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1.
J Endocrinol Invest ; 34(11): e398-402, 2011 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-21765241

RESUMEN

BACKGROUND: It has been reported that morning cortisol levels increase with age, although there is some controversy in the literature. AIM: The aim of this study was to examine associations of cortisol levels with advancing age in an elderly population and investigate possible interactions with metabolic and hormonal parameters. SUBJECTS AND METHODS: From 372 subjects initially evaluated, we studied 251 ambulatory subjects aged 51-90 yr, median 71 yr (169 women), all permanent residents of a small town in southern Greece. Anthropometric parameters, glucose, insulin, cortisol, and biochemical parameters were recorded. RESULTS: Fasting cortisol levels (08:00-09:00 h) varied between 150.9- 854 nmol/l (mean 362.4 nmol/l). A significant association was found between age and cortisol levels (Spearman's rho =0.170, p=0.01). There was a positive correlation between cortisol levels and creatinine (Spearman's rho =0.144, p=0.023), homocysteine (Spearman's rho =0.283, p<0.001) and a negative correlation with body mass index (Spearman's rho =-0.128, p=0.047). Multivariate analysis showed that when creatinine was taken into account, the association of cortisol with age and with homocysteine was no longer significant. When, however, diabetic subjects were included in the analysis, the adjusted for creatinine association of cortisol with age was significant (ß=0.168, p<0.05). CONCLUSIONS: It is concluded that, in elderly ambulatory subjects, the reported associations between cortisol levels, age, and homocysteine may be affected by coexisting co-morbidities or possibly by a decline in renal function. In subsequent studies it is important that fasting glycemia is taken into account.


Asunto(s)
Envejecimiento/sangre , Índice de Masa Corporal , Hidrocortisona/sangre , Anciano , Anciano de 80 o más Años , Envejecimiento/metabolismo , Glucemia/metabolismo , Estudios de Cohortes , Estudios Transversales , Femenino , Grecia/epidemiología , Homocisteína/sangre , Humanos , Insulina/sangre , Masculino , Persona de Mediana Edad , Relación Cintura-Cadera/métodos
2.
Neuroepidemiology ; 33(2): 96-102, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19494550

RESUMEN

BACKGROUND: We assessed the incidence and determinants of aphasia attributable to first-ever acute stroke. We also investigated early and long-term mortality and 1-year dependence in post-stroke patients. METHODS: A 10-year prospective hospital-based study was conducted in the prefecture of Athens, Greece. RESULTS: In total, 2,297 patients were included in the study, of whom 806 (35.1%) had aphasia. The presence of aphasia was independently associated with increasing age (OR: 1.19 per 10-year increase, 95% CI: 1.12-1.21) and atrial fibrillation (OR: 1.35, 95% CI: 1.08-1.67), and inversely associated with Scandinavian Stroke Scale (SSS) score (OR: 0.55 per 10-point increase, 95% CI: 0.52-0.59) and hypertension (OR: 0.77, 95% CI: 0.63-0.96). One-year dependence score (calculated with the modified Rankin score) was higher in aphasic patients compared to non-aphasics (p < 0.001). Moreover, severity of aphasia (estimated with a subscale of SSS) was found as an independent predictor of 1-year dependence. Most of the deaths in the aphasic patients were attributed to infections and neurological damage. Using the Kaplan-Meier limit method, the unadjusted probability of 10-year mortality was demonstrated to increase with the severity of aphasia (log-rank test: 233.9, p < 0.001) and, even after adjustment for several other factors, severity of aphasia remained an independent predictor of 10-year mortality. CONCLUSIONS: Increasing age, atrial fibrillation and severity of stroke were associated with the risk of aphasia after stroke. Severity of aphasia is a strong predictor of long-term mortality and dependence of post-stroke patients.


