Clinical genetic counselling and rehabilitation treatment of a patient with Guillain–Barré syndrome after COVID-19

The authors present a clinical case of rehabilitation after the development of Guillain–Barré syndrome, an acute autoimmune inflammatory polyradiculoneuropathy, in a patient who underwent a SARS CoV-2 infection. The patient previously manifested with severe comorbidities (arterial hypertension, hypercholesterolemia, type 2 diabetes mellitus, stenosing atherosclerosis of brachiocephalic arteries). A diagnostic panel of single nucleotide gene polymorphisms associated with risk factors of cardiovascular diseases, metabolic disorders, immunopathology, pharmacogenetics was applied using PCR-RT “Genetic Passport” test system, and the results were interpreted in order to predict potential complications, adverse drug reactions and the choice of biomarkers for preventive measures. We have compared clinical manifestations, comorbid background and the identified genotype features, as follows: minor homo- and heterozygous variants of ACE, AGT, CYP1A2, NOS3, PPARD, EDN, PALLD, SNX19 genes associated with predisposition to cardiovascular diseases, increasing the risk of dysregulation of blood pressure, development of endothelial dysfunction. The following gene variants were revealed: FXII, ITGA2, ITGB3, MTHFR, MTRR, MTR, PAI-1 that increase the risk of venous and arterial thrombosis, along with gene variants of ADRB3, FTO, INSIG2, KCNG11, LEP, PPARD, TCF7L2, ApoC3, PON1 associated with carbohydrate and lipid metabolism disorders; polymorphisms in the genes determining the immune response, i.e., IL4, IL6, IL8, IL10, CDH1, BDNF1, CRP, CCR5 (with del32 allele considered a risk factor of severe SARS-CoV-2), homozygous polymorphism of a gene of FCGR2 associated with risk of antigen-antibody-complement-mediated cytotoxicity, circulation arrest, deposition of immune complexes in endothelium of microvessels, decreased antithrombotic effects and increased procoagulant activity. Pharmacogenetic study revealed a variant of the CYP4F2 gene, a CYP2C19 gene polymorphism associated with delayed metabolism of a number of pharmaceuticals which requires higher drug dosage, or choosing a drug with a different mechanism of action; gene variants of CYP1A2, GSTP1, GSTT1 reducing efficiency of the cellular detoxification system; NAT2*5 and NAT2*6 variants determining a decrease in appropriate enzyme activities when administering a standard dose of drugs with slowdown of their detoxification, accumulation of toxic metabolites causing clinical adverse effects (hepatotoxicity, dyspepsia, lupus-like syndrome, polyneuritis). Based on the genotype that determines pathogenesis of the multifactorial pathology (including immune-mediated complications of COVID-19), a personalized approach is recommended to the patient, in terms of treatment and prevention of complications. On the basis of testing the biochemical, immunological and blood coagulation biomarkers, an adequate choice of pharmaceuticals is recommended for the patient.