APLASTIC ANEMIA AND VIRAL HEPATITIS
<p class="MsoNormal" style="margin: 0cm 0cm 0pt; line-height: 200%; text-align: justify;"><span style="font-size: small;"><span style="font-family: Times New Roman;">Acquired aplastic anemia(aAA) is a severe <sp...
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| Format: | Article |
| Language: | English |
| Published: |
PAGEPress Publications
2009-11-01
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| Series: | Mediterranean Journal of Hematology and Infectious Diseases |
| Subjects: | |
| Online Access: | http://www.mjhid.org/article/view/5225 |
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| Summary: | <p class="MsoNormal" style="margin: 0cm 0cm 0pt; line-height: 200%; text-align: justify;"><span style="font-size: small;"><span style="font-family: Times New Roman;">Acquired aplastic anemia(aAA) is a severe <span style="mso-ansi-language: EN-GB;" lang="EN-GB">and rare disease, characterized by hematopoietic bone marrow failure and peripheral cytopenia. The pathophysiology is immune mediated in most cases, activated T1 lymphocytes have been identified as effector cells . The disease can be successfully treated with combined immunosuppressive therapy or allogeneic hematopoietic stem cell transplantation.</span></span></span></p><p class="MsoNormal" style="margin: 0cm 0cm 0pt; line-height: 200%; text-align: justify;"><span style="mso-ansi-language: EN-GB;" lang="EN-GB"><span style="font-size: small;"><span style="font-family: Times New Roman;">Hepatitis-associated aplastic anemia (HAA)<span style="mso-spacerun: yes;"> </span>is a syndrome of bone marrow failure following the development of acute seronegative hepatitis. HAA syndrome most often affects young males who presented severe pancytopenia two to three months after an episode of acute hepatitis. The clinical course of hepatitis is more frequently benign but a fulminant severe course is also described. The bone marrow failure can be explosive and severe and it is usually fatal if untreated, no correlations have been observed between severity of hepatitis and AA.</span></span></span></p><p class="MsoNormal" style="margin: 0cm 0cm 0pt; line-height: 200%; text-align: justify;"><span style="mso-ansi-language: EN-GB;" lang="EN-GB"><span style="font-size: small;"><span style="font-family: Times New Roman;">In none of the<span style="mso-spacerun: yes;"> </span>studies a specific virus could be identified and most cases are seronegative for known hepatitis viruses. The clinical characteristics<span style="mso-spacerun: yes;"> </span>and response to immunotherapy indicate a central role for immune-mediated mechanism in the pathogenesis of HAA. The initial target organ of the immune<span style="mso-spacerun: yes;"> </span>response is the liver as suggested by the time interval between hepatitis and the onset of bone marrow failure.</span></span></span></p><p class="MsoNormal" style="margin: 0cm 0cm 0pt; line-height: 200%; text-align: justify;"><span style="mso-ansi-language: EN-GB;" lang="EN-GB"><span style="font-size: small;"><span style="font-family: Times New Roman;">Liver histology is characterized by T cell infiltrating the parenchyma as reported in acute hepatitis. </span></span></span></p><p class="MsoBodyText" style="margin: 0cm 0cm 0pt;"><span lang="EN-GB"><span style="font-size: small; font-family: Times New Roman;">Recently in HAA it has been demonstrated intrahepatic<span style="mso-spacerun: yes;"> </span>and blood lymphocytes with<span style="mso-spacerun: yes;"> </span>T cell repertoire similar to that of confirmed viral acute hepatitis. The expanded T cell clones return to a normal distribution after response to immunosuppressive treatment, suggesting the antigen or T cell clearance. Therapeutic options are the same as acquired aplastic anemia.</span></span></p> |
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| ISSN: | 2035-3006 |