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Severe Aplastic Anemia following Acute Hepatitis from Toxic Liver Injury: Literature Review and Case Report of a Successful Outcome.

Qureshi K, Sarwar U, Khallafi H - Case Reports Hepatol (2014)

Bottom Line: The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA.We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids.He was treated with IST with successful outcome without the need for a BMT.

View Article: PubMed Central - PubMed

Affiliation: Section of Gastroenterology and Hepatology, Division of Hepatology, Department of Medicine, Temple University School of Medicine, Temple University Health System, 3440 N Broad Street, Kresge Building West No. 209, Philadelphia, PA 19140, USA.

ABSTRACT
Hepatitis associated aplastic anemia (HAAA) is a rare syndrome in which severe aplastic anemia (SAA) complicates the recovery of acute hepatitis (AH). HAAA is described to occur with AH caused by viral infections and also with idiopathic cases of AH and no clear etiology of liver injury. Clinically, AH can be mild to fulminant and transient to persistent and precedes the onset SAA. It is assumed that immunologic dysregulation following AH leads to the development of SAA. Several observations have been made to elucidate the immune mediated injury mechanisms, ensuing from liver injury and progressing to trigger bone marrow failure with the involvement of activated lymphocytes and severe T-cell imbalance. HAAA has a very poor outcome and often requires bone marrow transplant (BMT). The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA. We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids. The liver injury slowly resolved with supportive care and after 4 months of attack of AH, he developed SAA. He was treated with IST with successful outcome without the need for a BMT.

No MeSH data available.


Related in: MedlinePlus

Graphical trends of the laboratory parameters of HAAA over six months.
© Copyright Policy - open-access
Related In: Results  -  Collection


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fig2: Graphical trends of the laboratory parameters of HAAA over six months.

Mentions: We describe a case of a 26-year-old Hispanic male, who presented (Day 1) to his primary care physician (PCP) office after he noticed progressively worsening yellowish discoloration of his eyes and skin for 10 days' duration. In addition, he had noticed dark urine for 2-3 weeks and pale colored stools for 5–7 days. He complained of nausea, generalized fatigue, and malaise but did not have any abdominal pain, fever, chills, diarrhea, or any skin rash. He was noted to have diffuse jaundice, hepatomegaly, and mild epigastric tenderness on examination. The laboratory evaluation revealed abnormalities in liver panel, with total bilirubin (TBili) of 12.2 mg/dL, alkaline phosphatase (AlkP) 272 IU/dL, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) of 2112 and 1055 IU/dL, respectively (Table 1). The complete blood count (CBC) and coagulation panel (INR) were normal at that time. He was admitted to our hospital where he underwent initial workup for painless jaundice. Upon initial evaluation by hepatology service, he informed us that he was originally from Puerto Rico and was living in the US for 17 years. He denied any history of significant illness as a child or any known history of liver disease in any family member. He denied any episodes of mental confusion and excessive sleepiness, as well as hematemesis, hematochezia, melena, or poor appetite. He also denied pruritus at any time and lower extremity edema or increased abdominal girth. He denied any recent sick contacts, animal exposure, or travel outside the US. He denied any history of incarceration, tattoos, or blood transfusions. He denied any history of tobacco use, illicit drug usage such as marijuana, cocaine, and heroin, or abuse of amphetamines. He reported drinking alcohol only on occasions and his last drink was approximately 7 months prior to this admission. However, he did report that he had been using over-the-counter anabolic steroids and a supplement from a vitamin store as a muscle-building high performance protein supplement (the ingredients are indicated in Table 3) on a daily basis for approximately 6 months. On examination, he appeared comfortable with diffuse jaundice and somewhat tender hepatomegaly. No clinical stigmata of advanced liver disease were identified on examination. The baseline serologic workup is shown in Table 2 which ruled out any infectious, autoimmune, or metabolic causes of his liver disease. The radiological workup with ultrasound, and a Magnetic Resonance Cholangiopancreatography did not reveal any biliary obstruction. He was suspected to have probable DILI with significant hyperbilirubinemia based on the negative etiologic workup. For further confirmation, he underwent a liver biopsy (Day 5) which revealed quite an impressive inflammatory process involving both portal areas and the lobules displaying also a pattern of sinusoidal lymphocytosis (Figure 1). The hepatocytic injury was identified and was more prominent in centrilobular (zone 3) location. Trichrome stain revealed only mild portal and periportal fibrosis and some perisinusoidal fibrosis especially in centrilobular location where the majority of the hepatocytic damage was identified along with mild collapse of the reticulin framework and likely was the result of hepatocytic dropout. Within the lobules, there was prominent “spotty necrosis,” highlighted with the PAS positive, diastase resistant stain, revealing macrophages loaded with phagocytic debris. Iron stores were not increased and immunostain for adenovirus, cytomegalovirus (CMV), herpes virus, and hepatitis B surface antigen were also negative on the histologic tissue. Iron stain was negative and copper stain showed no increased copper deposition in the hepatocytes. Based on the above findings, he was started on a short course of oral prednisone and ursodiol (Day 8) as the treatment for severe AH with cholestasis. His laboratory tests showed gradual improvement in hepatitis and subsequently he was discharged to be followed up as outpatient. He was seen in the clinic for monitoring (Day 35) and reported over all symptomatic improvement and he had started back his job as a residential painter. His follow-up monitoring laboratory testing 6 weeks later showed continued improvement in AH (Figure 2) while he stayed on low dose ursodiol.


