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  1. Article ; Online: Fatal acute haemolysis and methaemoglobinaemia in a man with renal failure and Alkaptonuria – Is nitisinone the solution?

    A.S. Davison / E. Luangrath / E. Selvi / L.R. Ranganath

    Molecular Genetics and Metabolism Reports, Vol 23, Iss , Pp - (2020)

    2020  

    Abstract: Haemolysis and methaemoglobinaemia (MetHb) are rare metabolic complications that can occur in Alkaptonuria (AKU), for which there is no curative treatment. Presented is a case of a man who had AKU, and serves as a reminder of life-threatening ... ...

    Abstract Haemolysis and methaemoglobinaemia (MetHb) are rare metabolic complications that can occur in Alkaptonuria (AKU), for which there is no curative treatment. Presented is a case of a man who had AKU, and serves as a reminder of life-threatening complications that can occur with haemolysis and MetHb. This case presents an opportunity to revisit important considerations relating to the investigation and treatment of haemolysis and MetHb with a view to raising awareness, and in doing so hopefully reducing the uniformly fatal outcome. Additionally it is proposed that treatment of haemolysis and MetHb with nitisinone is considered as a potentially lifesaving treatment as it is believed that reducing the concentration of circulating homogentisic acid will reduce oxidative stress.
    Keywords Oxidative stress ; Haemolysis ; Methaemoglobinaemia ; Alkaptonuria ; Nitisinone ; Renal failure ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-06-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Metabolomic studies in the inborn error of metabolism alkaptonuria reveal new biotransformations in tyrosine metabolism

    Brendan P. Norman / Andrew S. Davison / Juliette H. Hughes / Hazel Sutherland / Peter JM. Wilson / Neil G. Berry / Andrew T. Hughes / Anna M. Milan / Jonathan C. Jarvis / Norman B. Roberts / Lakshminarayan R. Ranganath / George Bou-Gharios / James A. Gallagher

    Genes and Diseases, Vol 9, Iss 4, Pp 1129-

    2022  Volume 1142

    Abstract: Alkaptonuria (AKU) is an inherited disorder of tyrosine metabolism caused by lack of active enzyme homogentisate 1,2-dioxygenase (HGD). The primary consequence of HGD deficiency is increased circulating homogentisic acid (HGA), the main agent in the ... ...

    Abstract Alkaptonuria (AKU) is an inherited disorder of tyrosine metabolism caused by lack of active enzyme homogentisate 1,2-dioxygenase (HGD). The primary consequence of HGD deficiency is increased circulating homogentisic acid (HGA), the main agent in the pathology of AKU disease. Here we report the first metabolomic analysis of AKU homozygous Hgd knockout (Hgd−/−) mice to model the wider metabolic effects of Hgd deletion and the implication for AKU in humans. Untargeted metabolic profiling was performed on urine from Hgd−/− AKU (n = 15) and Hgd+/− non-AKU control (n = 14) mice by liquid chromatography high-resolution time-of-flight mass spectrometry (Experiment 1). The metabolites showing alteration in Hgd−/− were further investigated in AKU mice (n = 18) and patients from the UK National AKU Centre (n = 25) at baseline and after treatment with the HGA-lowering agent nitisinone (Experiment 2). A metabolic flux experiment was carried out after administration of 13C-labelled HGA to Hgd−/−(n = 4) and Hgd+/−(n = 4) mice (Experiment 3) to confirm direct association with HGA. Hgd−/− mice showed the expected increase in HGA, together with unexpected alterations in tyrosine, purine and TCA-cycle pathways. Metabolites with the greatest abundance increases in Hgd−/− were HGA and previously unreported sulfate and glucuronide HGA conjugates, these were decreased in mice and patients on nitisinone and shown to be products from HGA by the 13C-labelled HGA tracer. Our findings reveal that increased HGA in AKU undergoes further metabolism by mainly phase II biotransformations. The data advance our understanding of overall tyrosine metabolism, demonstrating how specific metabolic conditions can elucidate hitherto undiscovered pathways in biochemistry and metabolism.
    Keywords Alkaptonuria ; Biotransformation ; Metabolism ; Metabolomics ; Mice ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Subject code 570
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Characterization of changes in the tyrosine pathway by 24-h profiling during nitisinone treatment in alkaptonuria

