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429 results on '"Strange, Richard C."'

1. Testosterone Replacement Therapy: Effects on Blood Pressure in Hypogonadal Men.

Author

Hackett, Geoffrey, Mann, Amar, Haider, Ahmad, Haider, Karim S., Desnerck, Pieter, König, Carola S., Strange, Richard C., and Ramachandran, Sudarshan

Subjects
MULTIPLE regression analysis, ANTIHYPERTENSIVE agents, HEMATOCRIT, WAIST circumference, BLOOD pressure
Abstract

Purpose: While testosterone therapy can improve the various pathologies associated with adult-onset testosterone deficiency (TD), Summary of Product Characteristics (SPC) of five testosterone preparations caution that treatment may be associated with hypertension. This paper evaluates the impact of testosterone undecanoate (TU) on blood pressure (BP) in men with adult-onset TD. Materials and Methods: Of 737 men with adult-onset TD in an on-going, observational, prospective, cumulative registry, we studied changes in BP using non-parametric sign-rank tests at final assessment and fixed time points. We used multiple regression analysis to establish factors (baseline BP, age, change/baseline waist circumference [WC] and hematocrit [HCT] and follow-up) potentially associated with BP change in men on TU. Results: TU was associated with significant reductions in systolic, diastolic BP and pulse pressure, regardless of antihypertensive therapy (at baseline or during follow-up), larger reductions were seen with concurrent antihypertensive therapy. In men never on antihypertensive agents, median changes (interquartile range [IQR]) in systolic BP, diastolic BP and pulse pressure were -12.5 (-19.0, -8.0), -8.0 (-14.0, -3.0), and -6.0 (-10.0, -1.0) mmHg, respectively at final assessment, with only baseline BP values inversely associated with these changes (HCT and WC were not significantly associated). In men not on TU, systolic BP, diastolic BP, and pulse pressure significantly increased. In the TU treated men only 1 of the 152 men (not on antihypertensive agents at baseline) were started on antihypertensives during follow-up. In contrast 33 of the 202 men on antihypertensives (at baseline or follow-up) had the antihypertensive agent discontinued by the end of the follow-up. Conclusions: TU was associated with lowering of BP during follow-up irrespective of antihypertensive therapy, with greater reductions in men with higher baseline BP. In the context of SPC warnings, our long-term data provide reassurance on the effect of TU on BP. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Testosterone replacement therapy: association with mortality in high‐risk patient subgroups.

Author

Mann, Amar, Strange, Richard C, König, Carola S, Hackett, Geoffrey, Haider, Ahmad, Haider, Karim Sultan, Desnerck, Peter, and Ramachandran, Sudarshan

Subjects
*TYPE 2 diabetes, *WAIST circumference, *TESTOSTERONE, *BLOOD pressure, MORTALITY risk factors
Abstract

Objectives: We describe studies determining the association between testosterone therapy (TTh) and mortality. Materials & methods: We used a registry database of 737 men with adult‐onset testosterone deficiency defined as presenting with low serum total testosterone (TT) levels ≤12.1 nmol/L and associated symptoms over a near 10‐year follow‐up. We compared associations between testosterone undecanoate (TU), cardio‐metabolic risk factors and mortality using non‐parametric statistics followed by separate Cox regression models to determine if any association between TU and morality was independent of age and cardio‐metabolic risk factors. Finally, the association between TU and mortality was studied in men stratified by cardio‐metabolic risk. Results: During a median follow‐up interquartile range (IQR) of 114 (84–132) months, 94 of the 737 men died. TU (ref: non‐treatment) was associated with mortality; hazard ratio = 0.23, 95% confidence intervals = 0.14–0.40. Cox's regression models showed the above association to be independent of baseline age, waist circumference, hemoglobin A1c, lipids, blood pressure, smoking, and type 2 diabetes. These variables remained associated with mortality. We finally stratified the men by the high‐risk baseline variables and established that the association between mortality and TU was only evident in men at higher risk. A possible explanation could lie with the "law of initial value," where greater improvements are evident following treatment in patients with worse baseline values. Conclusions: This study with long follow‐up confirms that TTh is associated with lower mortality in men with adult‐onset TD. This association was evident only in men with greater cardio‐metabolic risk factors who demonstrated greater benefit. [ABSTRACT FROM AUTHOR]

Published
2024
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3. Adult-onset testosterone deficiency:the usefulness of hormone replacement in reducing mortality in men with this common age-related condition

