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1. Pharmacogenomics of GLP-1 receptor agonists: a genome-wide analysis of observational data and large randomised controlled trials

Author

't Hart, L.M., Abdalla, M., Adam, J., Adamski, J., Adragni, K., Allin, K.H., Arumugam, M., Atabaki Pasdar, N., Baltauss, T., Banasik, K.B., Baum, P., Bell, J.D., Bergstrom, M., Beulens, J.W., Bianzano, S., Bizzotto, R., Bonneford, A., Brorsson, C.A.B., Brown, A.A., Brunak, S.B., Cabrelli, L., Caiazzo, R., Canouil, M., Dale, M., Davtian, D., Dawed, A.Y., De Masi, F.M., de Preville, N., Dekkers, K.F., Dermitzakis, E.T., Deshmukh, H.A., Dings, C., Donnelly, L., Dutta, A., Ehrhardt, B., Elders, P.J.M., Engel Thomas, C.E.T., Engelbrechtsen, L., Eriksen, R.G., Eriksen, R.E., Fan, Y., Fernandez, J., Ferrer, J., Fitipaldi, H., Forgie, I.M., Forman, A., Franks, P.W., Frau, F., Fritsche, A., Froguel, P., Frost, G., Gassenhuber, J., Giordano, G.N., Giorgino, T., Gough, S., Graefe-Mody, U., Grallert, H., Grempler, R., Groeneveld, L., Groop, L., Gudmundsdóttir, V.G., Gupta, R.G., Haid, M., Hansen, T., Hansen, T.H., Hattersley, A.T., Haussler, R.S., Heggie, A.J., Hennige, A.M., Hill, A.V., Holl, R.W., Hong, M.-G., Hudson, M., Jablonka, B., Jennison, C., Jiao, J., Johansen, J.J., Jones, A.G., Jonsson, A., Karaderi, T.K., Kaye, J., Klintenberg, M., Koivula, R.W., Kokkola, T., Koopman, A.D.M., Kurbasic, A, Kuulasmaa, T., Laakso, M., Lehr, T., Loftus, H., Lundbye Allesøe, R.L.A, Mahajan, A., Mari, A., Mazzoni, G.M., McCarthy, M.I., McDonald, T.J., McEvoy, D., McRobert, N., McVittie, I., Mourby, M., Musholt, P., Mutie, P, Nice, R., Nicolay, C., Nielsen, A.M.N., Nilsson, B.N., Palmer, C.N., Pattou, F., Pavo, I., Pearson, E.R., Pedersen, O., Pedersen, H.K.P., Perry, M.H., Pomares-Millan, H., Ramisch, A., Rasmussen, S.R., Raverdi, V., Ridderstrale, M., Robertson, N., Roderick, R.C., Rodriquez, M., Ruetten, H., Rutters, F., Sackett, W., Scherer, N., Schwenk, J.M., Shah, N., Sharma, S., Sihinevich, I., Sondertoft, N.B., Staerfeldt, H., Steckel-Hamann, B., Teare, H., Thomas, M.K., Thomas, E.L., Thomsen, H.S., Thorand, B., Thorne, C.E., Tillner, J., Troen Lundgaard, A.T.L., Troll, M., Tsirigos, K.D.T., Tura, A., Uhlen, M., van Leeuwen, N., van Oort, S., Verkindt, H., Vestergaard, H., Viñuela, A., Vogt, J.K, Wad Sackett, P.W.S, Wake, D., Walker, M., Wesolowska-Andersen, A., Whitcher, B., White, M.W., Wu, H., Dawed, Adem Y, Mari, Andrea, Brown, Andrew, McDonald, Timothy J, Li, Lin, Wang, Shuaicheng, Hong, Mun-Gwan, Sharma, Sapna, Robertson, Neil R, Mahajan, Anubha, Wang, Xuan, Walker, Mark, Gough, Stephen, Hart, Leen M ‘t, Zhou, Kaixin, Forgie, Ian, Ruetten, Hartmut, Pavo, Imre, Bhatnagar, Pallav, Jones, Angus G, and Pearson, Ewan R

