Bucharest, Romania
Bucharest, Romania

Time filter

Source Type

Ioacara S.,N Paulescu National Institute Of Diabetes | Guja C.,N Paulescu National Institute Of Diabetes | Fica S.,Elias Hospital | Ionescu-Tirgoviste C.,N Paulescu National Institute Of Diabetes
Diabetes Research and Clinical Practice | Year: 2013

Aim: To investigate the historical changes in survival with diabetes in elderly people with diabetes. Research design and methods: We analyzed 6504 deaths (44.5% males) registered in a large urban population, aged ≥65 years, and deceased between 1943 and 2009. We split the analysis into three time periods according to year of death: 1943-1965, 1966-1988 and 1989-2009. The parallel changes in the corresponding general population were available. Results: The mean age at diabetes onset was 70.8 ± 4.7 years, with mean disease duration at death 7.5 ± 5 years, and mean age at death 78.3 ± 5.9 years. The mean survival loss due to diabetes (expected minus observed survival) was 4.5 ± 5.1 years (4.9 ± 5.1 years for females versus 4.1 ± 5.2 years for males, p< 0.001). The mean disease duration at death was 6.4 ± 5.7 years in the period 1943-1965, followed by a significant (p= 0.019) rise to 7 ± 5 years in 1966-1988, and 8.3 ± 4.9 years (p< 0.001) in 1989-2009. There was a significant increase in coronary heart disease and stroke, and a significant decrease in infections and end-stage renal disease as causes of death. Conclusions: We found a significant increase in age at onset and survival with diabetes leading to a significant increase in age at death. Females had a higher survival loss due to diabetes compared with males. © 2012 Elsevier Ireland Ltd.


Ioacara S.,N Paulescu National Institute Of Diabetes | Guja C.,N Paulescu National Institute Of Diabetes | Ionescu-Tirgoviste C.,N Paulescu National Institute Of Diabetes | Fica S.,Elias Hospital | And 4 more authors.
Diabetes Research and Clinical Practice | Year: 2011

Aim: To investigate the historical changes in survival with diabetes in adult type 2 diabetes patients. Methods: We analyzed 9066 deaths, 54.2% males, registered at "I. Pavel" Bucharest Diabetes Centre, aged 40-64 years and deceased between 1943 and 2009. We split the analysis in three time periods according to year of death: 1943-1965, 1966-1988 and 1989-2009. Results: The mean age at diabetes onset was 55.5 ± 6.2 years, with mean disease duration at death 12.7 ± 8.2 years and mean age at death 68.2 ± 8.7 years. The mean disease duration at death was 9.9 ± 7.3 years in 1943-1965 period, followed by a significant (p< 0.001) rise to 12.2 ± 8.2 years in 1966-1988, and 14 ± 8.1 years (p< 0.001) in 1989-2009. There was a significant increase for coronary heart diseases and cancer and a significant decrease for infections and end-stage renal disease as causes of death. Conclusion: We found a significant increase in age at onset and survival with diabetes leading to a significant increase in age at death. © 2011 Elsevier Ireland Ltd.


Ioacara S.,Elias Hospital | Ioacara S.,Carol Davila University of Medicine and Pharmacy | Guja C.,Carol Davila University of Medicine and Pharmacy | Ionescu-Tirgoviste C.,Carol Davila University of Medicine and Pharmacy | And 4 more authors.
PLoS ONE | Year: 2014

Aims: To test the hypothesis that cumulative exposure to insulin and long-acting insulin analogs might be associated with cancer mortality in diabetes patients. Methods: All consecutive diabetes patients aged over 40 years, residing in a major urban area were screened at their first diabetes outpatient visit between 01/01/2001-12/31/2008 (n = 79869). Exclusion criteria were insulin treatment at screening, no insulin treatment until 12/31/2008, less than 6 months of glucose-lowering treatment alone before insulin initiation, insulin prescription before glargine became available, age <40/≥80 years at first insulin prescription, and <6 months of insulin exposure. A total 4990 subjects were followed-up for death based on death certificate, until 12/31/2011. Adjusted time-dependent competing risk regression analysis, with daily updates of treatment modalities was performed. Results are expressed for every 10,000 IU of cumulative dose or one year of cumulative time exposure to insulin. Results: Mean baseline age was 62±9 years, and follow-up 4.7±1.9 years. Glargine cumulative dose was associated with lower cancer mortality risk (subhazard ratio, SHR: 0.94 (95%CI 0.89-0.99, p = 0.033)). Cumulative exposure limited to that attained one year prior to death revealed lower SHRs for cumulative time (0.94 (95%CI 0.89-0.99, p = 0.018)) and cumulative dose of glargine (0.92 (95%CI 0.86-0.98, p = 0.014)). Glargine cumulative time and cumulative dose were significant predictors for lower pancreatic and breast cancer mortality, but not for deaths from lung, colorectal, female genital, liver, and urinary tract cancer. No increased hazards were found for any other subtypes of insulins. Conclusions: The cumulative dose exposure to insulin glargine was associated with a lower risk of cancer mortality in general, and of breast and pancreatic cancer in particular. This effect remained even after additional "fixed" cohort or propensity score analyses. © 2014 Ioacara et al.