Author

Mann, Amar, Strange, Richard C., Hackett, Geoff, König, Carola, Ramachandran, Sudarshan, Mann, Amar, Strange, Richard C., Hackett, Geoff, König, Carola, and Ramachandran, Sudarshan

Abstract

Adult-onset testosterone deficiency (TD) in men is diagnosed by the finding of low serum testosterone levels and recognised, associated symptoms. The condition has high prevalence in men over 50 years of age, particularly those with type 2 diabetes (T2DM). Accumulating data show adult-onset TD is associated with increased mortality risk. We review the literature and consider the evidence suggesting testosterone therapy (TTh) reduces mortality, especially in men with T2DM. We previously reported that in the Burntwood Lichfield Atherstone Sutton Coldfield Tamworth (BLAST) study screened cohort of men with adult-onset TD and T2DM adult-onset TD was associated with increased mortality with TTh decreasing this higher mortality. The data hinted that the effect was greater in older men. We confirmed this observation with statistical analyses to study the effect of age on the association between adult-onset TD and mortality; Cox regression analysis demonstrated that the reduced risk (hazard ratio: 0.61, 95% CI: 0.38–0.96) following TTh was restricted to men above the median age of 65.89 years. Finally, we speculate on putative mechanisms that may mediate these associations. Heterogeneity in men with adult-onset TD is expected in view of its definition of low testosterone levels together with associated clinical phenotypes that are not always directly related. Many of these classifying phenotypes are associated with increased mortality. Thus, it is perhaps possible that mechanism(s) of all-cause mortality reduction following TTh is via the impact on these associated phenotypes such as the metabolic syndrome (MetS), hyperglycaemia, hypertension, dyslipidaemia, low haematocrit, sex hormone binding levels, erectile dysfunction, etc. We propose that further research studying the effect of TTh takes heterogeneity into account.

Published
2024

11. Simultaneous identification of GSTP1 Ile105→Val105 and Ala114→Val114 substitutions using an amplification refractory mutation systempolymerase chain reactionassay: studies in patients with asthma

Author

Strange Richard C, Hepple Michael, Fryer Anthony A, Hemmingsen Anja, and Spiteri Monica A

Subjects
amplification refractory mutation system, asthma, bronchial hyperresponsiveness, GSTP1, Diseases of the respiratory system, RC705-779
Abstract

Abstract Background The glutathione S-transferase (GST) enzyme GSTP1 utilizes byproducts of oxidative stress. We previously showed that alleles of GSTP1 that encode the Ile105→Val105 substitution are associated with the asthma phenotypes of atopy and bronchial hyperresponsiveness (BHR). However, a further polymorphic site (Ala114→Val114) has been identified that results in the following alleles: GSTP1*A (wild-type Ile105→Ala114), GSTP1*B (Val105→Ala114), GSTP1*C (Val105→Val114) and GSTP1*D (Ile105→Val114). Methods Because full identification of GSTP1 alleles may identify stronger links with asthma phenotypes, we describe an amplification refractory mutation system (ARMS) assay that allows identification of all genotypes. We explored whether the GSTP1 substitutions influence susceptibility to asthma, atopy and BHR. Results Among 191 atopic nonasthmatic, atopic asthmatic and nonatopic nonasthmatic individuals, none had the BD, CD, or DD genotypes. GSTP1 BC was significantly associated with reduced risk for atopy (P = 0.031). Compared with AA, trend test analysis identified a significant decrease in the frequency of GSTP1 BC with increasing severity of BHR (P = 0.031). Similarly, the frequency of GSTP1 AA increased with increasing BHR. Conclusion These data suggest that GSTP1*B and possibly GSTP1*C are protective against asthma and related phenotypes.

Published
2001
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14. Meta-analysis and pooled analysis of GSTM1 and CYP1A1 polymorphisms and oral and pharyngeal cancers: a HuGE-GSEC review

Author

Varela-Lema, Leonor, Taioli, Emanuela, Ruano-Ravina, Alberto, Barros-Dios, Juan M., Anantharaman, Devasena, Benhamou, Simone, Boccia, Stefania, Bhisey, Rajani A., Cadoni, Gabriella, Capoluongo, Ettore, Chen, Chien-Jen, Foulkes, William D., Goloni-Bertollo, Eny Maria, Hatagima, Ana, Hayes, Richard B., Katoh, Takahiko, Koifman, Sergio, Lazarus, Phillip, Manni, Johannes J., Mahimkar, Manoj, Morita, Shunji, Park, Jong, Park, Kwang-Kyun, Bertelli, Erika Cristina Pavarino, de Souza Fonseca Ribeiro, Enilze Maria, Roy, Bidyut, Spitz, Margaret R., Strange, Richard C., Wei, Qingyi, and Ragin, Camille C.