Published
2023
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2. Pharmacogenomics of GLP-1 receptor agonists: a genome-wide analysis of observational data and large randomised controlled trials

Author

Dawed, Adem Y, primary, Mari, Andrea, additional, Brown, Andrew, additional, McDonald, Timothy J, additional, Li, Lin, additional, Wang, Shuaicheng, additional, Hong, Mun-Gwan, additional, Sharma, Sapna, additional, Robertson, Neil R, additional, Mahajan, Anubha, additional, Wang, Xuan, additional, Walker, Mark, additional, Gough, Stephen, additional, Hart, Leen M ‘t, additional, Zhou, Kaixin, additional, Forgie, Ian, additional, Ruetten, Hartmut, additional, Pavo, Imre, additional, Bhatnagar, Pallav, additional, Jones, Angus G, additional, Pearson, Ewan R, additional, 't Hart, L.M., additional, Abdalla, M., additional, Adam, J., additional, Adamski, J., additional, Adragni, K., additional, Allin, K.H., additional, Arumugam, M., additional, Atabaki Pasdar, N., additional, Baltauss, T., additional, Banasik, K.B., additional, Baum, P., additional, Bell, J.D., additional, Bergstrom, M., additional, Beulens, J.W., additional, Bianzano, S., additional, Bizzotto, R., additional, Bonneford, A., additional, Brorsson, C.A.B., additional, Brown, A.A., additional, Brunak, S.B., additional, Cabrelli, L., additional, Caiazzo, R., additional, Canouil, M., additional, Dale, M., additional, Davtian, D., additional, Dawed, A.Y., additional, De Masi, F.M., additional, de Preville, N., additional, Dekkers, K.F., additional, Dermitzakis, E.T., additional, Deshmukh, H.A., additional, Dings, C., additional, Donnelly, L., additional, Dutta, A., additional, Ehrhardt, B., additional, Elders, P.J.M., additional, Engel Thomas, C.E.T., additional, Engelbrechtsen, L., additional, Eriksen, R.G., additional, Eriksen, R.E., additional, Fan, Y., additional, Fernandez, J., additional, Ferrer, J., additional, Fitipaldi, H., additional, Forgie, I.M., additional, Forman, A., additional, Franks, P.W., additional, Frau, F., additional, Fritsche, A., additional, Froguel, P., additional, Frost, G., additional, Gassenhuber, J., additional, Giordano, G.N., additional, Giorgino, T., additional, Gough, S., additional, Graefe-Mody, U., additional, Grallert, H., additional, Grempler, R., additional, Groeneveld, L., additional, Groop, L., additional, Gudmundsdóttir, V.G., additional, Gupta, R.G., additional, Haid, M., additional, Hansen, T., additional, Hansen, T.H., additional, Hattersley, A.T., additional, Haussler, R.S., additional, Heggie, A.J., additional, Hennige, A.M., additional, Hill, A.V., additional, Holl, R.W., additional, Hong, M.-G., additional, Hudson, M., additional, Jablonka, B., additional, Jennison, C., additional, Jiao, J., additional, Johansen, J.J., additional, Jones, A.G., additional, Jonsson, A., additional, Karaderi, T.K., additional, Kaye, J., additional, Klintenberg, M., additional, Koivula, R.W., additional, Kokkola, T., additional, Koopman, A.D.M., additional, Kurbasic, A, additional, Kuulasmaa, T., additional, Laakso, M., additional, Lehr, T., additional, Loftus, H., additional, Lundbye Allesøe, R.L.A, additional, Mahajan, A., additional, Mari, A., additional, Mazzoni, G.M., additional, McCarthy, M.I., additional, McDonald, T.J., additional, McEvoy, D., additional, McRobert, N., additional, McVittie, I., additional, Mourby, M., additional, Musholt, P., additional, Mutie, P, additional, Nice, R., additional, Nicolay, C., additional, Nielsen, A.M.N., additional, Nilsson, B.N., additional, Palmer, C.N., additional, Pattou, F., additional, Pavo, I., additional, Pearson, E.R., additional, Pedersen, O., additional, Pedersen, H.K.P., additional, Perry, M.H., additional, Pomares-Millan, H., additional, Ramisch, A., additional, Rasmussen, S.R., additional, Raverdi, V., additional, Ridderstrale, M., additional, Robertson, N., additional, Roderick, R.C., additional, Rodriquez, M., additional, Ruetten, H., additional, Rutters, F., additional, Sackett, W., additional, Scherer, N., additional, Schwenk, J.M., additional, Shah, N., additional, Sharma, S., additional, Sihinevich, I., additional, Sondertoft, N.B., additional, Staerfeldt, H., additional, Steckel-Hamann, B., additional, Teare, H., additional, Thomas, M.K., additional, Thomas, E.L., additional, Thomsen, H.S., additional, Thorand, B., additional, Thorne, C.E., additional, Tillner, J., additional, Troen Lundgaard, A.T.L., additional, Troll, M., additional, Tsirigos, K.D.T., additional, Tura, A., additional, Uhlen, M., additional, van Leeuwen, N., additional, van Oort, S., additional, Verkindt, H., additional, Vestergaard, H., additional, Viñuela, A., additional, Vogt, J.K, additional, Wad Sackett, P.W.S, additional, Wake, D., additional, Walker, M., additional, Wesolowska-Andersen, A., additional, Whitcher, B., additional, White, M.W., additional, and Wu, H., additional

