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4. Computation of a cardiac severity score with left-censored biomarkers for patients with heart failure

Author

Vasudevan A, Munkres AG, Bottiglieri T, Won JI, Garg P, and McCullough PA

Subjects
cardiac biomarkers, left-censored, limit of detection, therapeutic index, myocardial injury summary score, Pathology, RB1-214
Abstract

Anupama Vasudevan,1,2 Alyssa G Munkres,3 Teodoro Bottiglieri,1,4 Jane I Won,1,2 Puja Garg,1,2 Peter A McCullough 1–3,5,6 1Baylor Research Institute, 2Baylor Heart and Vascular Institute, 3Texas A&M Health Science Center, College of Medicine, 4The Institute of Metabolic Disease, 5Baylor University Medical Center, Dallas, 6The Heart Hospital Baylor, Plano, TX, USA Introduction: Biomarkers reported as being less than the limit of detection (LOD) are challenging to be included in analyses without being dichotomized. Substitutions by the LOD, LOD/2, LOD/√2, or zero have been attempted for left-censored values. We calculated a novel Modified Myocardial Injury Summary Score (MMISS) by incorporating four biomarkers (B-type natriuretic peptide, troponin, galectin-3, and suppression of tumorigenicity 2) to efficiently stratify heart failure (HF) patients. The objective of this study is to evaluate the differences in associations between MMISS, calculated by different methods of substitution, and therapeutic intensity index (TII), a composite pharmacologic score. Methods and results: This is a cross-sectional study including 39 HF patients aged ≥18 years who were treated in the Baylor Health Care System. MMISS was calculated with the left-censored biomarkers substituted by zero, LOD, LOD/2, and LOD/√2. Patients with biomarker values more than LOD (complete cases) were also considered separately. The computed TII was regressed separately on MMISS for each substitution method, while controlling for age and gender. All substitution methods yielded negative associations; however, statistical significance for the association was not achieved using substitution by zero or when considering only the complete cases. The association was quite comparable with the substitution of left-censored values by LOD, LOD/2, and LOD/√2. Conclusion: Substantial loss of information is inevitable if only the data with values above the LOD are considered for analysis or when the left-censored values are substituted with zero. Keywords: cardiac biomarkers, left-censored, limit of detection, therapeutic index, myocardial injury summary score

