A woman we know has a rare blood disorder. Her body is trying to make red blood cells but something is preventing the process. If you have any suggestions -- including traditional and/or complimentary medicine -- we would be extremely grateful and blessed. Please write to us at email@example.com.
Below is a medical explanation from one of her doctors. Additional information is contained in a story that appeared in The New Sun called, A Birthday Gift that Suits Me.
Medical Explanation and History
(written in summer of '96)
The patient is a 39 year old white female with a history of anemia since 1989. Seven years ago she was found to have a hemoglobin (HGB) of 3.9 g/dL hematocrit (HCT) of 10, a reticulocyte count of ). The white blood count was normal and the platelets were elevate of 691,000/cmm. A bone marrow aspirate revealed only maturation arrest at the erythroblast stage. No evidence of dysplasia was noticed. Coombs test was negative, serum haptoglobin was normal, B12 and folate normal. Chromosome studies were normal. ANA was negative. Antibodies to CMV and EB were negative. CT scan revealed no enlarged thymus.
She was transfused, but her HGB fell shortly afterward. She then received 1) anazol and Prednisone with good results. Once the prednisone was tapered to 15mg daily the HGB began to fall. Further attempts to decrease the prednisone resulted in similar results.
I.V gamma globulin was initiated which resulted in a prompt rise in her HGB. The patient next received a course of low-dose Cyclophosphamide (initial dose 50 mg daily) and then increased to 100 mg for a period of 6 months. During this period the patient continued to require prednisone (15 mg daily) and gamma globulin every three weeks. The cyclophosphamide was discontinued (no added response).
Cyclosporin A was then used. Within 2 weeks HCT levels were normal and reties were 3%. This benefit was short lived. Cyclosporin was discontinued.
She was next treated with I.M. Methotrexate at 25 mg weekly. She had an initial response to this treatment.
A repeat bone marrow aspirate in 1991 revealed an improvement in maturation as compared to 1989. Cytogenetics were again normal.
The patient was placed back on gamma globulin, without prednisone, and continued to require therapy every 3 weeks. In 6/94 the patient underwent plasmapheresis. There was a significant improvement in the HGB. However, the patient continued to require gamma globulin. The added benefit of apheresis lasted for approximately 6 months. Plasmapheresis was repeated; however, this time the benefit was not as pronounced. The use of erythropoietin had no significant effect.
Laboratory studies were performed on the patient's bone marrow, plasma, and protein from the apheresis collection. All tests were suggestive of the presence of an inhibitor to red cell precursors.