Published
2023
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3. Genetic analysis of blood molecular phenotypes reveals regulatory networks affecting complex traits: a DIRECT study

Author

Petra J. M. Elders, Andrea Mari, Femke Rutters, Musholt P, Caiazzo R, Ana Viñuela, Harriet Teare, Fernandez J, H Grallert, McEvoy D, Kristine H. Allin, Pattou F, Jochen M. Schwenk, Pavo I, Mourby M, Dupuis T, Giuseppe N. Giordano, Tarja Kokkola, Andrew T. Hattersley, Adam J, Jagadish Vangipurapu, Ian M Forgie, Anubha Mahajan, Cédric Howald, Caroline Brorsson, Adamski J, Henrik Vestergaard, Gary Frost, Emmanouil T. Dermitzakis, Thomas Willum Hansen, Alison Heggie, Deborah Penet, Sapna Sharma, McDonald Tj, Mark Haid, De Masi F, Raverdy, Bernd Jablonka, Paul W. Franks, Robert W. Koivula, Andrew A. Brown, Søren Brunak, Mark I. McCarthy, Konstantinos D. Tsirigos, Angus G. Jones, Ridderstrale M, Mun-Gwan Hong, E R Pearson, Markku Laakso, Birgitte Nilsson, Davtian D, T’Hart Lm, Walker M, Oluf Pedersen, Ruetten H, Henna Cederberg, and Luciana Romano

Subjects
Genetics, Pleiotropy, Genetic variation, Genome-wide association study, Allelic heterogeneity, Biology, Genetic analysis, Gene, Phenotype, Genetic association
Abstract

Genetic variants identified by genome-wide association studies can contribute to disease risk by altering the production and abundance of mRNA, proteins and other molecules. However, the interplay between molecular intermediaries that define the pathway from genetic variation to disease is not well understood. Here, we evaluated the shared genetic regulation of mRNA molecules, proteins and metabolites derived from whole blood from 3,029 human donors. We find abundant allelic heterogeneity, where multiple variants regulate a particular molecular phenotype, and pleiotropy, where a single variant was associated with multiple molecular phenotypes over multiple genomic regions. We find varying proportions of shared genetic regulation across phenotypes, highest between expression and proteins (66.6%). We were able to recapitulate a substantial proportion of gene expression genetic regulation in a diverse set of 44 tissues, with a median of 88% shared associations for blood expression and 22.3% for plasma proteins. Finally, the genetic and molecular associations were represented in networks including 2,828 known GWAS variants. One sub-network shows the trans relationship between rs149007767 and RTEN, and identifies GRB10 and IKZF1 as candidates mediating genes. Our work provides a roadmap to understanding molecular networks and deriving the underlying mechanism of action of GWAS variants across different molecular phenotypes.