Published
2017

15. Abstracts from the sixth meeting of the international association of pancreatology, November 2–4, 1994, Chicago, IL

Author

Burdick, Michael, Hollingsworth, Tony, Gansauge, S., Gansauge, F., Link, K. H., Schoenberg, M. H., Poch, B., Beger, H. G., Wagner, A. C. C., Steffen, H., Göke, B., Gaisano, H. Y., Sheu, L., Foskett, J. K., Trimble, W. S., Lee, Y. L., Kwon, H. Y., Park, H. S., Lee, S. M., Park, H. J., aguchi, S., Green, G. M., Mitamura, K., Komatsu, Y., Arai, I., Yamaura, H., Wang, OJ, Adrian, TE, Teyssen, S., Niebel, W., Niebergall, E., Singer, M. V., Umehara, K, Ohara, T, Kataoka, K, Okamura, H, Kato, M, Sakagami, J, Ohta, A, Murase, M, Hosoda, M, Yamane, Y, Kashima, K, Ibata, Y, Balthazar, Emil J., Banks, P. A., Garzof, S. G., Langevin, R. E., Silverman, S. G., Sica, G. T., Bassi, C., Benini, A., Muner, A., Falconi, M., Abbas, H., Pederzoli, P., Salvia, R., Minelli, E. Bertazzoni, Shaskar, S. Shanmuga, Shearer, M. G., Imrie, C. W., Brodmerkel, G. J., Reed, P. A., Carr-Locke, DL, Musa, A, Lichtenstein, DR, Dam, J Van, Banks, PA, Eisele, S., Schoenberg, M. H., Böchjer, M., Beger, H. G., Foitzik, Th., Fern’andez-del Castillo, C., Rattner, D. W., Ferraro, M. J., Warshaw, A. L., Foitzik, Th., Schmidt, J., Hotz, H., Warshaw, A. L., Buhr, H. J., Klar, E., Heinisch, A., Kadow, R., Bioss, U., Schölmerich, J., Zimgibl, H., Leser, H. -G., Manes, G., Rabitti, P. G., Laccetti, M., Cavallera, A., Paceili, L., Gagiione, G., Uomo, G., Marinqhini, A., Zinsmeister, A. R., Melton, L. J., DiMagno, E. P., Marotta, F., Chui, D. H., Barbi, G., Zhong, G. G., Marotta, F., Chui, D. H., Tajiri, H., Bellini, O., Zhong, G. G., Barbi, G., McKay, C, Baxter, J. N., Imrie, C. W., Mithöfer, K., Fern’andez-delCastillo, C., Frick, T. W., Lewandrowski, K., Rattner, D. W., Warshaw, A. L., Pezzilli, R., Billi, P., Miniero, R., Gullo, L., Barakat, B., Migliuli, M., Rau, B., Schad, M., Schoenberg, M., Beger, H. G., Richter, F., Matthias, R., Sakagami, J, Kataoka, K, Ohta, A, Umehara, K, Imoto, M, Murase, M, Hosoda, M, Yamane, Y, Kato, M, Kashima, K, Ashihara, T, Schofield, D, Sharer, NM, Heywood, KM, Waters, HM, Braganza, JM, Scott, P, Sharer, NM, Bilton, D, Deardon, D, Lee, S, Taylor, PM, McCloy, RF, Braganza, JM, Shen, J., Shao, H., Wu, Z. P., Jin, J. J., Shiel, N, Cassidy, O, Sharma, H, Braganza, J. M., Soöckmann, F., Ahrens, J., Leonhardt, U., Otto, J., Ritzel, U., Ramadori, G., Tian, Fuzhou, Hu, JZ, Huang, DR, Wang, XH, Lian, HW, Zhang, BY, Miao, JG, Li, Xu, Zhou, HT, Uomo, G., Rabitti, P. G., Laccetti, M., Manes, G., Esposico, P., Perrocti, F., Visconci, M., Vaccaro, M. I., Dagrosa, M. A., Mora, M. I., Sordelli, D. O., Vogt, W., MeOmann, H., Heinisch, A., Linseis, A., Holstege, A., Schölmerich, J., Leser, H. -G., Weiser, M. R., Gibbs, S. A. L., Hechcman, H. B., Moore, F. D., Worthington, H. V., Runt, L. P., HcCloy, R. F., KacLennan, I. A., Braqanza, J. M., Heath, D, Alexander, D, Wilson, C, Larvin, M, Imrie, CW, McMahon, MJ, Larvin, M, Ward, J, Robinson, PJ, Chalmers, AG, McMahon, MJ, Apte, M, Wilson, J, McCaughan, G, Korsten, M, Norton, I, Piroia, R, Bimmler, D., Frick, T. W., Scheele, G. A., Bockman, Dale