    L.R. Ranganath / A.M. Milan / A.T. Hughes / A.S. Davison / M. Khedr / B.P. Norman / G. Bou-Gharios / J.A. Gallagher / M. Gornall / R. Jackson / R. Imrich / J. Rovensky / M. Rudebeck / B. Olsson

    Molecular Genetics and Metabolism Reports, Vol 30, Iss , Pp 100846- (2022)

    2022  

    Abstract: Background: Although changes in the tyrosine pathway during nitisinone therapy are known, a complete characterization of the induced tyrosinaemia is lacking to improve disease management. Patients and methods: Our research aims were addressed by 24-h ... ...

    Abstract Background: Although changes in the tyrosine pathway during nitisinone therapy are known, a complete characterization of the induced tyrosinaemia is lacking to improve disease management. Patients and methods: Our research aims were addressed by 24-h blood sampling. 40 patients with alkaptonuria (AKU), treated with 0, 1, 2, 4 and 8 mg nitisinone daily (n = 8), were studied over four weeks. Serum homogentisic acid (sHGA), tyrosine (sTYR), phenylalanine (sPHE), hydroxyphenylpyruvate (sHPPA), hydroxyphenyllactate (sHPLA) and nitisinone (sNIT) were measured at baseline and after four weeks. Results: sNIT showed a clear dose-proportional response. sTYR increased markedly but with less clear-cut dose responses after nitisinone. Fasting and average 24-h (Cav) sTYR responses were similar. Individual patient sTYR 24-h profiles showed significant fluctuations during nitisinone therapy. At week 4, sTYR, sHPPA and sHPPL all showed dose-related increases compared to V0, with the greatest difference between 1 and 8 mg nitisinone seen for HPLA, while there was no change from V0 in sPHE. sHGA decreased to values around the lower limit of quantitation. Discussion: There was sustained tyrosinaemia after four weeks of nitisinone therapy with significant fluctuations over the day in individual patients. Diet and degree of conversion of HPPA to HPLA may determine extent of nitisinone-induced tyrosinaemia. Conclusion: A fasting blood sample is recommended to monitor sTYR during nitisinone therapy Adaptations in HPPA metabolites as well as the inhibition of tyrosine aminotransferase could be contributing factors generating tyrosinaemia during nitisinone therapy.
    Keywords Alkaptonuria ; Homogentisic acid ; Tyrosine ; Hydroxyphenylpyruvate ; Hydroxyphenyllactate ; Phenylalanine ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 610 ; 616
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Quantification of the flux of tyrosine pathway metabolites during nitisinone treatment of Alkaptonuria

    A. M. Milan / A. T. Hughes / A. S. Davison / M. Khedr / J. Rovensky / E. E. Psarelli / T. F. Cox / N. P. Rhodes / J. A. Gallagher / L. R. Ranganath

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Volume 9

    Abstract: Abstract Nitisinone decreases homogentisic acid (HGA) in Alkaptonuria (AKU) by inhibiting the tyrosine metabolic pathway in humans. The effect of different daily doses of nitisinone on circulating and 24 h urinary excretion of phenylalanine (PA), ... ...

    Abstract Abstract Nitisinone decreases homogentisic acid (HGA) in Alkaptonuria (AKU) by inhibiting the tyrosine metabolic pathway in humans. The effect of different daily doses of nitisinone on circulating and 24 h urinary excretion of phenylalanine (PA), tyrosine (TYR), hydroxyphenylpyruvate (HPPA), hydroxyphenyllactate (HPLA) and HGA in patients with AKU was studied over a four week period. Forty AKU patients, randomised into five groups of eight patients, received doses of 1, 2, 4 or 8 mg of nitisinone daily, or no drug (control). Metabolites were analysed by tandem mass spectrometry in 24 h urine and serum samples collected before and after nitisinone. Serum metabolites were corrected for total body water and the sum of 24 hr urine plus total body water metabolites of PA, TYR, HPPA, HPLA and HGA were determined. Body weight and urine urea were used to check on stability of diet and metabolism over the 4 weeks of study. The sum of quantities of urine metabolites (PA, TYR, HPPA, HPLA and HGA) were similar pre- and post-nitisinone. The sum of total body water metabolites were significantly higher post-nitisinone (p < 0.0001) at all doses. Similarly, combined 24 hr urine:total body water ratios for all analytes were significantly higher post-nitisinone, compared with pre-nitisinone baseline for all doses (p = 0.0002 – p < 0.0001). Significantly higher concentrations of metabolites from the tyrosine metabolic pathway were observed in a dose dependant manner following treatment with nitisinone and we speculate that, for the first time, experimental evidence of the metabolite pool that would otherwise be directed towards pigment formation, has been unmasked.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2019-07-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Urine homogentisic acid and tyrosine: Simultaneous analysis by liquid chromatography tandem mass spectrometry