Published
2021

4. A reference map of potential determinants for the human serum metabolome

Author

Bar, N., Korem, T., Weissbrod, O., Zeevi, D., Rothschild, D., Leviatan, S., Kosower, N., Lotan-Pompan, M., Weinberger, A., Le Roy, C. I., Menni, C., Visconti, A., Falchi, M., Spector, T. D., Vestergaard, H., Arumugam, M., Hansen, T., Allin, K., Hong, Mun-Gwan, Schwenk, Jochen M., Häussler, Ragna S., Dale, Matilda, Giorgino, T., Rodriquez, M., Perry, M., Nice, R., McDonald, T., Hattersley, A., Jones, A., Graefe-Mody, U., Baum, P., Grempler, R., Thomas, C. E., Masi, F. D., Brorsson, C. A., Mazzoni, G., Allesøe, R., Rasmussen, S., Gudmundsdóttir, V., Nielsen, A. M., Banasik, K., Tsirigos, K., Nilsson, B., Pedersen, H., Brunak, S., Karaderi, T., Lundgaard, A. T., Johansen, J., Gupta, R., Sackett, P. W., Tillner, J., Lehr, T., Scherer, N., Dings, C., Sihinevich, I., Loftus, H., Cabrelli, L., McEvoy, D., Mari, A., Bizzotto, R., Tura, A., ’t Hart, L., Dekkers, K., Leeuwen, N., Slieker, R., Rutters, F., Beulens, J., Nijpels, G., Koopman, A., Oort, S., Groeneveld, L., Groop, L., Elders, P., Viñuela, A., Ramisch, A., Dermitzakis, E., Ehrhardt, B., Jennison, C., Froguel, P., Canouil, M., Boneford, A., McVittie, I., Wake, D., Frau, F., Staerfeldt, H. -H, Adragni, K., Thomas, M., Wu, H., Pavo, I., Steckel-Hamann, B., Thomsen, H., Giordano, G. N., Fitipaldi, H., Ridderstråle, M., Kurbasic, A., Pasdar, N. A., Pomares-Millan, H., Mutie, P., Koivula, R., McRobert, N., McCarthy, M., Wesolowska-Andersen, A., Mahajan, A., Abdalla, M., Fernandez, J., Holl, R., Heggie, A., Deshmukh, H., Hennige, A., Bianzano, S., Thorand, B., Sharma, S., Grallert, H., Adam, J., Troll, M., Fritsche, A., Hill, A., Thorne, C., Hudson, M., Kuulasmaa, T., Vangipurapu, J., Laakso, M., Cederberg, H., Kokkola, T., Jiao, Y., Gough, S., Robertson, N., Verkindt, H., Raverdi, V., Caiazzo, R., Pattou, F., White, M., Donnelly, L., Brown, A., Palmer, C., Davtian, D., Dawed, A., Forgie, I., Pearson, E., Ruetten, H., Musholt, P., Bell, J., Thomas, E. L., Whitcher, B., Haid, M., Nicolay, C., Mourby, M., Kaye, J., Shah, N., Teare, H., Frost, G., Jablonka, B., Uhlen, M., Eriksen, R., Vogt, J., Dutta, A., Jonsson, A., Engelbrechtsen, L., Forman, A., Sondertoft, N., de Preville, N., Baltauss, T., Walker, M., Gassenhuber, J., Klintenberg, M., Bergstrom, M., Ferrer, J., Adamski, J., Franks, P. W., Pedersen, O., Segal, E., consortium, The