Feasibility and Safety of Outpatient Total Laparoscopic Hysterectomy

Methods:We report a prospective, consecutive case series of 128 outpatient TLHs performed for benign gynecologic conditions in a tertiary care center.Results:Of the 295 women scheduled for a TLH, 151 (51%) were attempted as an outpatient procedure. A total of 128 women (85%) were actually discharged home the day of their surgery. The most common reasons for admission the same day were urinary retention (19%) and nausea (15%). Indications for hysterectomy were mainly leiomyomas (62%), menorrhagia (24%), and pelvic pain (9%). Endometriosis and adhesions were found in 23% and 25% of the cases, respectively. Mean estimated blood loss was 56 mL and mean uterus weight was 215 g, with the heaviest uterus weighing 841 g. Unplanned consultation and readmission were infrequent, occurring in 3.1% and 0.8% of cases, respectively, in the first 72 hours. At 3 months, unplanned consultation, complication, and readmission had occurred in a similar proportion of inpatient and outpatient TLHs (17.2%, 12.5%, and 4.7% versus 18.1%, 12.7%, and 5.4%, respectively). In a logistic regression model, uterus weight, presence of adhesions or endometriosis, and duration of the operation were not associated with adverse outcomes.Conclusion:Same-day discharge is a feasible and safe option for carefully selected patients who undergo an uncomplicated TLH, even in the presence of leiomyomas, severe adhesions, or endometriosis.     

Identification of Streptococcal M-Protein Cardiopathogenic Epitopes in Experimental Autoimmune Valvulitis

The M protein of rheumatogenic group A streptococci induces carditis and valvulitis in Lewis rats and may play a role in pathogenesis of rheumatic heart disease. To identify the epitopes of M5 protein that produce valvulitis, synthetic peptides spanning A, B, and C repeat regions contained within the extracellular domain of the streptococcal M5 protein were investigated. A repeat region peptides NT4, NT5/6, and NT7 induced valvulitis similar to the intact pepsin fragment of M5 protein. T cell lines from rats with valvulitis recognized M5 peptides NT5/6 and NT6. Passive transfer of an NT5/6-specific T cell line into naïve rats produced valvulitis characterized by infiltration of CD4+ cells and upregulation of VCAM-1, while an NT6-specific T cell line did not target the valve. Our new data suggests that M protein-specific T cells may be important mediators of valvulitis in the Lewis rat model of rheumatic carditis.     

Influence of obesity indices, metabolic parameters and age on cardiac autonomic function in abdominally obese men

Heart rate variability (HRV) is affected by age, hyperglycemia and accumulation of body fat. This study compares the predictive value of four measurements of adiposity/obesity on HRV and investigates the specific role of age, metabolic contributors and degree/distribution of fat in HRV alterations. The sample consisted of 97 non-diabetic and non-medicated men with features of the metabolic syndrome (50 ± 8 years of age, body mass index [BMI] 31 ± 3 kg/m², waist circumference [WC] 107 ± 9 cm, triglycerides 2.3 ± 0.7 mmol/L, fasting glucose 6.0 ± 0.5 mmol/L, insulin 156 ± 71 pmol/L; mean ± SD). WC, BMI, percent body fat (% fat, from dual energy X-ray absorptiometry) and visceral adipose tissue volume (VAT, from computed tomography) were used as measures of adiposity/obesity. HRV measures were obtained from 24-h, day- and night-time segments of Holter recordings. BMI presented no independent association with HRV. Percentage fat was the strongest obesity index to be associated with HRV: 24-h pNN50, rMSSD, HF and daytime pNN50, rMSSD, HF and LF (?0.27 ≤ std β ≤ ?0.20, P < .05). VAT was associated with 24-h SDNN, LF (std β = ?0.25 and ?0.20, P < .05, respectively) and daytime SDNN (std β = ?0.24, P < .05) while WC was associated with nighttime SDNN and SDANN (std β = 0.22 and 0.32, P < .05). In addition, age, fasting glucose, 2-h oral glucose tolerance test and triglycerides presented independent association with HRV. Adiposity/obesity measurements seem to be differently associated with HRV. An approach considering the combination of age, obesity and glucose metabolism factors could be helpful in the global cardiovascular risk management in abdominally obese men.     

Elastin accumulation is regulated at the level of degradation by macrophage metalloelastase (MMP-12) during experimental liver fibrosis

Elastin has been linked to maturity of liver fibrosis. To date, the regulation of elastin secretion and its degradation in liver fibrosis has not been characterized. The aim of this work was to define elastin accumulation and the role of the paradigm elastase macrophage metalloelastase (MMP-12) in its turnover during fibrosis. Liver fibrosis was induced by either intraperitoneal injections of carbon tetrachloride (CCl(4) ) for up to 12 weeks (rat and mouse) or oral administration of thioacetamide (TAA) for 1 year (mouse). Elastin synthesis, deposition, and degradation were investigated by immunohistochemistry, quantitative polymerase chain reaction (qPCR), western blotting, and casein zymography. The regulation of MMP-12 elastin degradation was defined mechanistically using CD11b-DTR and MMP-12 knockout mice. In a CCl(4) model of fibrosis in rat, elastin deposition was significantly increased only in advanced fibrosis. Tropoelastin expression increased with duration of injury. MMP-12 protein levels were only modestly changed and in coimmunoprecipitation experiments MMP-12 was bound in greater quantities to its inhibitor TIMP-1 in advanced versus early fibrosis. Immunohistochemistry and macrophage depletion experiments indicated that macrophages were the sole source of MMP-12. Exposure of CCl(4) in MMP-12(-/-) mice led to a similar degree of overall fibrosis compared to wildtype (WT) but increased perisinusoidal elastin. Conversely, oral administration of TAA caused both higher elastin accumulation and higher fibrosis in MMP-12(-/-) mice compared with WT. Conclusion: Elastin is regulated at the level of degradation during liver fibrosis. Macrophage-derived MMP-12 regulates elastin degradation even in progressive experimental liver fibrosis. These observations have important implications for the design of antifibrotic therapies.