els of functioning. Everyday tasks were described as requiring excessive effort. Also reported were sleep disturbances and fatigue resulting in a decreased quality of life (Wagner-Raphael, Jason & Ferrari, 1999).
No pathognomonic signs or diagnostic tests for CFS have been validated in scientific studies and no definitive treatment exists. Many illnesses however, are characterized by chronic fatigue as a major symptom, one of which is chronic depression. Biochemical imbalances have been identified as potential causal factors in diseases such as depression and long-term autoimmune diseases (Gimenez, Cash, Laing & Douglas, 1999; Wilson et al., 1996). This raises the possibility that an imbalance may lead to the identification of a CFS causing mechanism such as C-1 esterase inhibitor.
C-1 esterase inhibitor deficiency has been identified as resulting in hereditary and acquired angio-neurotic edema (HANE, AANE). C-1 esterase inhibitor deficiency results in unchecked classical complement activation (vasoactive substance release and increased vascular permeability) and recurrent mast cell degranulation (recurrent loss of connective tissue cell granules; mast cells physiologic function is unknown but may be capable of elaborating basophilic, metachromatic cytoplasmic granules containing histamine and heparin) (Alsenz, Bork & Loos, 1987; Kwong, Maalouf & Jones, 1998; Lovsin, Guzej, Vok, Kramar & Ravnikar, 1999).
Research linking C-1 esterase inhibitor deficiency with CFS is lacking. The literature provided examples of diseases that were found to result from this deficiency, therefore, it is logical to explore possible effects of C-1 esterase deficiencies with other diseases.
Chronic fatigue was first mentioned in the medical literature in 1869. The condition was described by an English physician who called it neurasthenia (Chronic Fatigue Syndrome, 1997). The search for causes of the problem of chronic fatigue began...