IMI DIRECT, Bar, N., Korem, T., Weissbrod, O., Zeevi, D., Rothschild, D., Leviatan, S., Kosower, N., Lotan-Pompan, M., Weinberger, A., Le Roy, C. I., Menni, C., Visconti, A., Falchi, M., Spector, T. D., Vestergaard, H., Arumugam, M., Hansen, T., Allin, K., Hong, Mun-Gwan, Schwenk, Jochen M., Häussler, Ragna S., Dale, Matilda, Giorgino, T., Rodriquez, M., Perry, M., Nice, R., McDonald, T., Hattersley, A., Jones, A., Graefe-Mody, U., Baum, P., Grempler, R., Thomas, C. E., Masi, F. D., Brorsson, C. A., Mazzoni, G., Allesøe, R., Rasmussen, S., Gudmundsdóttir, V., Nielsen, A. M., Banasik, K., Tsirigos, K., Nilsson, B., Pedersen, H., Brunak, S., Karaderi, T., Lundgaard, A. T., Johansen, J., Gupta, R., Sackett, P. W., Tillner, J., Lehr, T., Scherer, N., Dings, C., Sihinevich, I., Loftus, H., Cabrelli, L., McEvoy, D., Mari, A., Bizzotto, R., Tura, A., ’t Hart, L., Dekkers, K., Leeuwen, N., Slieker, R., Rutters, F., Beulens, J., Nijpels, G., Koopman, A., Oort, S., Groeneveld, L., Groop, L., Elders, P., Viñuela, A., Ramisch, A., Dermitzakis, E., Ehrhardt, B., Jennison, C., Froguel, P., Canouil, M., Boneford, A., McVittie, I., Wake, D., Frau, F., Staerfeldt, H. -H, Adragni, K., Thomas, M., Wu, H., Pavo, I., Steckel-Hamann, B., Thomsen, H., Giordano, G. N., Fitipaldi, H., Ridderstråle, M., Kurbasic, A., Pasdar, N. A., Pomares-Millan, H., Mutie, P., Koivula, R., McRobert, N., McCarthy, M., Wesolowska-Andersen, A., Mahajan, A., Abdalla, M., Fernandez, J., Holl, R., Heggie, A., Deshmukh, H., Hennige, A., Bianzano, S., Thorand, B., Sharma, S., Grallert, H., Adam, J., Troll, M., Fritsche, A., Hill, A., Thorne, C., Hudson, M., Kuulasmaa, T., Vangipurapu, J., Laakso, M., Cederberg, H., Kokkola, T., Jiao, Y., Gough, S., Robertson, N., Verkindt, H., Raverdi, V., Caiazzo, R., Pattou, F., White, M., Donnelly, L., Brown, A., Palmer, C., Davtian, D., Dawed, A., Forgie, I., Pearson, E., Ruetten, H., Musholt, P., Bell, J., Thomas, E. L., Whitcher, B., Haid, M., Nicolay, C., Mourby, M., Kaye, J., Shah, N., Teare, H., Frost, G., Jablonka, B., Uhlen, M., Eriksen, R., Vogt, J., Dutta, A., Jonsson, A., Engelbrechtsen, L., Forman, A., Sondertoft, N., de Preville, N., Baltauss, T., Walker, M., Gassenhuber, J., Klintenberg, M., Bergstrom, M., Ferrer, J., Adamski, J., Franks, P. W., Pedersen, O., Segal, E., and consortium, The IMI DIRECT

