Publications

BACKGROUND

Effective communication between referring and specialty providers is key to optimizing patient safety. Communication was assessed in an electronic referral system by review of referrals to a public urban health care system's gastroenterology clinic that were not scheduled for appointments.

METHODS

All electronic referrals to a publicly funded, urban health care system's adult gastroenterology clinic from November 1, 2009, to November 30, 2010, were reviewed that did not result in scheduling of appointments. An assessment was made of whether in-person visits were unnecessary by preconsultation exchange or whether the referrals remained unscheduled for other reasons. For the latter group, reasons why the referrals remained unscheduled were examined, and medical records were reviewed for actual patient harm when sufficient information was present in the chart or for potential harm when no further information about the referral complaint was available.

RESULTS

Eighty-six (32%) of 266 not-scheduled referrals were resolved via preconsultation exchange. For another 96 (36%), patients were not ultimately considered to require appointments or were scheduled via other routes. Nine patients received unplanned care while awaiting scheduling decisions, 5 of whom had harm that was related to referral complaints, although scheduling of appointments may not have avoided this harm. Of 75 patients for whom further information was not available about the referral complaints, most were not seen back in primary care, and 55 (73%) had potential for major harm.

CONCLUSION

Few adverse outcomes in electronic referrals not scheduled for in-person gastroenterology visits were found, and none were clearly due to communication lapses in the referral process. Contributors to the potential for harm in referrals that were unintentionally left unscheduled included discontinuity of care and lack of patient or provider follow-up.

Older Chinese immigrants are a growing population in the United States who experience multiple healthcare communication barriers such as limited English proficiency and low health literacy. Each of these obstacles has been associated with poor health outcomes but less is known about their effects in combination. This study examined the association between healthcare communication barriers and self-rated health among older Chinese immigrants. Cross-sectional survey data were obtained from 705 Chinese American immigrants ages 50-75 living in San Francisco, California. Communication barriers examined included spoken English proficiency, medical interpreter needs, and health literacy in written health information. The study sample (81 % females, mean age = 62) included 67 % who spoke English poorly or not at all, 34 % who reported needing a medical interpreter, and 37 % who reported "often" or "always" needing assistance to read health information. Two-thirds reported poor self-rated health; many reported having access to racial-concordant (74 %) and language-concordant (86 %) healthcare services. Both poor spoken English proficiency and low health literacy were associated with poor self-rated health, independent of other significant correlates (unemployment, chronic health conditions, and having a primary doctor who was ethnic Chinese). Results revealed that spoken English proficiency and print health literacy are independent communication barriers that are directly associated with health status among elderly Chinese American immigrants. Access to racial- or language-concordant health care services did not appear to resolve these barriers. These findings underscore the importance of addressing both spoken and written healthcare communication needs among older Chinese American immigrants.

Recent studies have focused on associations of the APOL1 risk variants with outcomes beyond kidney disease, including cardiovascular disease and mortality. Ma and colleagues now expand on this growing but contradicting body of work. Their analysis of a prevalent cohort of African American hemodialysis patients shows that the risk variants are associated with a survival benefit among nondiabetics. Whether this simply reflects a healthier status at hemodialysis initiation among those carrying 2 risk variants or whether these variants truly confer a survival advantage is unclear.

Osteoclasts require coordinated co-stimulation by several signaling pathways to initiate and regulate their cellular differentiation. Receptor activator for NF-κB ligand (RANKL or TNFSF11), a tumor necrosis factor (TNF) superfamily member, is the master cytokine required for osteoclastogenesis with essential co-stimulatory signals mediated by immunoreceptor tyrosine-based activation motif (ITAM)-signaling adaptors, DNAX-associated protein 12 kDa size (DAP12) and FcεRI gamma chain (FcRγ). The ITAM-signaling adaptors do not have an extracellular ligand-binding domain and, therefore, must pair with ligand-binding immunoreceptors to interact with their extracellular environment. DAP12 pairs with a number of different immunoreceptors including triggering receptor expressed on myeloid cells 2 (TREM2), myeloid DAP12-associated lectin (MDL-1), and sialic acid-binding immunoglobulin-type lectin 15 (Siglec-15); while FcRγ pairs with a different set of receptors including osteoclast-specific activating receptor (OSCAR), paired immunoglobulin receptor A (PIR-A), and Fc receptors. The ligands for many of these receptors in the bone microenvironment remain unknown. Here, we will review immunoreceptors known to pair with either DAP12 or FcRγ that have been shown to regulate osteoclastogenesis. Co-stimulation and the effects of ITAM-signaling have turned out to be complex, and now include paradoxical findings that ITAM-signaling adaptor-associated receptors can inhibit osteoclastogenesis and immunoreceptor tyrosine-based inhibitory motif (ITIM) receptors can promote osteoclastogenesis. Thus, co-stimulation of osteoclastogenesis continues to reveal additional complexities that are important in the regulatory mechanisms that seek to maintain bone homeostasis.

We have recently described a novel form of hyperalgesic priming (type II) induced by agonists at two clinically important Gi-protein-coupled receptors (Gi-GPCRs), mu-opioid and A1-adenosine. Like mu-opioids, the antimigraine triptans, which act at 5-HT1B/D Gi-GPCRs, have been implicated in pain chronification. We determined whether sumatriptan, a prototypical 5-HT1B/D agonist, produces type II priming. Characteristic of hyperalgesic priming, intradermal injection of sumatriptan (10 ng) induced a change in nociceptor function such that a subsequent injection of prostaglandin-E2 (PGE2) induces prolonged mechanical hyperalgesia. However, onset to priming was delayed 3 days, characteristic of type I priming. Also characteristic of type I priming, a protein kinase Cε, but not a protein kinase A inhibitor attenuated the prolongation phase of PGE2 hyperalgesia. The prolongation of PGE2 hyperalgesia was also permanently reversed by intradermal injection of cordycepin, a protein translation inhibitor. Also, hyperalgesic priming did not occur in animals pretreated with pertussis toxin or isolectin B4-positive nociceptor toxin, IB4-saporin. Finally, as observed for other agonists that induce type I priming, sumatriptan did not induce priming in female rats. The prolongation of PGE2 hyperalgesia induced by sumatriptan was partially prevented by coinjection of antagonists for the 5-HT1B and 5-HT1D, but not 5-HT7, serotonin receptors and completely prevented by coadministration of a combination of the 5-HT1B and 5-HT1D antagonists. Moreover, the injection of selective agonists, for 5-HT1B and 5-HT1D receptors, also induced hyperalgesic priming. Our results suggest that sumatriptan, which signals through Gi-GPCRs, induces type I hyperalgesic priming, unlike agonists at other Gi-GPCRs, which induce type II priming.