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Manuel Román

Hospital Universitario de La Princesa

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Francisco Abad‐Santos

Universidad Autónoma de Madrid

Dolores Ochoa

Universidad Autónoma de Madrid

Teresa Cabaleiro

Universidade de Santiago de Compostela

Gina Mejía‐Abril

Hospital Universitario de La Princesa

Pablo Zubiaur

Hospital Universitario de La Princesa

Miriam Saiz‐Rodríguez

Hospital Universitario de Burgos

Marcos Navares‐Gómez

Hospital Universitario de La Princesa

Samuel Martín‐Vílchez

Universidad Autónoma de Madrid

Carmen Belmonte

Hospital Universitario de La Princesa

Juan-Bautista Gutiérrez-Aroca

Cooperative Institutions

Universidad Autónoma de Madrid

Hospital Universitario de La Princesa

Hospital Universitario Reina Sofía

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas

Centro de Investigación Biomédica en Red

University of Córdoba

Hospital Universitario La Paz

Instituto Maimónides de Investigación Biomédica de Córdoba

Universidad Complutense de Madrid

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P670 Identification of new genetic variants related to thiopurineinduced myelotoxicity in inflammatory bowel disease (IBD) patients with normal thiopurine s-methyltransferase (TPMT): a genome-wide association study

Journal of Crohn s and Colitis (2013)

María Chaparro Anna González‐Neira Manuel Román Guillermo Pita Teresa Cabaleiro

Thiopurine methyltransferase

Genome-wide Association Study

Identification

Genetic Association

10.1016/s1873-9946(13)60691-1

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Histone modifications associated with biological drug response in moderate‐to‐severe psoriasis

Experimental Dermatology (2018)

María C. Ovejero‐Benito Alejandra Reolid Patricia Sánchez‐Jiménez Miriam Saiz‐Rodríguez Ester Muñoz‐Aceituno

Abstract Introduction Epigenetic factors play an important role in psoriasis onset and development. Biological drugs are used to treat moderate‐to‐severe psoriasis patients resistant to conventional systemic drugs. Although they are safe and effective, some patients do not respond to them. Therefore, it is necessary to find biomarkers that could predict response to these therapies. Objective To find epigenetic biomarkers that could predict response to biological drugs (ustekinumab, secukinumab, adalimumab, ixekizumab). Materials and methods Peripheral blood mononuclear cells ( PBMC s) were isolated from 39 psoriasis patients treated with biological therapies before and after drug administration and from 42 healthy subjects. Afterwards, histones were extracted from PBMC s. Four histone modifications (H3 and H4 acetylation, H3K4 and H3K27 methylation) were determined by ELISA . Data were analysed by IBM ‐ SPSS v.23. Results and conclusions Psoriasis patients presented reduced levels of acetylated H3 and H4 and increased levels of methylated H3K4 compared to controls. Non‐significant changes were observed after treatment administration in any of the histone modifications analysed. Nevertheless, significant changes in methylated H3K27 were found between responders and non‐responders to biological drugs at 3 months. As 28% of these patients also presented psoriatic arthritis (PsA), the former analysis was repeated in the subsets of patients with or without PsA. In patients without PsA, significant changes in methylated H3K4 were found between responders and non‐responders to biological drugs at 3 and 6 months. Although further studies should confirm these results, these findings suggest that H3K27 and H3K4 methylation may contribute to patients’ response to biological drugs in psoriasis.

Ixekizumab

Ustekinumab

10.1111/exd.13790

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Study of Genetic Polymorphisms in the Tumor Necrosis Factor α Promoter Region in Spanish Patients With Psoriasis

Actas Dermo-Sifiliográficas (2012)

Enrique Vázquez Gallo Teresa Cabaleiro Manuel Román Francisco Abad‐Santos E. Daudén

