Socio-economic disparities in the appropriateness of diabetes care in an Italian region: findings of AEQUITAS study

Background: To evaluate socio-economic disparities in diabetes prevalence and care in Marches (a region of central Italy) in 2003-2010 through a cross-sectional study. Methods: The databases of 52 general practitioners were mined for people with diabetes (age ≥20 years). These data were linked with records from other regional administrative databases. Healthcare disparities, specifically potentially preventable hospitalizations (PPH) related to diabetes and its complications, were analysed using participants’ gender, age, and education data and the Italian Deprivation Index. Crude, age-specific and gender-specific diabetes prevalence was estimated for each year of observation. A time-trend analysis was performed. Admissions that might have been prevented according to Agency for Healthcare Research and Quality criteria were used to calculate the PPH rate for each level of social condition indicators. Rate ratios and 95% confidence intervals were estimated with a multiple Poisson regression model. Results: The search found 6,494 participants with diabetes mellitus aged ≥20 years. Disease prevalence ranged from 5.4% (2003) to 7.8% (2010), with a significant 0.31% positive trend. Those aged ≤44 years were at significantly higher risk of PPH than older people. A significant PPH excess was found among people living in socio-economically disadvantaged areas. Education and gender did not significantly affect PPH. Conclusion. People with diabetes seem to use primary care services appropriately irrespective of socio-economic status. Outpatient services are not equally distributed on the regional territory; this may increase disease severity and/or the risk of diabetes complications and affect appropriateness of diabetes care

Computer-assisted evaluation of nipple-areola complex sensibility in macromastia and following superolateral pedicle reduction mammaplasty: A statistical analysis

BACKGROUND: The authors performed a prospective study quantifying nipple-areola complex sensibility by computer-assisted neurosensory testing in breast hypertrophy before and after superolateral breast reduction. METHODS: A superolateral pedicle breast reduction was performed on 30 macromastia patients. The mean age of the patients was 46 years. The cup sizes of the patients were as follows: D, 14 patients; E, 12 patients; and EE, four patients. Ptosis was 3 degrees in 12 and 4 degrees in 18; nipple elevation ranged from 4 to 18 cm; glandular resection ranged from 379 to 1850 g. Static and moving one- and two-point discrimination was tested preoperatively and 6 months postoperatively at the nipple-areola complex, evaluating the impact of breast hypertrophy (D versus E and EE cups), nipple elevation (<9 cm versus ≥9 cm), and glandular resection (<900 g versus ≥900 g). RESULTS: Statistical analyses revealed preoperatively significant higher pressure thresholds in the nipple-areola complex of larger versus smaller hypertrophies and in the nipple of longer nipple-areola complex transposition breasts for static and moving one-point discrimination. Postoperatively, worsening of sensibility was more significant in the nipple-areola complex of smaller versus larger hypertrophies and of shorter versus longer nipple-areola complex transposition breasts for moving one-point discrimination. CONCLUSIONS: This study confirms that macromastia patients present a reduced breast sensibility, which is not necessarily worsened by reduction mammaplasty. After reduction mammaplasty with the superolateral pedicle technique, nipple-areola complex sensibility might be slightly reduced, which is less detectable in large-breast hypertrophy because of lower preoperative levels of sensibility and less of a postoperative decrease. ©2007American Society of Plastic Surgeons

Availability of computerised reminders in primary care doesn’t reduce heart-failure repeated hospitalisations

Computerised reminders can be a support for clinical improvement. We verified their effect on heart-failure (HF) re-hospitalisation rate. Methods and Results: A software (Millewin®) widely used in Italian general practice enbedded an automatic reminder to help general practitioners (GPs) to identify HF patients and to prescribe them with recommended drugs. This reminder system was already activated in the first 2004 release, but required voluntary activation in the successive releases. We had no possibility to know who decided to keep using the reminders. We examined the 2004-2009 HF hospitalisations in Puglia, a Southern Italian Region with a population of over 4000000, and with high HF hospitalisation rate compared with the Italian mean7. We compared the hospitalisations for patients cared for by GPs who used Millewin® in 2004 to those of the patients cared for by GPs who never used Millewin®. Data were provided by the local Health Authority, and were extracted from the administrative database. Users of Millewin® cared for 4969 patients (mean age 76 y, sd 12; 48,6% men), the non-users cared for 48781 patients (mean age 76 y, sd 11; 50% men ): no significant difference as far as age and gender are concerned. We examined 17810 patients with > 2 hospitalisation. No difference in re-hospitalisations was observed. Conclusions: Availability of computerised automatic reminders aimed to improve detection of HF patients and prescription of recommended drugs doesn’t decrease repeated hospitalisation; these tools should be probably part of a more complex strategy, such as a long-term audit. KEYWORDS: Computerised reminder; heart failure; hospitalisatio

Socio-economic disparities in the appropriateness of diabetes care in an Italian region: Findings of AEQUITAS study

Background: To evaluate socio-economic disparities in diabetes prevalence and care in Marches (a region of central Italy) in 2003-2010 through a cross-sectional study. Methods: The databases of 52 general practitioners were mined for people with diabetes (age 6520 years). These data were linked with records from other regional administrative databases. Healthcare disparities, specifically potentially preventable hospitalizations (PPH) related to diabetes and its complications, were analysed using participants\u2019 gender, age, and education data and the Italian Deprivation Index. Crude, age-specific and gender-specific diabetes prevalence was estimated for each year of observation. A time-trend analysis was performed. Admissions that might have been prevented according to Agency for Healthcare Research and Quality criteria were used to calculate the PPH rate for each level of social condition indicators. Rate ratios and 95% confidence intervals were estimated with a multiple Poisson regression model. Results: The search found 6,494 participants with diabetes mellitus aged 6520 years. Disease prevalence ranged from 5.4% (2003) to 7.8% (2010), with a significant 0.31% positive trend. Those aged 6444 years were at significantly higher risk of PPH than older people. A significant PPH excess was found among people living in socio-economically disadvantaged areas. Education and gender did not significantly affect PPH. Conclusions: People with diabetes seem to use primary care services appropriately irrespective of socio-economic status. Outpatient services are not equally distributed on the regional territory; this may increase disease severity and/ or the risk of diabetes complications and affect appropriateness of diabetes care

