Might Helicobacter pylori infection be associated with distortion on taste perception?

Helicobacter pylori (H. pylori) has been found in dental plaque, saliva and lingual sites. To date, taste or olfaction disorders related to H. pylori infections have never been reported. In a review of the literature we found two papers just referring to a sour taste sensation during H. pylori infection. Studies in animal models suggest that changes in taste perception may relate to infections which damage taste buds. We observed an interesting clinical case of a 24-year-old Ghanaian woman with documented H. pylori gastric infection, complaining of cacosmia and cacogeusia. Taste evaluation indicated hypogeusia and highlighted a specific difficulty in discriminating between bitter and acid tastes. Saliva fluid was found positive for the ureA gene (H. pylori ureasi A). On the basis of this report, we hypothesize that taste perception might be correlated with a documented H. pylori infection. So, in a dyspeptic clinical picture in both pre and post diagnostic phase when H. pylori infection is suspected, taste evaluation might be important. Further studies are certainly needed in a large patient population to clarify the possible connection between H. pylori infection and smell-taste distortion.

The status of olfactory function and the striatal dopaminergic system in drug-induced parkinsonism.

Olfactory impairment has been reported in drug-induced parkinsonism (DIP), but the relationship between dopaminergic dysfunction and smell deficits in DIP patients has not been characterized. To this end, we studied 16 DIP patients and 13 patients affected by Parkinson's disease (PD) using the "Sniffin' Sticks" test and [(123)I] FP-CIT SPECT (single-photon emission computed tomography). DIP patients were divided based on normal (n = 9) and abnormal (n = 7) putamen dopamine transporter binding. Nineteen healthy age- and sex-matched subjects served as controls of smell function. Patients with DIP and pathological putamen uptake had abnormal olfactory function. In this group of patients, olfactory TDI scores (odor threshold, discrimination and identification) correlated significantly with putamen uptake values, as observed in PD patients. By contrast, DIP patients with normal putamen uptake showed odor functions-with the exception of the threshold subtest-similar to control subjects. In this group of patients, no significant correlation was observed between olfactory TDI scores and putamen uptake values. The results of our study suggest that the presence of smell deficits in DIP patients might be more associated with dopaminergic loss rather than with a drug-mediated dopamine receptor blockade. These preliminary results might have prognostic and therapeutic implications, as abnormalities in these individuals may be suggestive of an underlying PD-like neurodegenerative process.