Severe Aplastic Anemia following Acute Hepatitis from Toxic Liver Injury: Literature Review and Case Report of a Successful Outcome.

Qureshi K, Sarwar U, Khallafi H - Case Reports Hepatol (2014)

Graphical trends of the laboratory parameters of HAAA over six months.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4283356&req=5

fig2: Graphical trends of the laboratory parameters of HAAA over six months.
Mentions: We describe a case of a 26-year-old Hispanic male, who presented (Day 1) to his primary care physician (PCP) office after he noticed progressively worsening yellowish discoloration of his eyes and skin for 10 days' duration. In addition, he had noticed dark urine for 2-3 weeks and pale colored stools for 5–7 days. He complained of nausea, generalized fatigue, and malaise but did not have any abdominal pain, fever, chills, diarrhea, or any skin rash. He was noted to have diffuse jaundice, hepatomegaly, and mild epigastric tenderness on examination. The laboratory evaluation revealed abnormalities in liver panel, with total bilirubin (TBili) of 12.2 mg/dL, alkaline phosphatase (AlkP) 272 IU/dL, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) of 2112 and 1055 IU/dL, respectively (Table 1). The complete blood count (CBC) and coagulation panel (INR) were normal at that time. He was admitted to our hospital where he underwent initial workup for painless jaundice. Upon initial evaluation by hepatology service, he informed us that he was originally from Puerto Rico and was living in the US for 17 years. He denied any history of significant illness as a child or any known history of liver disease in any family member. He denied any episodes of mental confusion and excessive sleepiness, as well as hematemesis, hematochezia, melena, or poor appetite. He also denied pruritus at any time and lower extremity edema or increased abdominal girth. He denied any recent sick contacts, animal exposure, or travel outside the US. He denied any history of incarceration, tattoos, or blood transfusions. He denied any history of tobacco use, illicit drug usage such as marijuana, cocaine, and heroin, or abuse of amphetamines. He reported drinking alcohol only on occasions and his last drink was approximately 7 months prior to this admission. However, he did report that he had been using over-the-counter anabolic steroids and a supplement from a vitamin store as a muscle-building high performance protein supplement (the ingredients are indicated in Table 3) on a daily basis for approximately 6 months. On examination, he appeared comfortable with diffuse jaundice and somewhat tender hepatomegaly. No clinical stigmata of advanced liver disease were identified on examination. The baseline serologic workup is shown in Table 2 which ruled out any infectious, autoimmune, or metabolic causes of his liver disease. The radiological workup with ultrasound, and a Magnetic Resonance Cholangiopancreatography did not reveal any biliary obstruction. He was suspected to have probable DILI with significant hyperbilirubinemia based on the negative etiologic workup. For further confirmation, he underwent a liver biopsy (Day 5) which revealed quite an impressive inflammatory process involving both portal areas and the lobules displaying also a pattern of sinusoidal lymphocytosis (Figure 1). The hepatocytic injury was identified and was more prominent in centrilobular (zone 3) location. Trichrome stain revealed only mild portal and periportal fibrosis and some perisinusoidal fibrosis especially in centrilobular location where the majority of the hepatocytic damage was identified along with mild collapse of the reticulin framework and likely was the result of hepatocytic dropout. Within the lobules, there was prominent “spotty necrosis,” highlighted with the PAS positive, diastase resistant stain, revealing macrophages loaded with phagocytic debris. Iron stores were not increased and immunostain for adenovirus, cytomegalovirus (CMV), herpes virus, and hepatitis B surface antigen were also negative on the histologic tissue. Iron stain was negative and copper stain showed no increased copper deposition in the hepatocytes. Based on the above findings, he was started on a short course of oral prednisone and ursodiol (Day 8) as the treatment for severe AH with cholestasis. His laboratory tests showed gradual improvement in hepatitis and subsequently he was discharged to be followed up as outpatient. He was seen in the clinic for monitoring (Day 35) and reported over all symptomatic improvement and he had started back his job as a residential painter. His follow-up monitoring laboratory testing 6 weeks later showed continued improvement in AH (Figure 2) while he stayed on low dose ursodiol.

Bottom Line: The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA.We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids.He was treated with IST with successful outcome without the need for a BMT.

View Article: PubMed Central - PubMed

Affiliation: Section of Gastroenterology and Hepatology, Division of Hepatology, Department of Medicine, Temple University School of Medicine, Temple University Health System, 3440 N Broad Street, Kresge Building West No. 209, Philadelphia, PA 19140, USA.

ABSTRACT
Hepatitis associated aplastic anemia (HAAA) is a rare syndrome in which severe aplastic anemia (SAA) complicates the recovery of acute hepatitis (AH). HAAA is described to occur with AH caused by viral infections and also with idiopathic cases of AH and no clear etiology of liver injury. Clinically, AH can be mild to fulminant and transient to persistent and precedes the onset SAA. It is assumed that immunologic dysregulation following AH leads to the development of SAA. Several observations have been made to elucidate the immune mediated injury mechanisms, ensuing from liver injury and progressing to trigger bone marrow failure with the involvement of activated lymphocytes and severe T-cell imbalance. HAAA has a very poor outcome and often requires bone marrow transplant (BMT). The findings of immune related myeloid injury implied the use of immunosuppressive therapy (IST) and led to improved survival from HAAA. We report a case of young male who presented with AH resulting from the intake of muscle building protein supplements and anabolic steroids. The liver injury slowly resolved with supportive care and after 4 months of attack of AH, he developed SAA. He was treated with IST with successful outcome without the need for a BMT.

No MeSH data available.


Related in: MedlinePlus