Several studies have reported an association between tumor necrosis factor α (TNF-α) polymorphisms and inflammatory diseases such as psoriasis vulgaris and psoriatic arthritis, although the results vary according to the population studied. No studies have been performed in the Spanish population. To analyze the polymorphisms of the promoter region of the TNF-α gene in patients with moderate to severe psorasis and to identify potential differences in genotype compared to a group of healthy volunteers. Eighty-nine patients with moderate to severe psoriasis and 76 healthy controls with no personal or family history of psoriasis were selected. Polymorphisms of the TNF-α promoter region of both groups were genotyped. We observed a higher prevalence of the genotype with both wild-type alleles at positions -238 (GG genotype, 86.5% vs 70.4%, respectively) and -1031 (TT genotype, 80.2% vs 45.8%, respectively) in patients compared to the healthy control group. The differences at positions -308 and -857 were not significant. There are differences in polymorphisms at positions -238 and -1031 in patients with moderate to severe psoriasis compared to healthy volunteers. This observation provides further support for the importance of the part that TNF-α plays in the pathophysiology of this disease. En diversos estudios se ha descrito la asociación de los polimorfismos del factor de necrosis tumoral α (TNF-α) y patologías inflamatorias como la psoriasis vulgar y la artritis psoriásica, aunque los resultados son variables según la población de origen de la muestra. No se han realizado estudios previamente en población española. Analizar los polimorfismos de la región promotora del gen del TNF-α en pacientes con psoriasis moderada-grave y establecer las posibles diferencias genotípicas con los hallados en un grupo de voluntarios sanos. Se seleccionaron 89 pacientes con psoriasis moderada-grave y 76 controles sin antecedentes familiares ni personales de psoriasis. Se genotiparon los polimorfismos de la región promotora del gen del TNF-α en ambos grupos. Observamos una mayor prevalencia de genotipo con ambos alelos en estado silvestre en posición -238 (GG, 86,5% vs 70,4% respectivamente) y -1031 (TT, 80,2% vs 45,8% respectivamente) en el grupo de pacientes con psoriasis al compararlo con el grupo control. Las diferencias halladas en posición -308 y -857 no fueron significativas. Existen diferencias en los polimorfismos en las posiciones -238 y -1031 entre pacientes con psoriasis moderada-grave y voluntarios sanos, lo cual apoya la importancia del papel del TNF-α en la fisiopatología de esta entidad.

10.1016/j.adengl.2012.05.009

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Genetic Variation in CYP2D6 and SLC22A1 Affects Amlodipine Pharmacokinetics and Safety

Pharmaceutics (2023)

Paula Soria‐Chacartegui Pablo Zubiaur Dolores Ochoa Gonzalo Villapalos‐García Manuel Román

Amlodipine is an antihypertensive drug with unknown pharmacogenetic biomarkers. This research is a candidate gene study that looked for associations between amlodipine pharmacokinetics and safety and pharmacogenes. Pharmacokinetic and safety data were taken from 160 volunteers from eight bioequivalence trials. In the exploratory step, 70 volunteers were genotyped for 44 polymorphisms in different pharmacogenes. CYP2D6 poor metabolizers (PMs) showed higher half-life (t1/2) (univariate p-value (puv) = 0.039, multivariate p-value (pmv) = 0.013, β = -5.31, R2 = 0.176) compared to ultrarapid (UMs), normal (NMs) and intermediate metabolizers (IMs). SLC22A1 rs34059508 G/A genotype was associated with higher dose/weight-corrected area under the curve (AUC72/DW) (puv = 0.025; pmv = 0.026, β = 578.90, R2 = 0.060) compared to the G/G genotype. In the confirmatory step, the cohort was increased to 160 volunteers, who were genotyped for CYP2D6, SLC22A1 and CYP3A4. In addition to the previous associations, CYP2D6 UMs showed a lower AUC72/DW (puv = 0.046, pmv = 0.049, β = -68.80, R2 = 0.073) compared to NMs, IMs and PMs and the SLC22A1 rs34059508 G/A genotype was associated with thoracic pain (puv = 0.038) and dizziness (puv = 0.038, pmv = 0.014, log OR = 10.975). To our knowledge, this is the first work to report a strong relationship between amlodipine and CYP2D6 and SLC22A1. Further research is needed to gather more evidence before its application in clinical practice.

Amlodipine

Variation (astronomy)

10.3390/pharmaceutics15020404

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[THE MICROSCOPIC ALGAE AS HUMAN PATHOGENS].

Some microscopic algae can cause different infectious diseases in humans, including skin, bone, and disseminated. These little-known emerging disease are more severe in immunocompromised patients. The confirmatory microbiological diagnosis must be done differential with yeast-like fungi that can be confused. Anti-fungal drugs and surgery, being quite frequent treatment failure have been used in the treatment. Given the increase of immunosuppression in the current medicine and new possibilities of microbiological diagnostics, it is logical that these diseases tend to increase, by which all physician should know them.

