrition, 23:180-187, Mar 2020. URL: https://doi.org/10.5223/pghn.2020.23.2.180, doi:10.5223/pghn.2020.23.2.180. This article has 9 citations and is from a peer-reviewed journal.

  6. (cho2016giantcellhepatitis pages 1-2): Myung Hyun Cho, Hee Sun Park, Hye Seung Han, and Sun Hwan Bae. Giant cell hepatitis with autoimmune hemolytic anemia in a korean infant. Pediatrics International, 58:628-631, Feb 2016. URL: https://doi.org/10.1111/ped.12874, doi:10.1111/ped.12874. This article has 10 citations and is from a peer-reviewed journal.

  7. (perezatayde1994coombspositiveautoimmunehemolytic pages 1-4): Antonio R. Perez-Atayde, Scott M. Sirlin, and Maureen Jonas. Coombs-positive autoimmune hemolytic anemia and postinfantile giant cell hepatitis in children. Pediatric pathology, 14 1:69-77, Jan 1994. URL: https://doi.org/10.3109/15513819409022027, doi:10.3109/15513819409022027. This article has 33 citations.

  8. (bakula2014giantcellhepatitis pages 1-3): Agnieszka Bakula, Piotr Socha, Maja Klaudel‐Dreszler, Grazyna Karolczyk, Malgorzata Wozniak, Olga Rutynowska‐Pronicka, and Michal Matysiak. Giant cell hepatitis with autoimmune hemolytic anemia in children: proposal for therapeutic approach. Journal of Pediatric Gastroenterology and Nutrition, 58:669–673, May 2014. URL: https://doi.org/10.1097/mpg.0000000000000270, doi:10.1097/mpg.0000000000000270. This article has 33 citations and is from a peer-reviewed journal.

  9. (paganelli2014anticd20treatmentof pages 1-2): Massimiliano Paganelli, Natacha Patey, Lee M. Bass, and Fernando Alvarez. Anti-cd20 treatment of giant cell hepatitis with autoimmune hemolytic anemia. Pediatrics, 134:e1206-e1210, Oct 2014. URL: https://doi.org/10.1542/peds.2014-0032, doi:10.1542/peds.2014-0032. This article has 23 citations and is from a highest quality peer-reviewed journal.

  10. (whitington2014humoralimmunemechanism pages 1-1): Peter F. Whitington, Miriam B. Vos, Lee M. Bass, Hector Melin‐Aldana, Rene Romero, Claude C. Roy, and Fernando Alvarez. Humoral immune mechanism of liver injury in giant cell hepatitis with autoimmune hemolytic anemia. Journal of Pediatric Gastroenterology and Nutrition, 58:74–80, Jan 2014. URL: https://doi.org/10.1097/mpg.0b013e3182a98dbe, doi:10.1097/mpg.0b013e3182a98dbe. This article has 39 citations and is from a peer-reviewed journal.

  11. (marsalli2016efficacyofintravenous pages 4-5): Giulia Marsalli, Silvia Nastasio, Marco Sciveres, Pier Luigi Calvo, Ugo Ramenghi, Simona Gatti, Veronica Albano, Sara Lega, Alessandro Ventura, and Giuseppe Maggiore. Efficacy of intravenous immunoglobulin therapy in giant cell hepatitis with autoimmune hemolytic anemia: a multicenter study. Clinics and research in hepatology and gastroenterology, 40 1:83-9, Feb 2016. URL: https://doi.org/10.1016/j.clinre.2015.03.009, doi:10.1016/j.clinre.2015.03.009. This article has 24 citations and is from a peer-reviewed journal.

  12. (marsalli2016efficacyofintravenous pages 6-7): Giulia Marsalli, Silvia Nastasio, Marco Sciveres, Pier Luigi Calvo, Ugo Ramenghi, Simona Gatti, Veronica Albano, Sara Lega, Alessandro Ventura, and Giuseppe Maggiore. Efficacy of intravenous immunoglobulin therapy in giant cell hepatitis with autoimmune hemolytic anemia: a multicenter study. Clinics and research in hepatology and gastroenterology, 40 1:83-9, Feb 2016. URL: https://doi.org/10.1016/j.clinre.2015.03.009, doi:10.1016/j.clinre.2015.03.009. This article has 24 citations and is from a peer-reviewed journal.

  13. (kim2020successfultreatmentof pages 5-6): Young Ho Kim, Ju Whi Kim, Eun Joo Lee, Gyeong Hoon Kang, Hyoung Jin Kang, Jin Soo Moon, and Jae Sung Ko. Successful treatment of a korean infant with giant cell hepatitis with autoimmune hemolytic anemia using rituximab. Pediatric Gastroenterology, Hepatology & Nutrition, 23:180-187, Mar 2020. URL: https://doi.org/10.5223/pghn.2020.23.2.180, doi:10.5223/pghn.2020.23.2.180. This article has 9 citations and is from a peer-reviewed journal.

  14. (marsalli2016efficacyofintravenous pages 2-3): Giulia Marsalli, Silvia Nastasio, Marco Sciveres, Pier Luigi Calvo, Ugo Ramenghi, Simona Gatti, Veronica Albano, Sara Lega, Alessandro Ventura, and Giuseppe Maggiore. Efficacy of intravenous immunoglobulin therapy in giant cell hepatitis with autoimmune hemolytic anemia: a multicenter study. Clinics and research in hepatology and gastroenterology, 40 1:83-9, Feb 2016. URL: https://doi.org/10.1016/j.clinre.2015.03.009, doi:10.1016/j.clinre.2015.03.009. This article has 24 citations and is from a peer-reviewed journal.

  15. (whitington2014humoralimmunemechanism pages 3-6): Peter F. Whitington, Miriam B. Vos, Lee M. Bass, Hector Melin‐Aldana, Rene Romero, Claude C. Roy, and Fernando Alvarez. Humoral immune mechanism of liver injury in giant cell hepatitis with autoimmune hemolytic anemia. Journal of Pediatric Gastroenterology and Nutrition, 58:74–80, Jan 2014. URL: https://doi.org/10.1097/mpg.0b013e3182a98dbe, doi:10.1097/mpg.0b013e3182a98dbe. This article has 39 citations and is from a peer-reviewed journal.

  16. (whitington2014humoralimmunemechanism pages 6-6): Peter F. Whitington, Miriam B. Vos, Lee M. Bass, Hector Melin‐Aldana, Rene Romero, Claude C. Roy, and Fernando Alvarez. Humoral immune mechanism of liver injury in giant cell hepatitis with autoimmune hemolytic anemia. Journal of Pediatric Gastroenterology and Nutrition, 58:74–80, Jan 2014. URL: https://doi.org/10.1097/mpg.0b013e3182a98dbe, doi:10.1097/mpg.0b013e3182a98dbe. This article has 39 citations and is from a peer-reviewed journal.

  17. (whitington2014humoralimmunemechanism pages 1-2): Peter F. Whitington, Miriam B. Vos, Lee M. Bass, Hector Melin‐Aldana, Rene Romero, Claude C. Roy, and Fernando Alvarez. Humoral immune mechanism of liver injury in giant cell hepatitis with autoimmune hemolytic anemia. Journal of Pediatric Gastroenterology and Nutrition, 58:74–80, Jan 2014. URL: https://doi.org/10.1097/mpg.0b013e3182a98dbe, doi:10.1097/mpg.0b013e3182a98dbe. This article has 39 citations and is from a peer-reviewed journal.