44 research outputs found
Levels of non-transferrin-bound iron as an index of iron overload in patients with thalassaemia intermedia
No full textNon-transferrin-bound iron (NTBI) was evaluated as an index of iron overload in a cross-sectional randomised study in 74 non-transfused patients with thalassaemia intermedia (TI). Mean NTBI (2.92 ± 3.43 μmol/l), serum ferritin (1023 ± 780 ng/ml) and liver iron concentration (LIC; 9.0 ± 7.4 mg Fe/g dry weight) were increased above reference-range levels. Significant positive correlations occurred between mean NTBI and LIC (Pearson correlation 0.36; P = 0.002) and serum ferritin (Pearson correlation 0.421; P < 0.0001); with higher levels observed in splenectomised patients. NTBI assessment has potential as a simple reliable approach to determining iron status in TI
Hypovitaminosis D in developing countries-prevalence, risk factors and outcomes
No full textHypovitaminosis D is a prevalent disorder in developing countries. Clinical manifestations of hypovitaminosis D include musculoskeletal disorders, such as nonspecific muscle pain, poor muscle strength and low BMD, as well as nonmusculoskeletal disorders, such as an increased risk of respiratory infections, diabetes mellitus and possibly cardiovascular diseases. In developing countries, the prevalence of hypovitaminosis D varies widely by and within regions; prevalence ranges between 30-90percent, according to the cut-off value used within specific regions, and is independent of latitude. A high prevalence of the disorder exists in China and Mongolia, especially in children, of whom up to 50percent are reported to have serum 25-hydroxyvitamin D levels 12.5 nmol-l. Despite ample sunshine throughout the year, one-third to one-half of individuals living in Sub-Saharan Africa and the Middle East have serum 25-hydroxyvitamin D levels 25 nmol-l, according to studies published in the past decade. Hypovitaminosis D is also prevalent in children and the elderly living in Latin America. Risk factors for hypovitaminosis D in developing countries are similar to those reported in Western countries and include extremes of age, female sex, winter season, dark skin pigmentation, malnutrition, lack of sun exposure, a covered clothing style and obesity. Clinical trials to assess the effect of vitamin D supplementation on classical and nonclassical clinical outcomes in developing countries are needed. © 2010 Macmillan Publishers Limited. 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Hydatid cyst mimicking acute chest syndrome in a sickle thalassemia patient [4]
No full text[No abstract available]BEAUDOIN.A, 1967, ANN BIOL CLIN-PARIS, V25, P199; Sadjadi SM, 2006, PARASITOL INT, V55, pS197, DOI 10.1016-j.parint.2005.11.030; Vichinsky EP, 2000, NEW ENGL J MED, V342, P1855, DOI 10.1056-NEJM2000062234225020
Postprandial ghrelin and PYY responses of male subjects on low carbohydrate meals to varied balancing proportions of proteins and fats
No full textPurpose: This study was conducted to investigate whether a higher proportion of protein or fat is more favorable for optimal ghrelin and peptide YY (PYY) release in subjects consuming low carbohydrate meals. Methods: Eight normal weight men received, on three separate occasions, high protein low fat (HPLF) (40percent protein, 25percent fat), low protein high fat (LPHF) (10percent protein, 55percent fat) or medium protein medium fat (MPMF) (25percent protein, 40percent fat) meals, with equal low carbohydrates content in all three meals (35percent of