Aneuploid acute myeloid leukemia exhibits a signature of genomic alterations in the cell cycle and protein degradation machinery

BACKGROUND: Aneuploidy occurs in more than 20% of acute myeloid leukemia (AML) cases and correlates with an adverse prognosis. METHODS: To understand the molecular bases of aneuploid acute myeloid leukemia (A-AML), this study examined the genomic profile in 42 A-AML cases and 35 euploid acute myeloid leukemia (E-AML) cases. RESULTS: A-AML was characterized by increased genomic complexity based on exonic variants (an average of 26 somatic mutations per sample vs 15 for E-AML). The integration of exome, copy number, and gene expression data revealed alterations in genes involved in DNA repair (eg, SLX4IP, RINT1, HINT1, and ATR) and the cell cycle (eg, MCM2, MCM4, MCM5, MCM7, MCM8, MCM10, UBE2C, USP37, CK2, CK3, CK4, BUB1B, NUSAP1, and E2F) in A-AML, which was associated with a 3-gene signature defined by PLK1 and CDC20 upregulation and RAD50 downregulation and with structural or functional silencing of the p53 transcriptional program. Moreover, A-AML was enriched for alterations in the protein ubiquitination and degradation pathway (eg, increased levels of UHRF1 and UBE2C and decreased UBA3 expression), response to reactive oxygen species, energy metabolism, and biosynthetic processes, which may help in facing the unbalanced protein load. E-AML was associated with BCOR/BCORL1 mutations and HOX gene overexpression. CONCLUSIONS: These findings indicate that aneuploidy-related and leukemia-specific alterations cooperate to tolerate an abnormal chromosome number in AML, and they point to the mitotic and protein degradation machineries as potential therapeutic targets.status: publishe

Aneuploid acute myeloid leukemia exhibits a signature of genomic alterations in the cell cycle and protein degradation machinery

Background: Aneuploidy occurs in more than 20% of acute myeloid leukemia (AML) cases and correlates with an adverse prognosis. Methods: To understand the molecular bases of aneuploid acute myeloid leukemia (A-AML), this study examined the genomic profile in 42 A-AML cases and 35 euploid acute myeloid leukemia (E-AML) cases. Results: A-AML was characterized by increased genomic complexity based on exonic variants (an average of 26 somatic mutations per sample vs 15 for E-AML). The integration of exome, copy number, and gene expression data revealed alterations in genes involved in DNA repair (eg, SLX4IP, RINT1, HINT1, and ATR) and the cell cycle (eg, MCM2, MCM4, MCM5, MCM7, MCM8, MCM10, UBE2C, USP37, CK2, CK3, CK4, BUB1B, NUSAP1, and E2F) in A-AML, which was associated with a 3-gene signature defined by PLK1 and CDC20 upregulation and RAD50 downregulation and with structural or functional silencing of the p53 transcriptional program. Moreover, A-AML was enriched for alterations in the protein ubiquitination and degradation pathway (eg, increased levels of UHRF1 and UBE2C and decreased UBA3 expression), response to reactive oxygen species, energy metabolism, and biosynthetic processes, which may help in facing the unbalanced protein load. E-AML was associated with BCOR/BCORL1 mutations and HOX gene overexpression. Conclusions: These findings indicate that aneuploidy-related and leukemia-specific alterations cooperate to tolerate an abnormal chromosome number in AML, and they point to the mitotic and protein degradation machineries as potential therapeutic targets.Background: Aneuploidy occurs in more than 20% of acute myeloid leukemia (AML) cases and correlates with an adverse prognosis. Methods: To understand the molecular bases of aneuploid acute myeloid leukemia (A-AML), this study examined the genomic profile in 42 A-AML cases and 35 euploid acute myeloid leukemia (E-AML) cases. Results: A-AML was characterized by increased genomic complexity based on exonic variants (an average of 26 somatic mutations per sample vs 15 for E-AML). The integration of exome, copy number, and gene expression data revealed alterations in genes involved in DNA repair (eg, SLX4IP, RINT1, HINT1, and ATR) and the cell cycle (eg, MCM2, MCM4, MCM5, MCM7, MCM8, MCM10, UBE2C, USP37, CK2, CK3, CK4, BUB1B, NUSAP1, and E2F) in A-AML, which was associated with a 3-gene signature defined by PLK1 and CDC20 upregulation and RAD50 downregulation and with structural or functional silencing of the p53 transcriptional program. Moreover, A-AML was enriched for alterations in the protein ubiquitination and degradation pathway (eg, increased levels of UHRF1 and UBE2C and decreased UBA3 expression), response to reactive oxygen species, energy metabolism, and biosynthetic processes, which may help in facing the unbalanced protein load. E-AML was associated with BCOR/BCORL1 mutations and HOX gene overexpression. Conclusions: These findings indicate that aneuploidy-related and leukemia-specific alterations cooperate to tolerate an abnormal chromosome number in AML, and they point to the mitotic and protein degradation machineries as potential therapeutic targets