Published
2008
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17. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis

Author

Sawcer, Stephen, Hellenthal, Garrett, Pirinen, Matti, Spencer, Chris C. A., Patsopoulos, Nikolaos A., Moutsianas, Loukas, Dilthey, Alexander, Su, Zhan, Freeman, Colin, Hunt, Sarah E., Edkins, Sarah, Gray, Emma, Booth, David R., Potter, Simon C., Goris, An, Band, Gavin, Bang Oturai, Annette, Strange, Amy, Saarela, Janna, Bellenguez, Céline, Fontaine, Bertrand, Gillman, Matthew, Hemmer, Bernhard, Gwilliam, Rhian, Zipp, Frauke, Jayakumar, Alagurevathi, Martin, Roland, Leslie, Stephen, Hawkins, Stanley, Giannoulatou, Eleni, D’alfonso, Sandra, Blackburn, Hannah, Martinelli Boneschi, Filippo, Liddle, Jennifer, Harbo, Hanne F., Perez, Marc L., Spurkland, Anne, Waller, Matthew J., Mycko, Marcin P., Ricketts, Michelle, Comabella, Manuel, Hammond, Naomi, Kockum, Ingrid, McCann, Owen T., Ban, Maria, Whittaker, Pamela, Kemppinen, Anu, Weston, Paul, Hawkins, Clive, Widaa, Sara, Zajicek, John, Dronov, Serge, Robertson, Neil, Bumpstead, Suzannah J., Barcellos, Lisa F., Ravindrarajah, Rathi, Abraham, Roby, Alfredsson, Lars, Ardlie, Kristin, Aubin, Cristin, Baker, Amie, Baker, Katharine, Baranzini, Sergio E., Bergamaschi, Laura, Bergamaschi, Roberto, Bernstein, Allan, Berthele, Achim, Boggild, Mike, Bradfield, Jonathan P., Brassat, David, Broadley, Simon A., Buck, Dorothea, Butzkueven, Helmut, Capra, Ruggero, Carroll, William M., Cavalla, Paola, Celius, Elisabeth G., Cepok, Sabine, Chiavacci, Rosetta, Clerget-Darpoux, Françoise, Clysters, Katleen, Comi, Giancarlo, Cossburn, Mark, Cournu-Rebeix, Isabelle, Cox, Mathew B., Cozen, Wendy, Cree, Bruce A. C., Cross, Anne H., Cusi, Daniele, Daly, Mark J., Davis, Emma, de Bakker, Paul I. W., Debouverie, Marc, D’hooghe, Marie Beatrice, Dixon, Katherine, Dobosi, Rita, Dubois, Bénédicte, Ellinghaus, David, Elovaara, Irina, Esposito, Federica, Fontenille, Claire, Foote, Simon, Franke, Andre, Galimberti, Daniela, Ghezzi, Angelo, Glessner, Joseph, Gomez, Refujia, Gout, Olivier, Graham, Colin, Grant, Struan F. A., Rosa Guerini, Franca, Hakonarson, Hakon, Hall, Per, Hamsten, Anders, Hartung, Hans-Peter, Heard, Rob N., Heath, Simon, Hobart, Jeremy, Hoshi, Muna, Infante-Duarte, Carmen, Ingram, Gillian, Ingram, Wendy, Islam, Talat, Jagodic, Maja, Kabesch, Michael, Kermode, Allan G., Kilpatrick, Trevor J., Kim, Cecilia, Klopp, Norman, Koivisto, Keijo, Larsson, Malin, Lathrop, Mark, Lechner-Scott, Jeannette S., Leone, Maurizio A., Leppä, Virpi, Liljedahl, Ulrika, Lima Bomfim, Izaura, Lincoln, Robin R., Link, Jenny, Liu, Jianjun, Lorentzen, Åslaug R., Lupoli, Sara, Macciardi, Fabio, Mack, Thomas, Marriott, Mark, Martinelli, Vittorio, Mason, Deborah, McCauley, Jacob L., Mentch, Frank, Mero, Inger-Lise, Mihalova, Tania, Montalban, Xavier, Mottershead, John, Myhr, Kjell-Morten, Naldi, Paola, Ollier, William, Page, Alison, Palotie, Aarno, Pelletier, Jean, Piccio, Laura, Pickersgill, Trevor, Piehl, Fredrik, Pobywajlo, Susan, Quach, Hong L., Ramsay, Patricia P., Reunanen, Mauri, Reynolds, Richard, Rioux, John D., Rodegher, Mariaemma, Roesner, Sabine, Rubio, Justin P., Rückert, Ina-Maria, Salvetti, Marco, Salvi, Erika, Santaniello, Adam, Schaefer, Catherine A., Schreiber, Stefan, Schulze, Christian, Scott, Rodney J., Sellebjerg, Finn, Selmaj, Krzysztof W., Sexton, David, Shen, Ling, Simms-Acuna, Brigid, Skidmore, Sheila, Sleiman, Patrick M. A., Smestad, Cathrine, Sørensen, Per Soelberg, Søndergaard, Helle Bach, Stankovich, Jim, Strange, Richard C., Sulonen, Anna-Maija, Sundqvist, Emilie, Syvänen, Ann-Christine, Taddeo, Francesca, Taylor, Bruce, Blackwell, Jenefer M., Tienari, Pentti, Bramon, Elvira, Tourbah, Ayman, Brown, Matthew A., Tronczynska, Ewa, Casas, Juan P., Tubridy, Niall, Corvin, Aiden, Vickery, Jane, Jankowski, Janusz, Villoslada, Pablo, Markus, Hugh S., Wang, Kai, Mathew, Christopher G., Wason, James, Palmer, Colin N. A., Wichmann, H-Erich, Plomin, Robert, Willoughby, Ernest, Rautanen, Anna, Winkelmann, Juliane, Wittig, Michael, Trembath, Richard C., Yaouanq, Jacqueline, Viswanathan, Ananth C., Zhang, Haitao, Wood, Nicholas W., Zuvich, Rebecca, Deloukas, Panos, Langford, Cordelia, Duncanson, Audrey, Oksenberg, Jorge R., Pericak-Vance, Margaret A., Haines, Jonathan L., Olsson, Tomas, Hillert, Jan, Ivinson, Adrian J., De Jager, Philip L., Peltonen, Leena, Stewart, Graeme J., Hafler, David A., Hauser, Stephen L., McVean, Gil, Donnelly, Peter, and Compston, Alastair