E., Büchler, Markus, Beger, Hans G., Cavallini, G., Brunori, M. P., Rigo, L., Bovo, P., Filippini, M., Vaona, B., Di Francesco, V., Frulloni, L., Marcori, M., Farri, P. C., Laardini, M. T., Pederzoli, P., Chowdhury, Riaz, Ochi, Koji, Mizushima, Takaaki, Tsurumi, Tetsuya, Harada, Hideo, Laver, P., Hoist, J. J., Ohe, M. v. d., Goebell, H., Mi Zumoto, A., Sarr, M. G., DiMagno, E. P., Moore, R., Frey, C. F., Debas, H. T., Mulvihill, S. J., Onizuka, S., Kuroda, H., Kuroda, Y., Hongo, H., Matsuzaki, S., Ito, M., Sekine, L., Tsunoda, T., Pap, ’A., Hrisztov, V., Pap, ’A., Marosi, E., Simon, K., Tak’acs, T., Pederzoli, P., Falconi, M., Bassi, C., Bonora, A., Talamini, G., Saivia, R., Benini, L., Caldiron, E., Vesentini, S., Cavallini, G., Raijman, Isaac, Kortan, Paul, Haber, Gregory B., Ramesh, H, Varghese, CJ, Schofield, D, Kay, PM, Bottiglieri, T, Uden, S, Bilton, D, Braganza, JM, Gut, A, Segal, I, Snehalatha, C, Mohan, V, Braganza, JM, Silva, E., Ceneviva, R., Velludo, M. A. L., Silvan, E., Ruebner, B., Ceneviva, R., Velludo, M. A. L., Roselino, J. E. S., Foss, M. C., Talaraini, G., Falcaoi, M., Frmlltai, L, K Fraacesca, V., Maxwi, M., Vaosa, B., Baro, P., Baxu, C., Pedercoli, P., Cavalliai, G., Taiamini, G., Iacano, C., Faicsai, M., Frulloni, L., Rige, L., Castagnisi, A., Marcori, M., Angelini, G., Bassi, C., Bom, P., Vaoss, B., Vantini, I., Sen, G., Pederzali, P., Cavallini, G., Štimee, B, Bulajič, M, Milosavljevi’c, T, Krsti’c, R, Markovi’c, M, Korneti, V, Ugljcš’c, M, Abruzzesse, IL, Evans, DB, Larry, L, King, T, Raijman, I, Roubein, L, Frazier, M, lacono, C., Faca, E., Falezza, G., Bonora, E., Aurola PP, Serio, G., lacono, C., Nicoli, N., Mansueto, G. C., Zicari, M., Marchiori, L., Mangiante, G., Seno, G., Imarnura, M., Yamauchi, H., Inoue, M., Onda, M., UchlDa, E., Almqtq, T., Yamanaka, Y., Kqbayashi, T., Yokqyama, T., Aida, K., Sasajima, K., Tajiri, T., Egami, K., Yamashita, K., Naitq, Z., Asano, G., Lewandrowski, K. B., Kirby, R. E., Southern, J. F., Compton, C. C., Warshaw, A. L., Lip, J, Strömmer, L, Permert, J, Larsson, J, Adrian, TE, Loftus, E. V., Adkins, M. C., Olivares-Pakzad, B., Batts, K. P., Stephens, D. H., Farnell, M. B., Sarr, H. G., Thompson, G. B., van Heerden, J. A., Kelly, D. G., Miller, L. J., Pearson, R. K., Clain, J. E., Petersen, B. T., DiMagno, E. P., Matsumoto, Cancer S., Chowdhury, R., Mizushima, T., Ochi, K., Harada, H., Miki, H., Ozkan, Hnsan, Saisho, Hiromitsu, Yarnaguchi, Taketo, Ishihara, Takeshi, Kikuchi, Yasuharu, Tsuyuguchi, Toshio, Ohto, Masao, Pasqual, C., Sperti, C., Liesai, G., Guido, M., Pedrazzoli, S., Sperti, C., Pasquali, C., Khajeturian, E., Guolo, P., Pedrazzoli, S., Tadokoro, H., Watanabe, S., Moriyoshi, Y., Yoshida, K., Shiratori, K., Takeuchi, T., Uchida, E., Onda, M., Tajiri, T., Egami, K., Yamashita, K., Aida, K., Yamanaka, Y., Kobayashi, T., Aimoto, T., Yokoyama, T., Inoue, M., Naito, Z., Asano, G., Valentich, M. A., Monis, B., Barotto, N. N., and Herrera, P.

