Somervillesahl6162
Instability is a common reason for revision surgery after total hip arthroplasty (THA). Recent studies suggest that revisions performed in the early postoperative period are associated with higher complication rates. The purpose of this study is to assess the effect of timing of revision for instability on subsequent complication rates.
The Medicare Part A claims database was queried from 2010 to 2017 to identify revision THAs for instability. Patients were divided based on time between index and revision surgeries <1, 1-2, 2-3, 3-6, 6-9, 9-12, and >12 months. Complication rates were compared between groups using multivariate analyses to adjust for demographics and comorbidities.
Of 445,499 THAs identified, 9298 (2.1%) underwent revision for instability. Revision THA within 3 months had the highest rate of periprosthetic joint infection (PJI) 14.7% at <1 month, 12.7% at 1-2 months, and 10.6% at 2-3 months vs 6.9% at >12 months (P < .001). Adjusting for confounding factors, PJI risk remained elevated at earlier periods <1 month (adjusted odds ratio [aOR] 1.84, 95% confidence interval [CI] 1.51-2.23, P < .001), 1-2 months (aOR 1.45, 95% CI 1.16-1.82, P= .001), 2-3 months (aOR 1.35, 95% CI 1.02-1.78, P= .036). However, revisions performed within 9 months of index surgery had lower rates of subsequent instability than revisions performed >12 months (aOR 0.67-0.85, P < .050), which may be due to lower rates of acetabular revision and higher rates of head-liner exchange in this later group.
When dislocation occurs in the early postoperative period, delaying revision surgery beyond 3 months from the index procedure may be warranted to reduce risk of PJI.
When dislocation occurs in the early postoperative period, delaying revision surgery beyond 3 months from the index procedure may be warranted to reduce risk of PJI.An expert consensus panel convened by the Italian Association for Inherited and Familial Gastrointestinal Tumors (Associazione Italiana per lo Studio della Familiarità ed Ereditarietà dei Tumori Gastrointestinali, AIFEG) reviewed the literature and agreed on a number of position statements regarding the definition and management of polyposis coli without an identified pathogenic mutation on the APC or MUTYH genes, defined in the document as NAMP (non-APC/MUTYH polyposis).
In women with ovarian cancer, tumor features largely determine serum HE4 and CA125 levels, but non-tumor factors may also influence levels and be better understood by studying determinants in a well-characterized sample of women without cancer.
Serum HE4 and CA125 were measured in 2302 women from the 2001-2002 cohort of the National Heath and Nutritional Survey (NHANES). Publicly-available data on this cohort included demographic/reproductive variables, blood counts, and measurements of C-reactive protein (CRP), total homocysteine (tHcy), cotinine, and creatinine which were examined as predictors of HE4 and CA125 using multivariate models and correlational analyses.
HE4 increased non-linearly by age and current smokers had higher HE4. CA125 was lower in postmenopausal women and non-whites and trended downward with increasing BMI. Current-users of oral contraceptives (OCs) had lower HE4 and CA125; and a downward trend for CA125 was seen with increasing OC use. Pregnant women had higher CA125 and nursing women higher HE4. HE4 and CA125 were positively correlated with neutrophils, monocytes, and the neutrophil-to-lymphocyte ratio and inversely correlated with lymphocytes and the lymphocyte-to-monocyte ratio. CRP was positively correlated with both HE4 and CA125 in postmenopausal women. Strong positive correlations existed for HE4 with both tHcy and creatinine.
Serum levels of HE4 and CA125 are influenced by several hormonal or environmental stimuli which affect non-cancerous tissues normally expressing HE4 or CA125. Cytokine co-expression in those tissues may, in turn, affect white cell counts and account for their correlation with HE4 or CA125 levels.
Serum levels of HE4 and CA125 are influenced by several hormonal or environmental stimuli which affect non-cancerous tissues normally expressing HE4 or CA125. Cytokine co-expression in those tissues may, in turn, affect white cell counts and account for their correlation with HE4 or CA125 levels.
To identify whether antibiotics (ABX) impact immunotherapy (ICI) response rate (RR), progression-free survival (PFS), and overall survival (OS) in women with recurrent endometrial (EC), cervical (CC) and ovarian cancer (OC).
This retrospective cohort study included women with recurrent EC, CC, and OC treated with ICIs from 1/1/17-9/1/2020. ABX were defined as 30days before (pABX) or concurrently (cABX) with ICI. The impact of ABX upon PFS and OS was assessed by univariate analysis and multivariable Cox regression.
Of 101 women, 52.5% (n=53) had recurrent EC, 21.4% (n=22) CC and 25.7% (n=26) OC. Screening Library purchase 56.9% (n=58) received ABX, with 22.8% (n=23) pABX and 46.5% (n=47) cABX. While no difference was observed in ICI RR for any ABX vs. none (p=0.89) and cABX vs. none (p=0.33), pABX (n=23) were associated with decreased RR vs. none (n=78) (Partial Response - 8.7% vs. 30.8%; Complete Response - 4.3% vs. 9.0%; p=0.002). On univariate analysis, pABX were associated with worsened PFS (2.9 vs. 8.9months; HR 2.53, 95% CI 1.48-4.31, p<0.001) and OS (9.3 vs. 19.9months; HR 2.29, 95% CI 1.22-4.32, p=0.01). No PFS or OS difference was noted for cABX (PFS - 9.3 vs. 6.0months; HR 0.70, 95% CI 0.43-1.12; p=0.14; OS - 13.4 vs. 16.3months; HR 0.89, 95% CI 0.51-1.54; p=0.68). On multivariable analysis, pABX were associated with significantly decreased PFS (HR 3.10, 95% CI 1.75-5.49, p<0.001) and OS (HR 3.03, 95% CI 1.50-6.10, p=0.002).
In women with recurrent EC, OC, and CC receiving ICI, pABX, but not cABX, are associated with decreased RR, PFS, and OS. Further investigation is warranted to understand predictors of ICI response in women with gynecologic cancer.
In women with recurrent EC, OC, and CC receiving ICI, pABX, but not cABX, are associated with decreased RR, PFS, and OS. Further investigation is warranted to understand predictors of ICI response in women with gynecologic cancer.