Mocanu M.A.,University of Bucharest | Diculescu M.,Elias Hospital | Dumitrescu M.,Elias Hospital
Revista medico-chirurgicalǎ̌ a Societǎ̌ţii de Medici ş̧i Naturaliş̧ti din Iaş̧i | Year: 2013

The AIM of our study was to evaluate gastric, duodenal and gallbladder motility disorders in patients with gastroesophageal reflux disease (GERD) and metabolic syndrome. We studied 128 patients with GERD divided into two groups: first group with metabolic syndrome and the second without metabolic syndrome. By abdominal ultrasound we monitored our patients for the gastric emptying rate, the duodenal motility and the nonlithiasic pathology of gallbladder (cholesterolosis). We found that patients with metabolic syndrome had three kind of abnormal motility disorders including stomach, duodenum, and gallbladder. The patients without metabolic syndrome we found only two abnormal motility disorders: of the duodenum and gallbladder. Hyperglycemia and high serum cholesterol level in the first group were correlated with stomach, duodenum and gallbladder abnormal motilities. In our opinion metabolic syndrome can aggravate gastroesophageal reflux disease due to these metabolic abnormalities. We consider that treatment of reflux disease in these particular cases must also involve measures to correct metabolic disorders.


PubMed | Elias Hospital and University of Bucharest
Type: Journal Article | Journal: Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi | Year: 2014

The AIM of our study was to evaluate gastric, duodenal and gallbladder motility disorders in patients with gastroesophageal reflux disease (GERD) and metabolic syndrome.We studied 128 patients with GERD divided into two groups: first group with metabolic syndrome and the second without metabolic syndrome. By abdominal ultrasound we monitored our patients for the gastric emptying rate, the duodenal motility and the nonlithiasic pathology of gallbladder (cholesterolosis).We found that patients with metabolic syndrome had three kind of abnormal motility disorders including stomach, duodenum, and gallbladder. The patients without metabolic syndrome we found only two abnormal motility disorders: of the duodenum and gallbladder. Hyperglycemia and high serum cholesterol level in the first group were correlated with stomach, duodenum and gallbladder abnormal motilities. In our opinion metabolic syndrome can aggravate gastroesophageal reflux disease due to these metabolic abnormalities.We consider that treatment of reflux disease in these particular cases must also involve measures to correct metabolic disorders.


Voiosu T.,Stefan Cel Mare University of Suceava | Balanescu P.,Stefan Cel Mare University of Suceava | Bengus A.,Stefan Cel Mare University of Suceava | Voiosu A.,Stefan Cel Mare University of Suceava | And 7 more authors.
Clinical Laboratory | Year: 2014

Background: Endocan is a marker of angiogenesis previously studied in various types of cancer and inflammatory conditions. Its expression is influenced by vascular endothelial growth factor A (VEGF A) and tumor necrosis factor alpha (TNF alpha), cytokines involved in pathogenetic pathways in inflammatory bowel disease (IBD). The aim of this study was to determine whether serum endocan levels were increased in IBD patients. Methods: We conducted an exploratory pilot study. Serum endocan levels were determined in a group of 33 consecutive IBD patients from an observational cohort study ongoing at Colentina Hospital and compared to levels determined in two control groups: healthy controls and stage IV cancer patients. Results: Endocan levels were significantly higher in the IBD group as compared to both healthy controls (p < 0.001) and cancer patients (p < 0.01). There was no correlation found between endocan levels and disease activity as assessed by clinical or endoscopical activity scores. Conclusions: There is a potential role for endocan in future biomarker studies in IBD patients.


Martin C.S.,Carol Davila University of Medicine and Pharmacy | Martin C.S.,Elias Hospital | Blaga C.,Elias Hospital | Lambrescu I.M.,Carol Davila University of Medicine and Pharmacy | And 3 more authors.
Journal of Clinical Pharmacy and Therapeutics | Year: 2015

What is known and objective Budesonide, an oral glucocorticoid indicated for the treatment of Crohn's disease, rarely interferes with the hypothalamic-pituitary-adrenal axis because more than 80% of it is metabolized by cytochrome P450 enzymes. Case summary A 33-year-old female patient diagnosed with Crohn's disease, treated with oral budesonide, was admitted for Cushingoid symptoms and signs. The onset coincided with the use of fluvoxamine, a serotonin reuptake inhibitor and also a potent inhibitor of cytochrome P450 enzymes that presumably led to budesonide accumulation. What is new and conclusion Practitioners should take into consideration the possibility of iatrogenic Cushing's syndrome caused by the association of oral budesonide with a P450 cytochrome inhibitor. Iatrogenic Cushing's syndrome caused by the association of oral budesonide with a P450 cytochrome inhibitor. © 2015 John Wiley & Sons Ltd.


