Combining Interferon-a2b (IFN) and Intravenous Immunoglobulins IgG, IgM and IgA (IVIG) in Rapid Progressive Myelofibrosis (MF) With Trisomy 1

Combining Interferon-a2b (IFN) and Intravenous Immunoglobulins IgG, IgM and IgA (IVIG) in Rapid Progressive Myelofibrosis (MF) With Trisomy 1

Combining Interferon-a2b (IFN) and Intravenous Immunoglobulins IgG, IgM and IgA (IVIG) in Rapid Progressive Myelofibrosis (MF) With Trisomy 1

Combining physiological cell-secreted molecules may impact therapeutics.
Here we associate IFN and IVIG for MF after a 3-year experience with
chronic hepatitis C [1].
The 59-year-old male developed 21⁄2 years painful osteosclerosis. Two
dry tap marrow biopsies bent steel needles like straw. Failing 6-month
IFN-monotherapy (5 MU sc 3 times per week), transdermal fentanyl, ketorolac,
and transfusions (Hb 4.4 g/dl) became necessary. Splenectomy (4
kg) only alleviated metaplasia’s mechanical burden. Histology: hematopoiesis
(60–65%) and fibrosis mix with hemocatheresis and scattered lymphatic
tissue. Few, mostly intrasinusoidal, megakaryocytes—small and
large in balance; nuclei: atypical, hyposegmented. Blood: anemia, thrombocytopenia,
some immature leukocytes persisted (also tetraploid, pelgueroid),
reticulocytes fell, rising peripheral erythroblasts.
Improvement coincided with IVIG adding, (IgG: 2 g/kg) followed by
IgG + IgM + IgA (14 fortnight doses, 0.4, 0.06, 0.06 g/kg [Pentaglobin,
Biotest Pharma GmBH] respectively, weight adjustment, +19.5%, not
done). Regularly, the patient emphasized 2–3 days postinfusion pain relief.

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