Publications

BACKGROUND

The Veterans Health Administration (VHA) provides health care to large numbers of veterans afflicted with keratinocyte carcinoma (KC).

OBJECTIVE

To estimate the number of veterans treated for KCs and the related diagnosis, actinic keratosis (AK) and the costs of treating these conditions over a 1-year period.

MATERIALS AND METHODS

The authors conducted a cross-sectional analysis of veterans diagnosed with KC or AK during fiscal year 2012 using administrative data on outpatient encounters and prescription drugs provided or paid by VHA. Marginal costs of each condition were estimated from a regression model. The authors estimated counts of outpatient encounters, procedures, and costs related to KC and AK care.

RESULTS

In 2012, there were 49,229 veterans with basal cell carcinoma, 26,310 veterans with squamous cell carcinoma, and 8,050 veterans with unspecified invasive KC. There were also 197,041 veterans with AK and 6,388 veterans with KC-related diagnoses. The VHA spent $356 million on KC and AK outpatient treatment for procedures, prescription drugs, and other dermatologic care during FY2012.

CONCLUSION

There was high prevalence of KC and AK and considerable spending to treat these conditions in VHA. Treatment costs are not generalizable to care provided by non-VHA providers where a facility fee was not incurred.

Breast cancer risk assessment can inform the use of screening and prevention modalities. We investigated the performance of the Breast Cancer Surveillance Consortium (BCSC) risk model in combination with a polygenic risk score (PRS) comprised of 83 single nucleotide polymorphisms identified from genome-wide association studies. We conducted a nested case-control study of 486 cases and 495 matched controls within a screening cohort. The PRS was calculated using a Bayesian approach. The contributions of the PRS and variables in the BCSC model to breast cancer risk were tested using conditional logistic regression. Discriminatory accuracy of the models was compared using the area under the receiver operating characteristic curve (AUROC). Increasing quartiles of the PRS were positively associated with breast cancer risk, with OR 2.54 (95 % CI 1.69-3.82) for breast cancer in the highest versus lowest quartile. In a multivariable model, the PRS, family history, and breast density remained strong risk factors. The AUROC of the PRS was 0.60 (95 % CI 0.57-0.64), and an Asian-specific PRS had AUROC 0.64 (95 % CI 0.53-0.74). A combined model including the BCSC risk factors and PRS had better discrimination than the BCSC model (AUROC 0.65 versus 0.62, p = 0.01). The BCSC-PRS model classified 18 % of cases as high-risk (5-year risk ≥3 %), compared with 7 % using the BCSC model. The PRS improved discrimination of the BCSC risk model and classified more cases as high-risk. Further consideration of the PRS's role in decision-making around screening and prevention strategies is merited.

 Data from international settings suggest that isolates of with mutations testing phenotypically susceptible to rifampin (RIF) may have clinical significance. We analyzed treatment outcomes of California patients with discordant molecular-phenotypic RIF results.  We included tuberculosis (TB) patients, during 2003-2013, whose specimens tested RIF susceptible phenotypically but had a mutation determined by pyrosequencing. Demographic data were abstracted from the California TB registry. Phenotypic drug-susceptibility testing, medical history, treatment, and outcomes were abstracted from medical records.  Of 3330 isolates tested, 413 specimens had a mutation (12.4%). Of these, 16 (3.9%) had molecular-phenotypic discordant RIF results. Seven mutations were identified: 511Pro, 516Phe, 526Asn, 526Ser (AGC and TCC), 526Cys, and 533Pro. Fourteen (88%) had isoniazid (INH) resistance, 6 of whom were also phenotypically resistant to ethambutol (EMB) and/or pyrazinamide (PZA). Five patients (25%), 1 with 511Pro and 4 with 526Asn, relapsed or failed treatment. The initial regimen for 3 patients was RIF, PZA, and EMB; 1 patient received RIF, PZA, EMB, and a fluoroquinolone (FQN); and 1 patient received RIF, EMB, FQN, and some second-line medications. Upon retreatment with an expanded regimen, 3 (75%) patients completed treatment, 1 patient moved before treatment completion, and 1 patient continues on treatment. The remaining 11 patients had a successful outcome with 9 having received a FQN and/or a rifamycin.  Rifampin molecular-phenotypic discordance was rare, and most isolates had INH resistance. Patients who did not receive an expanded regimen had poor outcomes. These mutations may have clinical importance, and expanded treatment regimens should be considered.