    Hughes, A.T / A.M. Milan / A.S. Davison / G. Ross / J.A. Gallagher / J.J. Dutton / L.R. Ranganath / P. Christensen

    Journal of Chromatography B. 2014 July 15, v. 963

    2014  

    Abstract: Alkaptonuria (AKU) is a rare debilitating autosomal recessive disorder of tyrosine metabolism. Deficiency of homogentisate 1,2-dioxygenase results in increased homogentisic acid (HGA) which although excreted in gram quantities in the urine, is deposited ... ...

    Abstract Alkaptonuria (AKU) is a rare debilitating autosomal recessive disorder of tyrosine metabolism. Deficiency of homogentisate 1,2-dioxygenase results in increased homogentisic acid (HGA) which although excreted in gram quantities in the urine, is deposited as an ochronotic pigment in connective tissues, especially cartilage. Ochronosis leads to a severe, early-onset form of osteoarthritis, increased renal and prostatic stone formation and hardening of heart vessels. Treatment with the orphan drug, Nitisinone, an inhibitor of the enzyme 4-hydroxyphenylpyruvate dioxygenase has been shown to reduce urinary excretion of HGA, resulting in accumulation of the upstream pre-cursor, tyrosine. Using reverse phase LC–MS/MS, a method has been developed to simultaneously quantify urinary HGA and tyrosine. Using matrix-matched calibration standards, two product ion transitions were identified for each compound and their appropriate isotopically labelled internal standards. Validation was performed across the AKU and post-treatment concentrations expected. Intrabatch accuracy for acidified urine was 96–109% for tyrosine and 94–107% for HGA; interbatch accuracy (n=20 across ten assays) was 95–110% for tyrosine and 91–109% for HGA. Precision, both intra- and interbatch was <10% for tyrosine and <5% for HGA. Matrix effects observed with acidified urine (12% decrease, CV 5.6%) were normalised by the internal standard. Tyrosine and HGA were proved stable under various storage conditions and no carryover, was observed. Overall the method developed and validated shows good precision, accuracy and linearity appropriate for the monitoring of patients with AKU, pre and post-nitisinone therapy
    Keywords 4-hydroxyphenylpyruvate dioxygenase ; cartilage ; drugs ; excretion ; heart ; isotope labeling ; liquid chromatography ; metabolism ; monitoring ; osteoarthritis ; patients ; storage conditions ; tandem mass spectrometry ; therapeutics ; tyrosine ; urine
    Language English
    Dates of publication 2014-0715
    Size p. 106-112.
    Publishing place Elsevier B.V.
    Document type Article
    ISSN 1570-0232
    DOI 10.1016/j.jchromb.2014.06.002
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Outcomes after perioperative SARS-CoV-2 infection in patients with proximal femoral fractures