Published
1994
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23. Enhancement of recovery from psychiatric illness by methylfolate

Author

Godfrey, P.S.A., Toone, B.K., Carney, M.W.P., Flynn, T.G., Bottiglieri, T., Laundy, M., Chanarin, I., and Reynolds, E.H.

Subjects
Schizophrenia -- Causes of, Vitamin B12 deficiency -- Complications, Schizophrenia -- Drug therapy, Depression, Mental -- Drug therapy, Vitamins -- Psychological aspects, Depression, Mental -- Causes of, Folic acid -- Health aspects
Published
1990

30. Biochemical, physiological and clinical effects of l-methylfolate in schizophrenia: a randomized controlled trial

Author

Roffman, J L, primary, Petruzzi, L J, additional, Tanner, A S, additional, Brown, H E, additional, Eryilmaz, H, additional, Ho, N F, additional, Giegold, M, additional, Silverstein, N J, additional, Bottiglieri, T, additional, Manoach, D S, additional, Smoller, J W, additional, Henderson, D C, additional, and Goff, D C, additional

Published
2017
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35. Decreased Homovanilic Acid in Cerebrospinal Fluid Correlates with Impaired Neuropsychologic Function in HIV-1-Infected Patients

Author

Werner P, David M. Dorfman, David M. Simpson, di Rocco A, Morrison C, and Bottiglieri T

Subjects
Adult, Male, medicine.medical_specialty, AIDS-related complex, HIV Infections, Neuropsychological Tests, Central nervous system disease, Cerebrospinal fluid, Dopamine, Internal medicine, medicine, Humans, Dementia, Pharmacology (medical), Pharmacology, Dopaminergic, Cognitive disorder, Homovanillic Acid, Middle Aged, medicine.disease, Endocrinology, Immunology, HIV-1, Catecholamine, Female, Neurology (clinical), Psychology, medicine.drug
Abstract

To determine whether dopamine metabolism is abnormal in HIV infected patients and whether dopamine metabolism abnormalities are related to specific neuropsychologic characteristics in HIV-infected patients, we measured cerebrospinal fluid (CSF) levels of homovanilic acid (HVA), the primary dopamine metabolite, in 10 HIV-infected patients and compared it to HVA levels in CSF in a group of 13 healthy control subjects. HIV-infected patients were also assessed with a battery of neuropsychologic tests and HVA levels were then correlated with performance on specific neuropsychologic tests. The mean (+/-SD) HVA level in CSF was 100.9 +/- 29.3 nmol/L in the HIV-infected study group and 230.5 +/- 50.0 nmol/L in the non-HIV-infected control group (p < 0.0001). The decrease in concentrations of HVA in CSF correlated with impairment on performance on neuropsychologic testing (Spearman r = 0.67; p = 0.03). When the relationship between HVA levels and specific cognitive domains was evaluated, we observed trends for positive correlation between HVA levels and tests that measure motor speed (r = 0.59; p = 0.074) and those testing attention, concentration, and executive control (r = 0.54; p = 0.108). There was no relationship between performance on memory tests and CSF HVA levels (r = -0.0061; p = 0.987). These results further support the hypothesis that dopaminergic dysfunction plays an important role in the pathogenesis of AIDS dementia complex (ADC) and suggest that specific motor and cognitive abnormalities may be related to depressed dopaminergic activity. This may have important implications for the development of treatments or preventive strategies for ADC.

Published
2000

38. CEREBROSPINAL-FLUID S-ADENOSYLMETHIONINE (SAME) AND GLUTATHIONE CONCENTRATIONS IN HIV-INFECTION - EFFECT OF PARENTERAL TREATMENT WITH SAME

Author

CASTAGNA , ANTONELLA, LEGRAZIE C, ACCORDINI A, GIULIDORI P, CAVALLI G, BOTTIGLIERI T, LAZZARIN A., Castagna, Antonella, Legrazie, C, Accordini, A, Giulidori, P, Cavalli, G, Bottiglieri, T, and Lazzarin, A.