energy). Postprandial blood samples were collected before and 15, 30, 60, 120, 180 and 240 min following the ingestion of each meal. Plasma acylated ghrelin and PYY 3-36 as well as serum insulin, glucose and triglycerides were measured. Results: Comparing meals and considering each time point separately, a trend for a statistically significant difference in acylated ghrelin was observed between HPLF and LPHF meals and a statistically significant change of PYY from baseline was noted between HPLF and LPHF meals as compared to the MPMF meal at certain time points. When data were pooled together, a statistically significant difference in acylated ghrelin change from baseline was observed between HPLF and LPHF meals, while both HPLF and LPHF meals resulted in a significantly higher PYY3-36 release in comparison to MPMF meal. AUC data analysis for PYY3-36 revealed significantly higher values following HPLF in comparison to MPMF meal. Correlation analysis revealed a significant negative correlation between acylated ghrelin and insulin only with the HPLF meal. Postprandial glucose and triglyceride levels were not significantly different between the three meals. Conclusions: In subjects consuming low carbohydrate meals, higher concentrations of proteins to fat seem to have more favorable effects on postprandial appetite hormones. © 2010 Springer-Verlag.ADRIAN TE, 1985, GASTROENTEROLOGY, V89, P1070; Al Awar R, 2005, CLIN SCI, V109, P405, DOI 10.1042-CS20050072; Baba NH, 1999, INT J OBESITY, V23, P1202, DOI 10.1038-sj.ijo.0801064; Batterham RL, 2003, NEW ENGL J MED, V349, P941, DOI 10.1056-NEJMoa030204; Batterham RL, 2006, CELL METAB, V4, P223, DOI 10.1016-j.cmet.2006.08.001; Blom WAM, 2006, AM J CLIN NUTR, V83, P211; Bowen J, 2006, J CLIN ENDOCR METAB, V91, P1477, DOI 10.1210-jc.2005-1856; Cameron C, 2002, COCHRANE DB SYST REV, DOI [10.1002-14651858.CD003640, DOI 10.1002-14651858.CD003640]; Chan JL, 2006, DIABETOLOGIA, V49, P169, DOI 10.1007-s00125-005-0041-2; Cummings DE, 2003, ARCH SURG-CHICAGO, V138, P389, DOI 10.1001-archsurg.138.4.389; De Schepper H, 2004, NEUROGASTROENT MOTIL, V16, P567, DOI 10.1111-j1365-2982.2004.00533.x; El Khoury DTD, 2006, ANN NUTR METAB, V50, P260, DOI 10.1159-000091684; Essah PA, 2007, J CLIN ENDOCR METAB, V92, P4052, DOI 10.1210-jc.2006-2273; Farnsworth E, 2003, AM J CLIN NUTR, V78, P31; Foreyt JP, 2009, NUTR REV, V67, pS99, DOI 10.1111-j.1753-4887.2009.00169.x; GRANDT D, 1994, REGUL PEPTIDES, V51, P151, DOI 10.1016-0167-0115(94)90204-6; Greenman Y, 2004, CLIN ENDOCRINOL, V60, P382, DOI 10.1111-j.1365-2265.2004.01993.x; Helou N, 2008, ANN NUTR METAB, V52, P188, DOI 10.1159-000138122; Keire DA, 2000, AM J PHYSIOL-GASTR L, V279, pG126; Lawrence CB, 2002, ENDOCRINOLOGY, V143, P155, DOI 10.1210-en.143.1.155; Leonetti F, 2004, REGUL PEPTIDES, V122, P179, DOI 10.1016-j.regpep.2004.06.014; le Roux CW, 2006, ENDOCRINOLOGY, V147, P3, DOI 10.1210-en.2005-0972; Lin HC, 2003, REGUL PEPTIDES, V114, P131, DOI 10.1016-S0167-0115(03)00115-0; Little TJ, 2005, OBES REV, V6, P297, DOI 10.1111-j.1467-789X.2005.00212.x; Luscombe ND, 2003, INT J OBESITY, V27, P582, DOI 10.1038-sj.ijo.0802270; MacIntosh CG, 1999, AM J CLIN NUTR, V69, P999; Marzullo P, 2004, J CLIN ENDOCR METAB, V89, P936, DOI 10.1210-jc.2003-031328; Mohlig M, 2002, J ENDOCRINOL INVEST, V25, pRC36; Monteleone P, 2005, BIOL PSYCHIAT, V57, P926, DOI 10.1016-j.biopsych.2005.01.004; Monteleone P, 2003, J CLIN ENDOCR METAB, V88, P5510, DOI 10.1210-jc.2003-030797; Neary NM, 2003, GUT, V52, P918, DOI 10.1136-gut.52.7.918; Nilsson M, 