    T Richards / S Shaikh / S Rehman / A Khan / J Shah / C Smith / A Brown / S Singh / A P Arnaud / A Young / D Bowen / P Patel / S Williams / J Dunn / J John / M Loubani / A Hainsworth / A Kolias / PJ Hutchinson /
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Vives / CJ Gómez Díaz / CA Guariglia / C Soto Montesinos / L Sanchon / M Xicola Martínez / N Guàrdia / P Collera / R Diaz Del Gobbo / R Sanchez Jimenez / R Farre Font / R Flores Clotet / CEM Brathwaite / H Hakmi / AH Sohail / R Heckburn / D Townshend / N McLarty / A Shenfine / K Madhvani / M Hampton / AP Hormis / V Miu / K Sheridan / C Luney / MA Williams / A Alqallaf / A Ben-Sassi / R Crichton / J Sonksen / GR Layton / B Karki / S Pankhania / S Asher / A Folorunso / J Winyard / J Mangwani / BHB Babu / C Weerasinghe / M Ballabio / P Bisagni / T Armao / M Madonini / A Gagliano / P Pizzini / A Älgå / M Nordberg / G Sandblom / J El Kafsi / K Logishetty / A Saadya / R Midha / H Subbiah Ponniah / T Stockdale / T Bacarese-Hamilton / N Anjarwalla / D Marujo Henriques / R Hettige / C Baban / A Tenovici / F Anazor / SD King / S Kazzaz / S HKruijff / De Vries JPPM / PJ Steinkamp / PKC Jonker / WY Van der Plas / W Bierman / Y Janssen / ABJ Borgstein / D Enjuto / M Perez Gonzalez / P Díaz Peña / M Marqueta De Salas / P Martinez Pascual / L Rodríguez Gómez / R Garcés García / A Ramos Bonilla / N Herrera-Merino / P Fernández Bernabé / EP Cagigal Ortega / García de Castro Rubio E / I Cervera / MH Siddique / C Barmpagianni / A Basgaran / A Basha / V Okechukwu / A Bartsch / CA Leo / HK Ubhi / N Zafar / H Abdul-Jabar / F Mongelli / M Bernasconi / M Di Giuseppe / D Christoforidis / D La Regina / M Arigoni / A Al-Sukaini / S Mediratta / O Brown / M Boal / S Stanger / H Abdalaziz / J Constable / G Dovell / R Gopi reddy / A Dehal / HB Shah / GWV Cross / P Seyed-Safi / YW Smart / A Kuc / M Al-Yaseen / B Jayasankar / D Balasubramaniam / K Abdelsaid / N Mundkur / RE Soulsby / O Ryska / T Raymond / P Hawkin / G Kinnaman / I Sharma / K Freystaetter / JN Hadfield / A Hilley / S Arkani / M Youssef / I Shaikh / K Seebah / V Kouritas / D Chrastek / G Maryan / DF Gill / F Khatun / J Parakh / V Sarodaya / A Daadipour / KD Bosch / V Bashkirova / LS Dvorkin / VK Kalidindi / A Choudhry / M Espino Segura-Illa / G Sánchez Aniceto / AM Castaño-Leon / L Jimenez-Roldan / J Delgado Fernandez / A Pérez Núñez / A Lagares / D Garcia Perez / M Santas / I Paredes / O Esteban Sinovas / L Moreno-Gomez / E Rubio / V Vega / A Vivas Lopez / M Labalde Martinez / O García Villar / PM Pelaéz Torres / J Garcia Borda / E Ferrero Herrero / C Eiriz Fernandez / C Ojeda-Thies / JM Pardo Garcia / H Wynn Jones / H Divecha / C Whelton / E Powell-Smith / M Alotaibi / A Maashi / A Zowgar / M Alsakkaf / O Izquierdo / D Ventura / D Escobar / U Garcia de cortazar / Villamor Garcia / A Cioci / K Rakoczy / W Pavlis / R Saberi / A Khaleel / A Unnithan / K Memon / RR Pala Bhaskar / F Maqboul / F Kamel / A Al-Samaraee / R Madani / H Llaquet Bayo / N Duchateau / C De Gheldere / A Fayad / ML Wood / G Groot / I Hakami / C Boeker / J Mall / AF Haugstvedt / ML Jönsson / P Caja Vivancos / Villalabeitia Ateca / M Prieto Calvo / P Martin Playa / A Gainza / EJ Aragon Achig / A Rodriguez Fraga / Melchor Corcóstegui / G Mallabiabarrena Ormaechea / JJ Garcia Gutierrez / L Barbier / MA Pesántez Peralta / M Jiménez Jiménez / JA Municio Martín / J Gómez Suárez / G García Operé / LA Pascua Gómez / M Oñate Aguirre / A Fernandez-Colorado / M De la Rosa-Estadella / A Gasulla-Rodriguez / M Serrano-Martin / A Peig-Font / S Junca-Marti / M Juarez-Pomes / S Garrido-Ondono / L Blasco-Torres / M Molina-Corbacho / Y Maldonado-Sotoca / A Gasset-Teixidor / J Blasco-Moreu / V Turrado-Rodriguez / AM Lacy / FB de Lacy / X Morales / A Carreras-Castañer / P Torner / M Jornet-Gibert / M Balaguer-Castro / M Renau-Cerrillo / P Camacho-Carrasco / M Vives-Barquiel / B Campuzano-Bitterling / I Gracia / R Pujol-Muncunill / M Estaire Gómez / D Padilla-Valverde / S Sánchez-García / D Sanchez-Pelaez / E Jimenez Higuera / R Picón Rodríguez / Fernández Camuñas À / C Martínez-Pinedo / EP Garcia Santos / V Muñoz-Atienza / A Moreno Pérez / CA Cano / D Crego-Vita / M Huecas-Martinez / A Roselló Añón / MJ Sangüesa / JC Bernal-Sprekelsen / JC Catalá Bauset / P Renovell Ferrer / C Martínez Pérez / O Gil-Albarova / J Gilabert Estellés / K Aghababyan / R Rivas / J Escartin / JL Blas Laina / B Cros / Talal El-Abur / J Garcia Egea / C Yanez / JH Kauppila / E Sarjanoja / S Tzedakis / PA Bouche / S Gaujoux / D Gossot / A Seguin-Givelet / D Fuks / M Grigoroiu / R Sanchez Salas / X Cathelineau / P Macek / Y Barbé / F Rozet / E Barret / A Mombet / N Cathala / E Brian / F Zadegan / AJ Baldwin / E Gammeri / A Catton / S Marinos Kouris / J Pereca / M Kaushal / A Kler / V Reghuram / S Tezas / V Oktseloglou / F Mosley / MFI De La Cruz Monroy / P Bobak / S Ahad / E Lostis / GK Ambler / J Manara / M Doe / T Jichi / GD Stewart / J Ramzi / AA Singh / J Ashcroft / OJ Baker / P Coughlin / Durst AZED / A Abood / A Habeeb / VE Hudson / B Lamb / L Luke / S Mitrasinovic / Ngu AWT / S Waseem / F Georgiades / XS Tan / J Pushpa-rajah / I Abu-Nayla / S Rooney / E Irune / MHV Byrne / A Durrani / A Sethuraman Venkatesan / T Combellack / G Tahhan / M Kornaszewska / V Valtzoglou / I Deglurkar / M Koutentakis / Syed Nong Chek SAH / M Shinkwin / F Ayeni / H Tustin / M Bordenave / N Manu / N Eardley / OL Serevina / S Roy Mahapatra / K Mohankumar / I Khawaja / A Palepa / T Doulias / Y Premakumar / Y Jauhari / Z Koshnow / A Uberai / F Hirri / BM Stubbs / J Manickavasagam / S Dalgleish / R Kanitkar / CJ Payne / Ng CE / DE Henshall / T Drake / EM Harrison / A Tambyraja / RJE Skipworth / G Linder / R McGregor / J Mayes / R Pasricha / A Razik / S Thrumurthy / D Howden / Z Baxter / L Osagie / M Bence / GE Fowler / N Rajaretnam / A Goubran / JS McGrath / JRA Phillips / DA Raptis / JM Pollok / F Soggiu / S Xyda / C Hidalgo Salinas / H Tzerbinis / T Pissanou / R Mirnezami / N Angamuthu / T Shakir / H Capitelli-McMahon / L Hitchman / A Andronic / A Aboelkassem Ibrahim / J Totty / S Tayeh / T Chase / J Ayorinde / T Cuming / A Trompeter / C Hing / P Tsinaslanidis / MW Benjamin / A Leyte / J Smelt / G Santhirakumaran / A Labib / O Lyons / S Onida / KM Sarraf / S Erridge / S Yalamanchili / A