Abstract

The methylation and transsulfuration pathways are intimately linked and have been implicated in the progression of neurologic damage and immune cell depletion caused by human immunodeficiency virus (HIV) infection. We studied the following metabolites related to these pathways: S-adenosylmethionine (SAMe), homocysteine, cysteine, cysteinyl-glycine, and glutathione (GSH) in blood and CSF of 16 HIV-infected patients with neurologic complications and 20 HIV-negative control patients undergoing lumbar punctures for other medical reasons, We confirmed recent studies of decreased CSF SAMe concentrations in HIV infection and demonstrated that diastereomers of SAMe are present in CSF but not in plasma or erythrocytes from both HIV-infected and HIV-negative patients, In HIV-infected patients, CSF GSH and cysteinyl-glycine, but not homocysteine or cysteine, were significantly reduced, This is the first report of decreased CSF GSH induced by HIV infection. GSH has a regulatory effect on the synthesis of SAMe in hepatic tissue, and the same mechanism may also apply in the CNS. Administration of SAMe-butanedisulphonate, 800 mg/d intravenously for 14 days, was associated with significant increases in CSF SAMe and GSH. These findings have potentially important therapeutic implications for the use of SAMe in protecting against SAMe and GSH deficiency in the CNS of HIV-infected patients.

Published
1995

39. Homocysteine and methylmalonic acid concentrations in cerebrospinal fluid: relation with age and Alzheimer's disease

Author

Bottiglieri T, Barbé F, Montagne P, Arning E, Franck P, Serot Jm, and Nicolas Jp

Subjects
Vitamin, Adult, Male, medicine.medical_specialty, Homocysteine, Methylmalonic acid, Short Report, Pathogenesis, Central nervous system disease, chemistry.chemical_compound, Cerebrospinal fluid, Alzheimer Disease, Internal medicine, medicine, Dementia, Humans, Aged, business.industry, food and beverages, Middle Aged, medicine.disease, Surgery, Psychiatry and Mental health, Endocrinology, chemistry, Female, Neurology (clinical), Alzheimer's disease, business, Methylmalonic Acid
Abstract

Homocysteine may be involved in the pathogenesis of late onset Alzheimer's disease. It is implicated in the metabolism of several important pathways in the brain. Methylmalonic acid (MMA) is related to the metabolism of branched chained amino acids and fatty acids.To compare cerebrospinal fluid (CSF) total homocysteine and MMA in elderly subjects, patients with Alzheimer's disease, and younger healthy controls.CSF samples were obtained from 33 patients under 20 years of age; 28 patients aged 21 to 60 years; 22 normal elderly subjects aged over 60; and 38 Alzheimer patients aged over 60.CSF total homocysteine increased with age (mean (SD): 57 (35) nmol/l in the youngest group v 123 (89) nmol/l in the elderly group (p0.001)). There was no difference between the elderly group and Alzheimer patients (115 (62) nmol/l). CSF MMA did not differ in the elderly group and the Alzheimer group (38 (13) v 35 (14) ng/ml). In the youngest group, it was significantly higher (60 (15) ng/ml).CSF total homocysteine is not increased in Alzheimer's disease compared with age matched controls. CSF total homocysteine was correlated with age. The decrease in CSF MMA levels with age eliminates a lack of vitamin B-12 at neuronal level.

Published
2005

41. Biochemical, physiological and clinical effects of l-methylfolate in schizophrenia: a randomized controlled trial

Author

Roffman, J L, Petruzzi, L J, Tanner, A S, Brown, H E, Eryilmaz, H, Ho, N F, Giegold, M, Silverstein, N J, Bottiglieri, T, Manoach, D S, Smoller, J W, Henderson, D C, and Goff, D C