Asunto(s)
Afasia/etiología , Accidente Cerebrovascular/complicaciones , Anciano , Afasia/mortalidad , Afasia/terapia , Causas de Muerte , Estudios de Cohortes , Femenino , Escala de Coma de Glasgow , Grecia/epidemiología , Hospitalización , Humanos , Hipertensión/complicaciones , Hipertensión/epidemiología , Estimación de Kaplan-Meier , Masculino , Modelos de Riesgos Proporcionales , Estudios Prospectivos , Factores de Riesgo , Accidente Cerebrovascular/mortalidad , Accidente Cerebrovascular/terapia , Resultado del Tratamiento
3.
Int J Artif Organs ; 30(7): 564-76, 2007 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-17674332

RESUMEN

The central concept of the cardiorenal syndrome (CRS) is that the heart and the kidney should be regarded not solely as individual organs but rather as a dipole with multiple interconnections. The interplay between the heart and the kidney seems complex and multifactorial: cardiac output, regulation of extracellular volume, blood pressure and renal sodium handling are the major parameters that determine the crosstalk between the 2 organs. These basic parameters are controlled through mediators (renin-angiotensin system, endothelin) and the relevant antagonists (natriuretic peptides). Recently, it has been shown that the nitric oxide / reactive oxygen species balance, sympathetic nervous system activation and the presence of systemic inflammation aggravate atherosclerosis, promote structural alterations in left ventricular geometry and favor progression of renal disease. Although the prevalence of the CRS is high, major clinical trials for heart failure have only partially addressed this issue. The present review tries to dissect the role of various components of the CRS in a way that could potentially facilitate the implementation of specific therapeutic strategies. The multiple factors that participate in the pathogenesis of this syndrome are studied in detail in an effort to better understand this syndrome and address effectively its various components, since a holistic approach could (ideally) alter the syndrome's course and hence ameliorate the prognosis of the CRS.


Asunto(s)
Insuficiencia Cardíaca/fisiopatología , Enfermedades Renales/fisiopatología , Acidosis/fisiopatología , Acidosis/terapia , Anemia/fisiopatología , Anemia/terapia , Enfermedad Crónica , Insuficiencia Cardíaca/diagnóstico , Humanos , Hipertensión/fisiopatología , Hipertensión/terapia , Inflamación/fisiopatología , Enfermedades Renales/terapia , Minerales/metabolismo , Óxido Nítrico/fisiología , Especies Reactivas de Oxígeno/metabolismo , Sistema Renina-Angiotensina/fisiología , Sistema Nervioso Simpático/fisiología , Síndrome
5.
Hippokratia ; 15(Suppl 1): 39-43, 2011 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-21897757

RESUMEN

Anemia is a common finding in patients with CKD, with a prevalence that increases gradually as eGFR declines. The prevalence of renal anemia depends on the size of the study and the selection of participants. Diabetic status increases the prevalence of anemia in patients with CKD. Anemia in CKD is due primarily to reduced production of erythropoietin in the kidney and secondarily to shortened red cell survival. Erythropoeitin (EPO) is produced by peritubular cells in the kidneys of the adult and in hepatocytes in the fetus. These cells are sensitive to hypoxia that once sensed leads to an increase in EPO production. EPO circulates in the plasma and induces redcell production in the bone marrow after successful binding to erythroid progenitor cells. Apart from EPO, folate, B(12) and iron are needed to assure effective erythropoiesis. Factors that can dysregulate this process include inflammation, uremic toxins, hypothyroidism, hypersplenism and ongoing infection.The investigation of renal anemia requires the assessment of a variety of biological indices. Among them, the complete blood count, the reticulocyte index, B(12), folate, ferritin levels and the saturation of transferrin are the most valuable tools in revealing the cause of renal anemia.

6.
Hippokratia ; 15(Suppl 1): 53-68, 2011 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-21897760

RESUMEN

Albeit the considerable progress that has been made both in our understanding of the pathophysiology of acute renal failure (ARF) and in its treatment (continuous renal replacement therapies), the morbidity of this complex syndrome remains unacceptably high. The current review focuses on recent developments concerning the definition of ARF, new strategies for the prevention and pharmacological treatment of specific causes of ARF, dialysis treatment in the intensive care setting and provides an update on critical care issues relevant to the clinical nephrologist.

7.
Hippokratia ; 14(3): 215-6, 2010 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-20981174

RESUMEN

With the exception of the catastrophic antiphospholipid syndrome (APS), the management of patients with APS has been largely supportive aiming at avoiding a recurrent thrombotic event; it is noteworthy that data concerning therapy targeting the triggering factor (the antiphopsholipid antibodies) are scarce. We report a case of APS manifested as recurrent fetal losses, ischemic stroke and renal dysfunction with concomitant nephrotic syndrome successfully treated with the combination of plasmapheresis and anti-CD20 antibody.

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