Abstract

The serum metabolome contains a plethora of biomarkers and causative agents of various diseases, some of which are endogenously produced and some that have been taken up from the environment1. The origins of specific compounds are known, including metabolites that are highly heritable2,3, or those that are influenced by the gut microbiome4, by lifestyle choices such as smoking5, or by diet6. However, the key determinants of most metabolites are still poorly understood. Here we measured the levels of 1,251 metabolites in serum samples from a unique and deeply phenotyped healthy human cohort of 491 individuals. We applied machine-learning algorithms to predict metabolite levels in held-out individuals on the basis of host genetics, gut microbiome, clinical parameters, diet, lifestyle and anthropometric measurements, and obtained statistically significant predictions for more than 76% of the profiled metabolites. Diet and microbiome had the strongest predictive power, and each explained hundreds of metabolites—in some cases, explaining more than 50% of the observed variance. We further validated microbiome-related predictions by showing a high replication rate in two geographically independent cohorts7,8 that were not available to us when we trained the algorithms. We used feature attribution analysis9 to reveal specific dietary and bacterial interactions. We further demonstrate that some of these interactions might be causal, as some metabolites that we predicted to be positively associated with bread were found to increase after a randomized clinical trial of bread intervention. Overall, our results reveal potential determinants of more than 800 metabolites, paving the way towards a mechanistic understanding of alterations in metabolites under different conditions and to designing interventions for manipulating the levels of circulating metabolites., QC 20211001

Published
2020
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6. Genetic analysis of blood molecular phenotypes reveals common properties in the regulatory networks affecting complex traits.

Author

Brown AA, Fernandez-Tajes JJ, Hong MG, Brorsson CA, Koivula RW, Davtian D, Dupuis T, Sartori A, Michalettou TD, Forgie IM, Adam J, Allin KH, Caiazzo R, Cederberg H, De Masi F, Elders PJM, Giordano GN, Haid M, Hansen T, Hansen TH, Hattersley AT, Heggie AJ, Howald C, Jones AG, Kokkola T, Laakso M, Mahajan A, Mari A, McDonald TJ, McEvoy D, Mourby M, Musholt PB, Nilsson B, Pattou F, Penet D, Raverdy V, Ridderstråle M, Romano L, Rutters F, Sharma S, Teare H, 't Hart L, Tsirigos KD, Vangipurapu J, Vestergaard H, Brunak S, Franks PW, Frost G, Grallert H, Jablonka B, McCarthy MI, Pavo I, Pedersen O, Ruetten H, Walker M, Adamski J, Schwenk JM, Pearson ER, Dermitzakis ET, and Viñuela A

Subjects
Humans, Phenotype, RNA, Messenger, Research Personnel, Multifactorial Inheritance, Genomics
Abstract

We evaluate the shared genetic regulation of mRNA molecules, proteins and metabolites derived from whole blood from 3029 human donors. We find abundant allelic heterogeneity, where multiple variants regulate a particular molecular phenotype, and pleiotropy, where a single variant associates with multiple molecular phenotypes over multiple genomic regions. The highest proportion of share genetic regulation is detected between gene expression and proteins (66.6%), with a further median shared genetic associations across 49 different tissues of 78.3% and 62.4% between plasma proteins and gene expression. We represent the genetic and molecular associations in networks including 2828 known GWAS variants, showing that GWAS variants are more often connected to gene expression in trans than other molecular phenotypes in the network. Our work provides a roadmap to understanding molecular networks and deriving the underlying mechanism of action of GWAS variants using different molecular phenotypes in an accessible tissue., (© 2023. Springer Nature Limited.)

Published
2023
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7. Gene expression kinetics of Exaiptasia pallida innate immune response to Vibrio parahaemolyticus infection.