Abstract

Folic acid supplementation confers modest benefit in schizophrenia, but its effectiveness is influenced by common genetic variants in the folate pathway that hinder conversion to its active form. We examined physiological and clinical effects of l-methylfolate, the fully reduced and bioactive form of folate, in schizophrenia. In this randomized, double-blind trial, outpatients with schizophrenia (n=55) received l-methylfolate 15 mg or placebo for 12 weeks. Patients were maintained on stable doses of antipsychotic medications. The pre-defined primary outcome was change in plasma methylfolate at 12 weeks. Secondary outcomes included change in symptoms (Positive and Negative Syndrome Scale (PANSS), Scale for Assessment of Negative Symptoms, Calgary Depression Scale for Schizophrenia), cognition (Measurement and Treatment Research to Improve Cognition in Schizophrenia composite) and three complementary magnetic resonance imaging measures (working memory-related activation, resting connectivity, cortical thickness). Primary, mixed model, intent-to-treat analyses covaried for six genetic variants in the folate pathway previously associated with symptom severity and/or response to folate supplementation. Analyses were repeated without covariates to evaluate dependence on genotype. Compared with placebo, l-methylfolate increased plasma methylfolate levels (d=1.00, P=0.0009) and improved PANSS Total (d=0.61, P=0.03) as well as PANSS Negative and General Psychopathology subscales. Although PANSS Total and General Psychopathology changes were influenced by genotype, significant PANSS Negative changes occurred regardless of genotype. No treatment differences were seen in other symptom rating scales or cognitive composite scores. Patients receiving l-methylfolate exhibited convergent changes in ventromedial prefrontal physiology, including increased task-induced deactivation, altered limbic connectivity and increased cortical thickness. In conclusion, l-methylfolate supplementation was associated with salutary physiological changes and selective symptomatic improvement in this study of schizophrenia patients, warranting larger clinical trials. ClinicalTrials.gov, NCT01091506.

Published
2018
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44. Homocysteine, folate, methylation, and monoamine metabolism in depression.

Author

Bottiglieri T, Laundy M, Crellin R, Toone BK, Carney MWP, Reynolds EH, Bottiglieri, T, Laundy, M, Crellin, R, Toone, B K, Carney, M W, and Reynolds, E H

Abstract

Objectives: Previous studies suggest that folate deficiency may occur in up to one third of patients with severe depression, and that treatment with the vitamin may enhance recovery of the mental state. There are, however, difficulties in interpreting serum and red cell folate assays in some patients, and it has been suggested that total plasma homocysteine is a more sensitive measure of functional folate (and vitamin B12) deficiency. Other studies suggest a link between folate deficiency and impaired metabolism of serotonin, dopamine, and noradrenaline (norepinephrine), which have been implicated in mood disorders. A study of homocysteine, folate, and monoamine metabolism has, therefore, been undertaken in patients with severe depression.Methods: In 46 inpatients with severe DSM III depression, blood counts, serum and red cell folate, serum vitamin B12, total plasma homocysteine, and, in 28 patients, CSF folate, S-adenosylmethionine, and the monoamine neurotransmitter metabolites 5HIAA, HVA, and MHPG were examined. Two control groups comprised 18 healthy volunteers and 20 patients with neurological disorders, the second group undergoing CSF examination for diagnostic purposes.Results: Twenty four depressed patients (52%) had raised total plasma homocysteine. Depressed patients with raised total plasma homocysteine had significant lowering of serum, red cell, and CSF folate, CSF S-adenosylmethionine and all three CSF monoamine metabolites. Total plasma homocysteine was significantly negatively correlated with red cell folate in depressed patients, but not controls.Conclusions: Utilising total plasma homocysteine as a sensitive measure of functional folate deficiency, a biological subgroup of depression with folate deficiency, impaired methylation, and monoamine neurotransmitter metabolism has been identified. Detection of this subgroup, which will not be achieved by routine blood counts, is important in view of the potential benefit of vitamin replacement. [ABSTRACT FROM AUTHOR]

Published
2000

46. Reduced Arginine Bioavailability in Sepsis.

Author

Gough, MS, primary, Morgan, MM, additional, Mack, CM, additional, Darling, DC, additional, Frasier, LM, additional, Doolin, KP, additional, Apostolakos, MJ, additional, Arning, E, additional, Bottiglieri, T, additional, Mooney, R, additional, Frampton, MW, additional, and Pietropaoli, AP, additional

Published
2009
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