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Hormones and Metabolism

The development of acute leukemia is accompanied by abnormalities in levels of cholesterol and some lipids (Baroni S et al 1994; Baroni S et al 1996; Moschovi M et al 2004). In particular, AML and ALL patients have low levels of high-density-lipoprotein cholesterol (Baroni S et al 1994; Baroni S et al 1996; Moschovi M et al 2004). Upon treatment, cholesterol levels return to normal in patients that respond to treatment, suggesting that cholesterol could be used as a marker to monitor chemotherapy (Baroni S et al 1994; Baroni S et al 1996; Moschovi M et al 2004). Research using specific types of leukemia cells (HL-60 cells) and showing that cholesterol is required for cells to progress through cell division (Fernandez C et al 2004) may explain the link between low cholesterol levels and acute leukemia that is characterized by the failure of cells to reach maturity.

Levels of the anti-inflammatory hormone cortisol are elevated in AML, CML,(Everaus H et al 1997; Singh JN et al 1989) and CLL (Everaus H 1992) patients. These high levels of cortisol, a powerful immunosuppressive agent, are associated with impaired immune cell responses (Everaus H 1992; Everaus H et al 1997) and may be partially responsible for the immune dysfunction seen in these patients.

DHEA. The hormone dehydroepiandrosterone (DHEA) has been shown to favorably alter inflammatory cytokines such as interleukin-2 in leukemic mice (raghi-Niknam M et al 1997). DHEA favorably modulated the immune dysfunction that occurred during leukemia retrovirus infection in old mice (Inserra P et al 1998) and prevented leukemia growth (Catalina F et al 2003).

DHEA might be effective in supporting healthy immune function in leukemia patients with a DHEA deficiency, which can be determined by a blood test (Uozumi K et al 1996). DHEA is contraindicated in both men and women with certain hormone-related cancers.