Missed diagnosis of cancer in primary care: Insights from malpractice claims data.

BACKGROUND: In the ambulatory setting, missed cancer diagnoses are leading contributors to patient harm and malpractice risk; however, there are limited data on the malpractice case characteristics for these cases. OBJECTIVE: The aim of this study was to examine key features and factors identified in missed cancer diagnosis malpractice claims filed related to primary care and evaluate predictors of clinical and claim outcomes. METHODS: We analyzed 2155 diagnostic error closed malpractice claims in outpatient general medicine. We created multivariate models to determine factors that predicted case outcomes. RESULTS: Missed cancer diagnoses represented 980 (46%) cases of primary care diagnostic errors, most commonly from lung, colorectal, prostate, or breast cancer. The majority (76%) involved errors in clinical judgment, such as a failure or delay in ordering a diagnostic test (51%) or failure or delay in obtaining a consult or referral (37%). These factors were independently associated with higher-severity patient harm. The majority of these errors were of high severity (85%). CONCLUSIONS: Malpractice claims involving missed diagnoses of cancer in primary care most often involve routine screening examinations or delays in testing or referral. Our findings suggest that more reliable closed-loop systems for diagnostic testing and referrals are crucial for preventing diagnostic errors in the ambulatory setting.

Regulation by SREBP-2 defines a potential link between isoprenoid and adenosylcobalamin metabolism.

Mevalonate kinase (MVK) catalyses an early step in cholesterol biosynthesis converting mevalonate to phosphomevalonate. Cob(I)alamin adenosyltransferase (MMAB) converts cob(I)alamin to adenosylcobalamin, functionally required for mitochondrial methylmalonyl-CoA mutase activity and succinyl-CoA formation. These two synthenic genes are found in a head-to-head formation on chromosome 12 in man and chromosome 5 in mouse. The 330bp intergenic region showed several conserved NF-Y sites indicative of potential bidirectional regulatory SREBP synergism. Both MVK and MMAB appear to be regulated in a similar manner, to a large extent by SREBP-2, since their tissue expression pattern was similar and both genes were suppressed by an excess of cholesterol as well as SREBP-2 knockdown. Statin treatment in mice upregulated both Mvk and Mmab mRNA levels indicating that this treatment may be useful in inborn errors of cblB complementation associated with methylmalonic aciduria as well as hyper IgD and periodic fever syndrome (HIDS).