Abstract
Up to the present time the etiology of polycythemia vera has not been clarified nor have the methods of treatment proposed met with lasting success. It is generally agreed (Vaquez 1 and Osier 2 that the hematopoietic tissues are primarily at fault. One group of workers look upon erythremia as a neoplasm of the bone marrow (Minot and Buckman 3 ), another as an excessive response to agents formed in the liver, stomach (Marshall 4 and Morris 5 ), and endocrine organs (Gunther, 6 Moehlig and Bates, 7 and others), and a third group visualizes the disease as an anoxemic response induced by subintimal and advential fibrosis in the arteries and arterioles of the bone marrow (Reznikoff, Foot and Bethea 8 ).
In polycythemia the patho-physiological changes in the peripheral blood are characterized by an increase in the number of red blood cells per cmm., an increase in the hemoglobin, an increase in the volume of packed cells with a corresponding decrease in plasma volume (hematocrit reading) and an increase in the total circulating blood volume.
When one searches for a means of correcting this anomaly, the state of myxoedema presents itself. It has been shown (Minot, 9 Emery, 10 Mackenzie, 11 and Stone 12 ) that anemia is a frequent if not constant finding in myxoedema; and there is abundant evidence (Tatum, 13 Lim, 14 and Kunde 15 ) to indicate that the abolition of thyroid function would depress erythropoiesis. Myxoedema is also associated with a decreased blood volume (Thompson, 16 Goldbloom and Libin 17 ). It seemed, therefore, a rational therapeutic procedure to subject a patient with polycythemia vera to a total thyroidectomy.
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