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Page 313 Guerra et al. J Transl Genet Genom 2022;6:304-21 https://dx.doi.org/10.20517/jtgg.2022.08

Name: Perindopril Mechanistic genes: SFRP4, ACE, AGT, AGTR1, MMP2, TGFB1
IUPAC name: 1H-Indole-2-carboxylic acid, 1-[2-[[1-(ethoxycarbonyl)butyl]amino]-1-oxopropyl]octahydro-, [2S- Metabolic genes:
[1[R*(R*)],2α,3aβ,7aβ]]- Substate: BCHE
Molecular Formula: C H N O C H N Transporter genes: SLC15A1, SLC15A2
19 32 2 5 4 11
Molecular Weight: 441.60 g/mol
Mechanism: A prodrug for perindoprilat, which acts as competitive inhibitor of angiotensin-converting enzyme. Prevents
c conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, and causes an increase in plasma renin activity
and reduction in aldosterone secretion.
Effect: Angiotensin-converting enzyme inhibitors

Name: Levetiracetam Mechanistic genes: SV2A, CACNA1B, MT-TK
IUPAC name: 1-Pyrrolidineacetamide, α-ethyl-2-oxo-, (α S)- Metabolic genes:
Molecular Formula: C H N O Unknown: CYP2D6, CYP3A4
8 14 2 2
Molecular Weight: 170.21 g/mol Transporter genes: ABCB1
Mechanism: The precise mechanism by which levetiracetam exerts its antiepileptic effect is unknown and does not
appear to derive from any interaction with known mechanisms involved in inhibitory and excitatory neurotransmission.
Effect: Anticonvulsants, miscellaneous

The T allele of rs17601696 (parent gene FGFR2) is reported to be associated with ND .
[72]

PHARMACOGENETICS OF DRUGS EMPLOYED IN OTHER ASSOCIATED OROPHARYNGEAL SYMPTOMS IN NEUROGENIC

DYSPHAGIA
Together with strategies aimed at controlling ND, it is also important to manage those factors that may exacerbate symptoms and increase the risk of

aspiration. Many patients with CNS conditions exhibit sialorrhea, hiccups, xerostomia, or reflux with swallowing difficulties. Prior to considering systemic
drugs, it is recommended that local treatment or physical measures be initiated first [Table 4] .
[37]

Sialorrhea
The most used treatments for the control of hypersalivation in patients with neurological damage are based on their anticholinergic profiles. This includes a
heterogeneous group of drugs such as amitriptyline, scopolamine, glycopyrronium chloride, trihexyphenidyl, atropine, or thiopium bromide. These

[73]
anticholinergic agents present an added benefit in the control of other motor symptoms, as occurs in patients with Parkinson’s disease . However, their main
drawback is the occurrence of frequent side effects that include sedation, cognitive deficits, constipation, urinary retention, tremor, and blurred vision. Within
a population where the prevalence of dementia is high, elderly patients often use drugs with anticholinergic effects, and frequently in combination.

Furthermore, in this patient population, polymedication may mask symptoms that are misdiagnosed as pathology unrelated to drug toxicity .
[74]

Concerning the pharmacogenetic profile, anticholinergic drug exposure shows associated variants located at chromosome 3p21.1 locus, with the top
SNP rs1076425 in the inter-alpha-trypsin inhibitor heavy chain 1 (ITIH1) gene . Subjects with CYP2D6/CYP2C19 PM phenotype increase the risk of adverse
[75]
reactions due to increased serum drug concentrations . In contrast, polymorphisms of the ARGEF10, ADRB3, ROCK2, and CYP3A4 genes in the cholinergic
[76]