PubMed | Carol Davila University of Medicine and Pharmacy and Elias Hospital
Type: Journal Article | Journal: Hormones (Athens, Greece) | Year: 2016

Thyroid hormones influence the GH/IGF1 axis, but previous studies have reported discrepant results regarding serum IGF1 levels in hyperthyroidism. We have therefore investigated, at diagnosis, the relationship between serum IGF1 levels and the main characteristics of Graves disease (GD): severity of hyperthyroidism, goiter size, presence of active Graves ophthalmopathy (GO), antythyroid antibodies status and titer.This cross-sectional study included 98 newly diagnosed hyperthyroid patients with GD who presented consecutively at our clinic. The main measured parameters were: TSH, FT4, FT3, TT3, thyroglobulin,anti-thyroid peroxidase antibodies (TPOAb), anti-thyroglobulin antibodies (ATA), thyrotropin receptor antibodies (TRAb), IGF1. Patients were considered IGF deficient if IGF1 z score was ≤-2SD from mean for age.In GD patients, men had higher IGF1 levels (p=0.023) and IGF1 z scores (p=0.013) than women. 18.4% of GD patients were, at diagnosis, IGF1 deficient. Compared to patients without IGF1 deficiency, these patients presented higher thyroglobulin (median=72.55, IQR=116.02 vs median=11.40, IQR=80.74 ng/ml, p=0.002) and FT3 (median=11.30, IQR=7.64 vs median=7.33, IQR=5.72 pg/ml, p=0.027), and lower ATA (median=20, IQR=0 vs median=34.05, IQR=161 iu/ml, p<0.001) levels. Thyroglobulin was independently associated with IGF1 deficiency (AUROC=0.732, 95% CI: 0.620-0.844, p=0.002; cut-off for thyroglobulin=50.40 ng/ml, Se=77.8%, Sp=70%). IGF1 status was not influenced by gender (p=0.084), current smoking (p=0.558), goiter size (p=0.533), active ophthalmopathy (p=0.334), TRAb (p=0.239) or TPOAb status (p=0.367).Nearly one fifth of newly diagnosed GD patients had IGF1 deficiency. IGF1 deficiency was associated with lower ATA titers, higher thyroglobulin levels and more severe FT3 hyperthyroidism at diagnosis.


PubMed | Carol Davila University of Medicine and Pharmacy and Elias Hospital
Type: | Journal: Journal of clinical pharmacy and therapeutics | Year: 2015

Budesonide, an oral glucocorticoid indicated for the treatment of Crohns disease, rarely interferes with the hypothalamic-pituitary-adrenal axis because more than 80% of it is metabolized by cytochrome P450 enzymes.A 33-year-old female patient diagnosed with Crohns disease, treated with oral budesonide, was admitted for Cushingoid symptoms and signs. The onset coincided with the use of fluvoxamine, a serotonin reuptake inhibitor and also a potent inhibitor of cytochrome P450 enzymes that presumably led to budesonide accumulation.Practitioners should take into consideration the possibility of iatrogenic Cushings syndrome caused by the association of oral budesonide with a P450 cytochrome inhibitor.


PubMed | Carol Davila University of Medicine and Pharmacy and Elias Hospital
Type: | Journal: Endocrine | Year: 2016

We investigated, at diagnosis, the relationship between serum immunoglobulin G4 levels and the main characteristics of Graves disease: hyperthyroidism severity, goiter size, presence of active Graves ophthalmopathy, antithyroid antibodies status, and titer.This prospective study included 80 newly diagnosed Graves disease patients. The main parameters measured at diagnosis: thyroid-stimulating hormone, free thyroxine, free triiodothyronine, total triiodothyronine, thyroglobulin, antithyroid peroxidase antibodies, anti-thyroglobulin antibodies, thyroid-stimulating hormone receptor antibodies, immunoglobulin G4.In Graves disease patients, serum immunoglobulin G4 levels were higher than in general population (p=0.028) and higher in men compared to women (p=0.002). Only one female patient with intense hypoechoic goiter, high anti-thyroglobulin antibody, and antithyroid peroxidase antibody titers had an elevated serum immunoglobulin G4 level at diagnosis. Patients with immunoglobulin G4 levels above the 75th percentile (>237.52mg/dl, N=20) were younger at Graves ophthalmopathy onset (p<0.001), had higher antithyroid peroxidase antibody (p=0.01), and anti-thyroglobulin antibody levels (p=0.006) and required shorter duration of the first methimazole treatment cycle (p=0.041) than patients with immunoglobulin G4 below the 75th percentile. At diagnosis, patients with immunoglobulin G4 levels above the 90th percentile (>286.28mg/dl, N=8) had lower total triiodothyronine values (p=0.001) than patients with IgG below the 90th percentile. No significant correlations were found between smoking status (p=0.58), goiter size (p=0.50), the presence of ophthalmopathy (p=0.42) or thyroid-stimulating hormone receptor antibody titers (p=0.45) and the mean value of immunoglobulin G4 levels at diagnosis.Our data suggest that Graves disease patients with elevated immunoglobulin G4 levels at diagnosis have a phenotype characterized by higher anti-thyroglobulin antibody and antithyroid peroxidase antibody titers, less severe T3 hyperthyroidism, younger age at ophthalmopathy onset and require a shorter duration of the first methimazole treatment cycle.

Loading Elias Hospital collaborators
Loading Elias Hospital collaborators