According to such hypotheses chemical exposures at minute levels are thought to trigger sensitization processes through olfactory-limbic pathways. Because of the lack of scientific data major medical organizations do not recognize MCS as a clinical syndrome. Depending on the enzyme and primary organ affected, they are grouped into hepatic, erythropoietic, or both. Depending on the enzyme involved, they present either as acute or chronic syndromes with symptoms triggered by exposure to drugs or toxins. Abdominal pain and neurologic abnormalities are the main features of acute porphyrias during an attack.
Chronic porphyrias have prominent skin manifestations.
Latent cases as well as organ-specific deficiencies can only be detected by assay of the activity of the deficient enzyme. Lead poisoning or rarely drugs, such as carbamazepine, or other chemicals, can produce clinical and biochemical findings that resemble acute porphyria. The assay uses erythrocytes, however, which do not contain mitochondria. The substrates used for the assay have to pass through several earlier enzymatic steps to yield the immediate substrate for the coproporphyrinogen oxidase. Any variation in the yield of intermediate products would alter the substrate availability for the enzyme.