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14 recordsLinked to original sources
PubMed2004

Post-liver-transplant anemia: etiology and management.

Anemia is common after liver transplantation, with the incidence ranging from 4.3% to 28.2% depending on the criteria used to define anemia. The cause of anemia is unidentified in the majority of patients, and it is likely to be multifactorial. Immunosuppressive-medication-induced bone marrow suppression is perhaps the most common cause of unexplained anemia. Chronic blood loss, iron deficiency, hemolysis, and renal insufficiency are other potential causes of chronic anemia. Rare causes, somewhat unique to transplantation, include aplastic anemia, graft-versus-host disease (GVHD), and lymphoproliferative disease. Anemia due to immunosuppressive medication is challenging, since almost all drugs currently used for this purpose cause anemia, but the renal-sparing property of sirolimus may benefit the subgroup in which renal insufficiency is contributing to anemia. Aplastic anemia is seen in young patients transplanted for non-A, non-B, non-C, fulminant hepatic failure. It is thought to be immunologically mediated, secondary to an unknown viral infection, and is associated with a grave prognosis. GVHD is another infrequent (approximately 1% of transplant recipients) but serious cause of severe anemia that carries a dismal prognosis. Lymphoproliferative disorder, too may rarely rare cause anemia and it may respond to reduction of immunosuppression. Recipients of solid-organ transplants do not mount a significant increase in erythropoietin in response to anemia. In conclusion, though there are no data on the response of anemia to erythropoietin in liver transplant recipients, it appears to benefit other solid-organ-transplant recipients with anemia.

Anemia↗
PubMed1989

Diamond-blackfan anemia: etiology, pathophysiology, and treatment.

Diamond-Blackfan anemia (DBA) is manifested by a wide variety of clinical and in vitro abnormalities. Despite this biological diversity, the hematological phenotype is remarkably similar for all patients and consists of a normochromic-macrocytic anemia in early childhood, reticulocytopenia, and a normocellular marrow with a selective deficiency of red cell precursors. Fetal hemoglobin is usually increased, distributed heterogeneously, has a fetal G gamma/A gamma pattern, and is associated with increased expression of red cell i antigen. Although most cases are sporadic, there are examples of autosomal recessive and autosomal dominant inheritance patterns. Approximately 70% of patients with DBA respond to prednisone, and many can be maintained on tapered doses. Those who are steroid-dependent at high dosage as well as those who do not respond are managed on a transfusion and iron chelation program. Claims of efficacy for other therapies, such as cyclosporine or high-dose intravenous methylprednisolone, require substantiation. Bone marrow transplantation has been successfully performed in patients who have tissue-matched donors, and the procedure cures the anemia. Recombinant growth factors may be a therapy of the future. Regarding pathophysiology, initial reports of humoral or cellular inhibitors of erythropoiesis were not confirmed in all laboratories. However, some patients have lymphocyte dysfunction with decreased T cells, decreased T4/T8 ratios, and defective lymphocyte-mediated suppression of lymphoproliferation. A large body of data indicates that the erythroid stem cells are intrinsically defective in DBA, and they are partly or completely refractory to erythropoietin. The role of elevated red cell adenosine deaminase activity in the pathogenesis of this abnormal erythropoiesis is not clear, but this finding is characteristic of the syndrome in most patients. Present studies using recombinant growth factors have demonstrated a diversity of defects in erythropoiesis in patients with DBA. Blocks in red cell production and red cell maturation were seen at various levels along the differentiation pathway. Of clinical interest, interleukin-3 has a corrective effect in vitro on the aberrant marrow erythropoiesis of steroid-refractory patients, and, hence, it may have therapeutic application.

Adrenal Cortex Hormones↗
PubMed1993

Abnormal uterine bleeding associated with iron-deficiency anemia. Etiology and role of hysteroscopy.

We reviewed the clinical and histologic records of 61 consecutive premenopausal women with abnormal uterine bleeding and moderate to severe iron-deficiency anemia investigated in a tertiary care and referral center. Excessive bleeding was caused by benign lesions in 67% of the cases and by anovulation in 25% and was unexplained in 8%. Hysteroscopy revealed an organic intrauterine lesion (submucous myomas in 38%, endometrial polyps in 13%, submucous adenomyomas in 3%) that could be treated endoscopically in more than half the patients. In populations without nutritional deficiencies, a woman of reproductive age with sideropenic anemia and no other evident cause of blood loss or systemic disease should be considered menorrhagic until proven otherwise. Hysteroscopy should be included in evaluations of abnormal uterine bleeding.

Adenomyoma↗