2004, AM J CLIN NUTR, V80, P1246; Poppitt SD, 2006, EUR J CLIN NUTR, V60, P77, DOI 10.1038-sj.ejcn.1602270; Roth CL, 2005, J CLIN ENDOCR METAB, V90, P6386, DOI 10.1210-jc.2005-1357; Saad MF, 2002, J CLIN ENDOCR METAB, V87, P3997, DOI 10.1210-jc.87.8.3997; Shick SM, 1998, J AM DIET ASSOC, V98, P408, DOI 10.1016-S0002-8223(98)00093-5; Smeets AJ, 2008, J NUTR, V138, P698; Stubbs RJ, 1998, P NUTR SOC, V57, P341, DOI 10.1079-PNS19980052; Tentolouris N, 2004, HORM METAB RES, V36, P559, DOI 10.1055-s-2004-825761; Tome D, 2004, BRIT J NUTR, V92, pS27, DOI 10.1079-BJN20041138; Torbay N, 2002, NUTR RES, V22, P587, DOI 10.1016-S0271-5317(02)00359-7; Veldhorst M, 2008, PHYSIOL BEHAV, V94, P300, DOI 10.1016-j.physbeh.2008.01.003; Wren AM, 2001, J CLIN ENDOCR METAB, V86, P5992, DOI 10.1210-jc.86.12.5992; ZULET MA, 2005, CURR NUTR FOOD SCI, V1, P13, DOI 10.2174-157340105295327665
Myocardial infarction in a 28-year-old thalassemia intermedia patient
No full textA 28-year-old Lebanese thalassemia intermedia (TI) patient with homozygous IVS1-110 mutation sustained atypical chest pain of 1 day's duration. The EKG reading revealed ST segment elevation in the chest leads V1 to V 5. Coronary angiography showed 2 plaques in the left anterior descending coronary artery. He underwent subsequent angioplasty with stenting of the left anterior descending coronary artery. An extensive thrombophilia profile was negative. He was started on medication, and his medical condition improved and chest pain ceased. This is the first case report of myocardial infarction in a TI patient among thalassemics. We propose that such cases will emerge more frequently as our population ages, keeping in mind a possible thrombotic mechanism.Fridlender ZG, 2004, AM J HEMATOL, V75, P52, DOI 10.1002-ajh.10454; Karimi M, 2006, ANN HEMATOL, V85, P29, DOI 10.1007-s00277-005-1101-x; Namazi MR, 2002, MED HYPOTHESES, V59, P361, DOI 10.1016-S0306-9877(02)00264-5; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; Taher A, 2006, BLOOD CELL MOL DIS, V37, P12, DOI 10.1016-j.bcmd.2006.04.0050
Beta-thalassemia intermedia: An overview
No full text[No abstract available]Aessopos A, 2005, CHEST, V127, P1523, DOI 10.1378-chest.127.5.1523; Aessopos A, 2001, BLOOD, V97, P3411, DOI 10.1182-blood.V97.11.3411; CAPELLINI MD, 2002, HEMATOL J, V65; CAPELLINI MD, 2007, GUIDELINES CLIN MANA, pCH11; Cappellini MD, 2005, SEMIN HEMATOL, V42, pS19, DOI 10.1053-j.seminhematol.2005.01.001; Cappellini MD, 2000, BRIT J HAEMATOL, V111, P467, DOI 10.1046-j.1365-2141.2000.02376.x; Castelli R, 2004, AM J MED SCI, V328, P299, DOI 10.1097-00000441-200411000-00012; Chehal Aref, 2003, Spine (Phila Pa 1976), V28, pE245, DOI 10.1097-00007632-200307010-00024; Dixit A, 2005, ANN HEMATOL, V84, P441, DOI 10.1007-s00277-005-1026-4; Eldor A, 2002, BLOOD, V99, P36, DOI 10.1182-blood.V99.1.36; GIMMON Z, 1982, PLAST RECONSTR SURG, V69, P320, DOI 10.1097-00006534-198202000-00023; Karimi M, 2005, J PEDIAT HEMATOL ONC, V27, P380, DOI 10.1097-01.mph.0000174386.13109.28; Kushner J P, 2001, Hematology Am Soc Hematol Educ Program, P47; Mourad FH, 2003, BRIT J HAEMATOL, V121, P187, DOI 10.1046-j.1365-2141.2003.04240.x; Origa R, 2005, ANN NY ACAD SCI, V1054, P451, DOI 10.1196-annals.1345.051; PERRINE SP, 1993, NEW ENGL J MED, V328, P81, DOI 10.1056-NEJM199301143280202; St Pierre TG, 2005, BLOOD, V105, P855, DOI 10.1182-blood-2004-01-0177; Taher A, 2006, THROMB HAEMOSTASIS, V96, P488, DOI 10.1160-TH06-05-0267; TAHER A, 2006, BLOOD CELL MOL DIS, V27, P12; TAHER A, 2007, ASH ANN M, V110, P3818; Weatherall DJ, 2001, J HEMATOL S1, V86, P18694
