Table 7 Summary of clues from blood profile to role of infection in aetiology/pathogenesis of idiopathic parkinsonism.

Blood lymphocyte count

Reduced count in probands and their spouses cf contemporaneous controls.

Viral origin would fit, especially in context of:-

(i) prevalent abnormal bowel function, starting prodromally in probands, and found in spouses

(ii) evidence of premonitory parkinsonian state in spouses.

Serum Immunoglobulin (IgM, IgG, IgA) concentrations

Strong associations with sporadic cardinal features of parkinsonism in controls suggest premonitory infection.

Serum IgM concentration

Differential effect of Helicobacter seropositivity between probands and controls.

Sequestration to site gastric inflammation no longer obtains in established parkinsonism or there is increased production of poly-specific IgM (in response to Helicobacter or SIBO).

Serum autoantibody titres

ANA associated with failure of, and functional deterioration after, Helicobacter eradication therapy in probands.

Autoimmune element to response to Helicobacter in probands. Hence, importance of residual low-density infection.

Serum haematinic and homocysteine concentrations

Elevated homocysteine prevalent in probands: explained only in small part by haematinics.

Immunoinflammatory activation likely cause.

Importance of SIBO suggested by association of breath-hydrogen with iron absorption (ferritin & MCHC markers) in a setting where moderate/severe gastric atrophy uncommon. Reduction of gastric acid by inflammatory cytokine likely mechanism.