Published
2011
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33. Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk

Author

Benhamou, Simone, Lee, Won Jin, Alexandrie, Anna-Karin, Boffetta, Paolo, Bouchardy, Christine, Butkiewicz, Dorota, Brockmöller, Jurgen, Clapper, Margie L., Daly, Ann, Dolzan, Vita, Ford, Jean, Gaspari, Laura, Haugen, Aage, Hirvonen, Ari, Husgafvel-Pursiainen, Kirsti, Ingelman-Sundberg, Magnus, Kalina, Ivan, Kihara, Masahiro, Kremers, Pierre, Le Marchand, Loïc, London, Stephanie J., Nazar-Stewart, Valle, Onon-Kihara, Masako, Rannug, Agneta, Romkes, Marjorie, Ryberg, David, Seidegard, Janeric, Shields, Peter, Strange, Richard C., Stücker, Isabelle, To-Figueras, Jordi, Brennan, Paul, and Taioli, Emanuela

Published
2002

42. Basal cell carcinoma

Author

Ramachandran, Sudarshan, Fryer, Anthony A., Smith, Andrew G., Lear, John T., Bowers, Bill, Griffiths, Christopher E.M., Jones, Peter W., and Strange, Richard C.

Subjects
Basal cell carcinoma -- Physiological aspects, Tumors -- Medical examination, Disease susceptibility -- Research, Health
Published
2000

46. Association of polymorphism in glutathione S-transferase loci in susceptibility and outcome in rheumatoid arthritis: comparison with shared epitope

Author

Mattey, Derek L., Hassell, Andrew B., Plant, Michael, Dawes, Peter T., Ollier, William R., Jones, Peter W., Fryer, Anthony A., Alldersea, Julie E., and Strange, Richard C.

Subjects
Rheumatoid arthritis -- Genetic aspects, Glutathione transferase -- Genetic aspects, Health
Abstract

Genes controlling the production and activity of the glutathione S-transferase (GST) enzyme may have some influence on the risk or outcome of rheumatoid arthritis. GST enzymes use byproducts of oxidation that can damage cells and cause inflammation. Researchers compared the genes of 277 patients with rheumatoid arthritis and 577 healthy people. Particular genetic types were more common in patients with arthritis, and gene type appeared to influence the severity of disease and the functional abilities of patients.

Published
1999

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