Impact of electronic documentation on Pap screening rates in an urban health center.

Providers and non-physician staff in primary care settings have reported barriers to full electronic health record (EHR) utilization. This study evaluates the effectiveness of EHR use for accurately documenting cervical cancer screening in a community healthcare setting, and proposes strategies to improve documentation. An electronic query generated data on average-risk patients aged 21-64 who had a medical visit at Fenway Health in 2012 and were overdue for a Papanicolaou (Pap) test according to the 2012 American Society for Colposcopy and Cervical Pathology guidelines. We then conducted a manual review of these records to determine the accuracy of EHR documentation. Of a total 5,279 patients, the electronic query classified 2,982 (56.5%) as up-to-date (UTD) for a Pap and 2,297 patients (43.5%) as overdue. Upon manual review, 65 (2.2%) patients thought to be UTD were actually overdue. Of those 2,297 patients classified by the query as overdue, 816 (35.5%) were reclassified as UTD due to evidence of a recent Pap in their chart that was not extractable by electronic query and 208 (9.1%) were ineligible for a Pap; only 1,272 patients (55.4%) of the 2,297 classified by the query were truly overdue. The cervical cancer screening rate indicated by electronic query was 56.5 %; after manual review, the adjusted rate was 73.6%. Overall, 1,090 patients (20.6%) were misclassified by the query. Inefficient EHR use can have serious implications for clinical practice and performance measures. Primary care practices need to develop mechanisms to capture outside medical records and create a team-based approach to facilitate accurate EHR documentation.

Human sterile alpha motif domain 9, a novel gene identified as down-regulated in aggressive fibromatosis, is absent in the mouse.

BACKGROUND: Neoplasia can be driven by mutations resulting in dysregulation of transcription. In the mesenchymal neoplasm, aggressive fibromatosis, subtractive hybridization identified sterile alpha motif domain 9 (SAMD9) as a substantially down regulated gene in neoplasia. SAMD9 was recently found to be mutated in normophosphatemic familial tumoral calcinosis. In this study, we studied the gene structure and function of SAMD9, and its paralogous gene, SAMD9L, and examined these in a variety of species. RESULTS: SAMD9 is located on human chromosome 7q21.2 with a paralogous gene sterile alpha motif domain 9 like (SAMD9L) in the head-to-tail orientation. Although both genes are present in a variety of species, the orthologue for SAMD9 is lost in the mouse lineage due to a unique genomic rearrangement. Both SAMD9 and SAMD9L are ubiquitously expressed in human tissues. SAMD9 is expressed at a lower level in a variety of neoplasms associated with beta-catenin stabilization, such as aggressive fibromatosis, breast, and colon cancers. SAMD9 and SAMD9L contain an amino-terminal SAM domain, but the remainder of the predicted protein structure does not exhibit substantial homology to other known protein motifs. The putative protein product of SAMD9 localizes to the cytoplasm. In vitro data shows that SAMD9 negatively regulates cell proliferation. Over expression of SAMD9 in the colon cancer cell line, SW480, reduces the volume of tumors formed when transplanted into immune-deficient mice. CONCLUSION: SAMD9 and SAMD9L are a novel family of genes, which play a role regulating cell proliferation and suppressing the neoplastic phenotype. This is the first report as far as we know about a human gene that exists in rat, but is lost in mouse, due to a mouse specific rearrangement, resulting in the loss of the SAMD9 gene.