Spontaneous perforation of primary gastric B‐cell lymphoma of MALT: a case report and literature review
No full textLa justicia constitucional desde la perspectiva de la filosofía de Jeremy Waldron y la experiencia venezolana reciente
No full textThe article reviews Jeremy Waldron’s theory about the legitimacy and moral authority of the various forms of constitutional justice. According to this theory, it is always illegitimate insofar as it violates the principle of majority decision, the only moral principle of legitimate legal authority.The author explains the conditions that, according to Waldron, a political community must gather so that his theory is applicable. He also ventures into forwarding some criticisms to the author regarding these conditions.Specially, the problem of the regressivity of Waldron’s argument and the problem of stability of his conditions are explored. However, it is assumed that Waldron’s theory off ers important contributions and a reflection is made in the face of the Venezuelan constitutional reality. Finally, a theoretical outline is used to combine the institution of constitutional justice with the most relevant criticisms of Waldron.El artículo repasa la teoría de Jeremy Waldron en torno a la legitimidad y autoridad moral de las diversas formas de justicia constitucional. Según esta teoría, la justicia constitucional siempre es ilegítima en la medida en que vulnera el principio de decisión mayoritaria, único de autoridad jurídica legítima. El autor expone las condiciones que, bajo el criterio de Waldron, debe reunir una comunidad política para que su teoría sea aplicable y ensaya algunas críticas al autor respecto de dichas condiciones.Especialmente, se contempla el problema de la regresividad del argumento de Waldron y el problema de la estabilidad que de las condiciones que el propio autor sugiere. Sin embargo, se asume que esta teoría ofrece aportes importantes y se hace una refl exión de ellos de cara a la realidad constitucional venezolana. Finalmente, se ensaya un bosquejo teórico que permita conjugar la institución de la justicia constitucional con las críticas más pertinentes de Waldron
Complications of β-thalassemia intermedia: A 12-year Lebanese experience
No full text[No abstract available]CAPELLINI MD, 2002, HEMATOL J S2, V3, P65; Rund D, 2005, NEW ENGL J MED, V353, P1135, DOI 10.1056-NEJMra050436; Singer ST, 2006, AM J HEMATOL, V81, P670, DOI 10.1002-ajh.20640; Wood JC, 2007, AM J HEMATOL, V82, P1132, DOI 10.1002-ajh.2109911
PTH level but not 25 (OH) vitamin D level predicts bone loss rates in the elderly
No full textWe assessed the impact of calciotropic hormones on bone loss in 195 elderly subjects. After a median follow up of 4 years, parathyroid hormone (PTH) correlated negatively with changes in bone mineral density (BMD) at all skeletal sites. After adjustment for potential predictors of bone loss in the elderly, PTH level alone explained 3percent of the variance in BMD changes at the hip. Introduction: This study assessed the impact of calciotropic hormones on bone loss rates in an elderly population-based cohort of 195 ambulatory men and women, aged 65-85 years and followed up for a median of 4 years. Methods: Calcium intake, serum calcium, and phosphorus were assessed at baseline. Serum creatinine was measured at follow up visit. The 25 (OH) vitamin D [25-OHD] and PTH were measured at baseline and at follow up. Bone mass at the lumbar spine, hip, forearm and total body, as well