Immunosuppression

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T74EFFECTS OF THE ATYPICAL ANTIPSYCHOTIC ARIPIPRAZOLE ON PLASMA PROLACTIN LEVELS RELATED TO PHARMACOGENETICS IN HEALTHY VOLUNTEERS

European Neuropsychopharmacology (2019)

Dóra Koller Carmen Belmonte Miriam Saiz‐Rodríguez Manuel Román Dolores Ochoa

10.1016/j.euroneuro.2019.08.273

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Detección de genotipos de alto riesgo de HPV. Resultados preliminares

Ángel D. García-Mayorgas Juan-Bautista Gutiérrez-Aroca Manuel Román

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Reemplazamiento valvular aórtico con autoinjerto pulmonar (operación de Ross), en pacientes adultos y pediátricos. Estudio preliminar

Revista Española de Cardiología (1999)

Manuel Concha Jaime Casares Donald N. Ross Lorenzo González-Lavin Manuel Franco

10.1016/s0300-8932(99)74878-5

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DRD2 Taq1A Polymorphism Modulates Prolactin Secretion Induced by Atypical Antipsychotics in Healthy Volunteers

Journal of Clinical Psychopharmacology (2011)

Rosario López‐Rodríguez Manuel Román Jesús Novalbos Maria Laura Pelegrina Dolores Ochoa

Hyperprolactinemia mediated by antagonism of dopaminergic neurotransmission in the pituitary gland is a common adverse effect of antipsychotics. Recent studies have suggested that polymorphisms of dopamine receptors can affect the therapeutic response to antipsychotics. Thus, our aim was to evaluate whether 2 such polymorphisms (DRD2 Taq1A and DRD3 Ser9Gly) modulate prolactin release in healthy volunteers (n = 119) receiving a single dose of quetiapine (25 mg, n = 26), olanzapine (5 mg, n = 57), or risperidone (1 mg, n = 36). The increases in maximum concentration and in area under the curve were calculated from plasma prolactin levels after subtraction of pretreatment levels. Multiple regression analyses revealed that prolactin increases in maximum concentration and in area under the curve depended on drug (quetiapine < olanzapine < risperidone; P < 0.001), sex (women > men; P < 0.001), and Taq1A polymorphism (A1+ > A2/A2; P < 0.05). Analysis of the individual drugs revealed that prolactin secretion was modulated by sex and Taq1A polymorphism in olanzapine and risperidone (P < 0.05); however, these factors were not linked to prolactin secretion in quetiapine.

10.1097/jcp.0b013e31822cfff2

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Effect of the Most Relevant CYP3A4 and CYP3A5 Polymorphisms on the Pharmacokinetic Parameters of 10 CYP3A Substrates

Biomedicines (2020)

Miriam Saiz‐Rodríguez Susana Almenara Marcos Navares‐Gómez Dolores Ochoa Manuel Román

Several cytochrome P450 (CYP) CYP3A polymorphisms were associated with reduced enzyme function. We aimed to evaluate the influence of these alleles on the pharmacokinetic parameters (PK) of several CYP3A substrates. We included 251 healthy volunteers who received a single dose of ambrisentan, atorvastatin, imatinib, aripiprazole, fentanyl, amlodipine, donepezil, olanzapine, fesoterodine, or quetiapine. The volunteers were genotyped for CYP3A4 and CYP3A5 polymorphisms by qPCR. To compare the PK across studies, measurements were corrected by the mean of each parameter for every drug and were logarithmically transformed. Neither CYP3A phenotype nor individual CYP3A4 or CYP3A5 polymorphisms were significantly associated with differences in PK. However, regarding the substrates that are exclusively metabolized by CYP3A, we observed a higher normalized AUC (p = 0.099) and a tendency of lower normalized Cl (p = 0.069) in CYP3A4 mutated allele carriers what was associated with diminished drug metabolism capacity. CYP3A4 polymorphisms did not show a pronounced influence on PK of the analysed drugs. If so, their impact could be detectable in a very small percentage of subjects. Although there are few subjects carrying CYP3A4 double mutations, the effect in those might be relevant, especially due to the majority of subjects lacking the CYP3A5 enzyme. In heterozygous subjects, the consequence might be less noticeable due to the high inducible potential of the CYP3A4 enzyme.

CYP3A

10.3390/biomedicines8040094

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