Clinical Trial: Incidence of Iron Deficiency in Polycythemia Vera (PV) and Association With Disease Features
Study Status: Not yet recruiting
Recruit Status: Not yet recruiting
Study Type: Observational
Official Title: Incidence of Iron Deficiency in Polycythemia Vera (PV) and Association With Disease Features
Brief Summary:
Iron deficiency is a known feature of PV, occurs because of accelerated erythropoiesis, gastrointestinal blood loss and phlebotomy. Incidence and effect of iron deficiency in these patients is not well characterized. The study will assess the incidence of iron deficiency at diagnosis and during the course of PV, assess effect of iron deficiency on patient symptoms and its correlation with disease features.
This is a multicenter, non-interventional, non-randomized, prospective, observational study in an adult population (patients >18 years old) of patients who have been diagnosed with PV and are being followed in either community or academic medical centers in Israel.
Detailed Summary:
Background:
Within intestinal epithelial cells, some of the imported iron is incorporated into ferritin and other storage forms. A fraction of the iron taken up from the intestinal lumen passes through the cell, and is exported across the basolateral membrane to enter the body. Ferroportin, a metal ion transporter, serves as the basolateral iron exporter. Hepcidin regulates basolateral iron export by binding to ferroportin to trigger its internalization and lysosomal degradation. Each day, normal adults need 25 mg of iron to support hemoglobin production in maturing erythrocytes. This amount is much greater than the iron absorbed daily through the intestine. Obviously, iron needed for erythropoiesis must be acquired from supplies already existing in the body. The primary source of plasma iron is the reticuloendothelial macrophage system, which recovers iron from senescent and damaged erythrocytes. Other significant site of iron exchange is the liver.
Dietary iron absorption is enhanced in response to insufficient iron stores, increased erythropoietic demand or hypoxia. It is diminished in response to iron surfeit and inflammation. Based on these observations, four different "regulators" have been defined functionally: 1) The stores regulator modulates absorption several fold, increasing it in iron deficiency and decreasing it in iron overload. 2) The erythroid regulator is more potent—it can increase iron absorption 6- to 10-fold when erythropoiesis becomes iron -restricted, result either from iron deficiency or from accelerated production of erythroid precursors. 3) The hypoxia regulator mediates an increase in iron absorption in response to hypoxia, to allow for production of hemoproteins that bind and carry oxygen. 4) An inflammatory regulator also exists, which acts to decrease iron absorption in respon
Sponsor: Rambam Health Care Campus
Current Primary Outcome: Incidence of iron deficiency in patients with PV [ Time Frame: 2 years ]
Original Primary Outcome: Same as current
Current Secondary Outcome:
- Association between iron deficiency and other clinical features [ Time Frame: 2 years ]
- Influence of therapy (phlebotomies, hydroxyurea, other therapies) on iron parameters [ Time Frame: 2 years ]
- Influence of iron parameters on Patient-reported symptoms [ Time Frame: 2 years ]
- Influence of iron deficiency on arterial and venous thrombosis rate [ Time Frame: 2 years ]
Original Secondary Outcome: Same as current
Information By: Rambam Health Care Campus
Dates:
Date Received: June 18, 2016
Date Started: July 2016
Date Completion: August 2018
Last Updated: June 21, 2016
Last Verified: June 2016