as body composition was measured at baseline and at follow up by dual energy X-ray absorptiometry. Results: Mean 25-OHD level was 14.7 ± 6.4 ng-ml and mean PTH level was 47.9 ± 30.4 pg-ml. Age correlated negatively with percent changes in BMD at all skeletal sites (p 0.05). Changes in body mass index (BMI) and in body composition correlated positively with BMD changes at all sites, except at the forearm. There was no correlation between 25-OHD and changes in BMD except at the trochanter (r = 0.19, p 0.008). Conversely, PTH negatively correlated with changes in BMD at all skeletal sites (r = -0.14 to -0.27, p 0.05). This correlation persisted after adjustment for age, changes in BMI, changes in fat mass and lean mass, serum creatinine, calcium intake, and 25-OHD levels. PTH level alone explained 3percent of the variance in BMD changes at all hip subregions. Conclusions: Serum PTH, but not 25-OHD, predicted bone loss rates in the elderly. Thus, it is important to normalize PTH level when correcting hypovitaminosis D in the elderly. © 2011 International Osteoporosis Foundation and National Osteoporosis Foundation.Adami S, 2009, OSTEOPOROSIS INT, V20, P239, DOI 10.1007-s00198-008-0650-y; Arabi A, 2006, BONE, V39, P268, DOI 10.1016-j.bone.2006.01.140; Baddoura R, 2007, BONE, V40, P1066, DOI 10.1016-j.bone.2006.11.016; Bischoff-Ferrari HA, 2005, JAMA-J AM MED ASSOC, V293, P2257, DOI 10.1001-jama.293.18.2257; Bischoff-Ferrari HA, 2004, JAMA-J AM MED ASSOC, V291, P1999, DOI 10.1001-jama.291.16.1999; Bischoff-Ferrari HA, 2004, AM J MED, V116, P634, DOI 10.1016-j.amjmed.2003.12.029; Bjornerem A, 2007, CALCIFIED TISSUE INT, V81, P65, DOI 10.1007-s00223-007-9035-z; Blain H, 2004, J GERONTOL A-BIOL, V59, P1285; Boonen S, 2007, J CLIN ENDOCR METAB, V92, P1415, DOI 10.1210-jc.2006-1404; Collins D, 1998, OSTEOPOROSIS INT, V8, P110, DOI 10.1007-BF02672505; Deane A, 2007, BMC MUSCULOSKEL DIS, V8, DOI 10.1186-1471-2474-8-3; Dennison E, 1999, OSTEOPOROSIS INT, V10, P384, DOI 10.1007-s001980050244; Emaus N, 2006, AM J EPIDEMIOL, V163, P441, DOI 10.1093-aje-kwj055; Ensrud KE, 2009, J CLIN ENDOCR METAB, V94, P2773, DOI 10.1210-jc.2008-2786; Fradinger EE, 2001, OSTEOPOROSIS INT, V12, P24, DOI 10.1007-s001980170153; Garnero P, 2007, BONE, V40, P716, DOI 10.1016-j.bone.2006.09.026; Gennari L, 2003, J CLIN ENDOCR METAB, V88, P5327, DOI 10.1210-jc.2003-030736; Hannan MT, 2000, J BONE MINER RES, V15, P710, DOI 10.1359-jbmr.2000.15.4.710; Ho-Pham LT, 2010, BMC MUSCULOSKEL DIS, V26, P59; KROLNER B, 1982, ACTA RADIOL DIAGN, V23, P517; Kuchuk NO, 2007, CLIN ENDOCRINOL, V67, P295, DOI 10.1111-j.1365-2265.2007.02882.x; Mellstrom D, 2008, J BONE MINER RES, V23, P1548; Mosekilde L, 2008, CLIN ENDOCRINOL, V69, P1, DOI 10.1111-j.1365-2265.2007.03162.x; Pottelbergh V, 2003, J CLIN ENDOCR METAB, V88, P075; Rand T, 1997, CALCIFIED TISSUE INT, V35, P667; Reid IR, 2008, OSTEOPOROSIS INT, V19, P595, DOI 10.1007-s00198-007-0492-z; RIGGS BL, 1986, NEW ENGL J MED, V314, P1676, DOI 10.1056-NEJM198606263142605; Sahota O, 2004, BONE, V35, P312, DOI 10.1016-j.bone.2004.02.003; Salamoun MM, 2005, EUR J CLIN NUTR, V59, P177, DOI 10.1038-sj.ejcn.1602056; Stewart KJ, 2005, AM J PREV MED, V28, P453, DOI 10.1016-j.amepre.2005.02.003; Stone K, 1998, J BONE MINER RES, V13, P1167, DOI 10.1359-jbmr.1998.13.7.1167; van Schoor NM, 2008, BONE, V42, P260, DOI 10.1016-j.bone.2007.11.002; Yoshimura N, 2011, J BONE MINER METAB, V29, P96, DOI 10.1007-s00774-010-0197-9; Zhai G, 2008, OSTEOPOROSIS INT, V19, P1211, DOI 10.1007-s00198-008-0562-x17141