Author

Seneca F, Davtian D, Boyer L, and Czerucka D

Subjects
Animals, Gene Expression, Immunity, Innate genetics, Kinetics, Sea Anemones genetics, Vibrio parahaemolyticus
Abstract

Background: Recent sequencing projects on early-diverging metazoans such as cnidarians, have unveiled a rich innate immunity gene repertoire; however, little is known about immunity gene regulation in the host's early response against marine bacterial pathogens over time. Here, we used RNA-seq on the sea anemone Exaiptasia pallida (Ep) strain CC7 as a model to depict the innate immune response during the onset of infection with the marine pathogenic bacteria Vibrio parahaemolyticus (Vp) clinical strain O3:K6, and lipopolysaccharides (LPS) exposure. Pairwise and time series analyses identified the genes responsive to infection as well as the kinetics of innate immune genes over time. Comparisons between the responses to live Vp and purified LPS was then performed., Results: Gene expression and functional analyses detected hundreds to thousands of genes responsive to the Vp infection after 1, 3, 6 and 12 h, including a few shared with the response to LPS. Our results bring to light the first indications that non-canonical cytoplasmic pattern recognition receptors (PRRs) such as NOD-like and RIG-I-like receptor homologs take part in the immune response of Ep. Over-expression of several members of the lectin-complement pathways in parallel with novel transmembrane and Ig containing ficolins (CniFLs) suggest an active defense against the pathogen. Although lacking typical Toll-like receptors (TLRs), Ep activates a TLR-like pathway including the up-regulation of MyD88, TRAF6, NF-κB and AP-1 genes, which are not induced under LPS treatment and therefore suggest an alternative ligand-to-PRR trigger. Two cytokine-dependent pathways involving Tumor necrosis factor receptors (TNFRs) and several other potential downstream signaling genes likely lead to inflammation and/or apoptosis. Finally, both the extrinsic and intrinsic apoptotic pathways were strongly supported by over-expression of effector and executioner genes., Conclusions: To our knowledge, this pioneering study is first to follow the kinetics of the innate immune response in a cnidarian during the onset of infection with a bacterial pathogen. Overall, our findings reveal the involvement of both novel immune gene candidates such as NLRs, RLRs and CniFLs, and previously identified TLR-like and apoptotic pathways in anthozoan innate immunity with a large amount of transcript-level evidence.

Published
2020
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8. [Level of leukotrienes B4 and C4 in the blood of patients with periodic disease].

Author

Gabrielian ES, Grigorian SV, Davtian DG, Mkhitarian GS, and Panosian AG

Subjects
Colchicine therapeutic use, Familial Mediterranean Fever drug therapy, Familial Mediterranean Fever therapy, Humans, Hyperbaric Oxygenation, Familial Mediterranean Fever blood, Leukotriene B4 blood, SRS-A blood
Abstract

The level of LTB4 and LTC4 in blood plasma of patients with familial mediterranean fever is significantly higher than in healthy donors: 53 + 10 pg/ml for LTB4 (normal - 25 + 5 pg/ml) and 175 + 22 pg/ml for LTC4 (normal 67 + 19 pg/ml). The more increase of the LTB4 and LTC4 content in plasma is observed during attacks of fever - 107 + 21 pg/ml (LTB4) and 249 + 34 pg/ml (LTC4). Hyperbaric oxygenation of patients, used to relieve pain and fever, reduces the level of leukotrienes.

Published
1990

10. [Metabolism of arachidonic acid in the thrombocytes of patients with periodic disease].

Author

Panosian AG, Grigorian SV, Davtian DG, Gevorkian GA, and Gabrielian ES

Subjects
Arachidonic Acid, Humans, In Vitro Techniques, Arachidonic Acids blood, Blood Platelets metabolism, Familial Mediterranean Fever blood
Abstract

Washed platelets of patients with familial Mediterranean fever (FMF) were incubated with I-14C arachidonic acid (AA). Only 10% of AA were transformed into thromboxane A2, 12(S)-12-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE) and 12(S)-12-hydroxy-5Z,8Z,10E-heptadecatrienoic acid (HHT), which strongly indicates the suppression of platelet lipoxygenase and cyclooxygenase or the deficit in these enzymes in FMF. However, there were no noticeable alterations in AA platelet metabolism during attacks of fever and immediately after hyperbaric oxygenation used to relieve pain and fever. The data obtained suggest that arachidonic acid metabolism plays an important role in the pathogenesis of FMF.

Published
1986

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