Abuown / D Davenport / S Wheatstone / SM Andreani / MF Bath / A Sahni / L Rigueros Springford / C Sohrabi / J Bacarese-Hamilton / FG Taylor / P Patki / C Tanabalan / ME Alexander / CJ Smart / L Abdeh / M Zeiton / R Advani / S Nikolaou / T Oni / N Ilahi / K Ballantyne / Z Woodward / R Merh / B Robertson-Smith / P Ameerally / JG Finch / C Gnanachandran / I Pop / D Dass / G Thiruchandran / Toh SKC / A Allana / C Bellis / O Babawale / YC Phan / U Lokman / T Koc / L Duggleby / S Shamoon / H Clancy / A Mansuri / A Thakrar / L Wickramarachchi / S Sivayoganathan / E Karam / HV Colvin / A Badran / A Cadersa / A Cumpstey / R Aftab / F Wensley / V Morrison-Jones / GK Sekhon / H Shields / Z Shakoor / T Talbot / A Alzetani / J Rooney / M Rudic / A Aladeojebi / M Kitchen / R Lefroy / P Nanjaiah / AD Rajgor / RJ Scurrah / LJ Watson / T Royle / B Steel / Luk ACO / VG Thiruvasagam / W Marlow / C Konstantinou / D Yershov / A Denning / E Mangos / T Nambirajan / I Flindall / V Mahendran / J De Marchi / NF Davis / A Picciariello / V Papagni / DF Altomare / S Granieri / C Cotsoglou / A Cabeleira / P Serralheiro / T Teles / C Canhoto / J Simões / AC Almeida / O Nogueira / R Athayde Nemésio / MJ Amaral / A Valente da Costa / R Martins / P Guerreiro / A Ruivo / D Breda / JM Oliveira / AL De Oliveira Lopez / M Colino / J De Barros / AP Soares / H Morais / T Revez / MI Manso / JC Domingues / P Henriques / Cardoso N Ribeiro VI / G Martins dos Santos / M Peralta Ferreira / J Ascensão / B Costeira / L Rio Rodrigues / M Sousa Fernandes / P Azevedo / I Lourenço / G Mendinhos / A Nobre Pinto / H Taflin / H Abdou / L O'Meara / Z Cooper / SA Hirji / BU Okafor / V Roxo / CP Raut / JS Jolissaint / DA Mahvi / C Reinke / S Merola / A Ssentongo / P Ssentongo / Oh JS / J Hazelton / J Maines / N Gusani / RCG Martin / N Bhutiani / R Choron / F Soliman / MD E Dauer / E Renza-Stingone / E Gokcen / E Kropf / H Sufrin / J Sewards / J Poggio / K Sanserino / L Rae / M Philp / M Metro / P McNelis / R Petrov / T Pazionis / DB Lumenta / SP Nischwitz / E Richtig / M Pau / P Srekl-Filzmaier / N Eibinger / B Michelitsch / M Fediuk / A Papinutti / TU Cohnert / E Kantor / J Kahiu / S Hosny / A Sultana / M Taggarsi / L Vitone / OP Vaz / I Sarantitis / S Timbrell / A Shugaba / GP Jones / SS Tripathi / MS Greenhalgh / H Emerson / K Vejsbjerg / W McCormick / K Singisetti / Y Aawsaj / R Vanker / M Ghobrial / S Kanthasamy / H Fawi / M Awadallah / J Cheung / S Tingle / F Abbadessa / A Sachdeva / CD Chan / I McPherson / F Mahmoud Ali / S Pandanaboyana / T Grainger / S Nandhra / N Dawe / C McCaffer / J Riches / J Moir / H Elamin Ahmed / C Saleh / RM Koshy / LJ Rogers / PL Labib / N Hope / K Emslie / P Panahi / E Clough / I Enemosah / J Natale / N Raza / JI Webb / M Antar / J Noel / R Nunn / F Eriberto / R Tanna / S Lodhia / C Osório / J Antunes / P Balau / M Godinho

    BMJ Open, Vol 11, Iss

    an international cohort study

    2021  Volume 11

    Keywords Medicine ; R
    Language English
    Publishing date 2021-11-01T00:00:00Z
    Publisher BMJ Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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