Miscommunication in Doctor-Patient Communication

The effectiveness of medical treatment depends on the quality of the patient–clinician relationship. It has been proposed that this depends on the extent to which the patient and clinician build a shared understanding of illness and treatment. Here, we use the tools of conversation analysis (CA) to explore this idea in the context of psychiatric consultations. The CA “repair” framework provides an analysis of the processes people use to deal with problems in speaking, hearing, and understanding. These problems are especially critical in the treatment of psychosis where patients and health care professionals need to communicate about the disputed meaning of hallucinations and delusion. Patients do not feel understood, they are frequently non‐adherent with treatment, and many have poor outcomes. We present an overview of two studies focusing on the role of repair as a mechanism for producing and clarifying meaning in psychiatrist–patient communication and its association with treatment outcomes. The first study shows patient clarification or repair of psychiatrists’ talk is associated with better patient adherence to treatment. The second study shows that training which emphasizes the importance of building an understanding of patients’ psychotic experiences increases psychiatrists’ self‐repair. We propose that psychiatrists are working harder to make their talk understandable and acceptable to the patient by taking the patient's perspective into account. We conclude that these findings provide evidence that repair is an important mechanism for building shared understanding in doctor–patient communication and contributes to better therapeutic relationships and treatment adherence. The conversation analytic account of repair is currently the most sophisticated empirical model for analyzing how people construct shared meaning and understanding. Repair appears to reflect greater commitment to and engagement in communication and improve both the quality and outcomes of communication. Reducing potential miscommunication between psychiatrists and their patients with psychosis is a low‐cost means of enhancing treatment from both the psychiatrist and patient perspective. Given that misunderstanding and miscommunication are particularly problematic in psychosis, this is critical for improving the longer term outcomes of treatment for these patients who often have poor relationships with psychiatrists and health care services more widely

Improvement of Therapeutic Efficacy of Oral Immunotherapy in Combination with Regulatory T Cell-Inducer Kakkonto in a Murine Food Allergy Model

<div><p>Oral immunotherapy (OIT) has been considered a promising approach for food allergies (FAs). However, the current OIT strategy is limited in terms of the long-term efficacy and safety. We have previously demonstrated that kakkonto, a traditional Japanese herbal medicine, suppresses the occurrence of allergic symptoms in a murine model of ovalbumin (OVA)-induced FA, which is attributed to the induction of the Foxp3⁺ CD4⁺ regulatory T cells. In this study, we established an OIT model using the FA mice with already established allergic symptoms and determined whether kakkonto could improve the efficacy of OIT. The OIT method consisted of initially administrating a very small amount of OVA and slowly increasing the amount. Allergic symptoms decreased in the OIT-treated FA mice. OIT significantly downregulated Th2 immune response-related gene expression in the FA mouse colon, and decreased the level of mouse mast cell protease-1, a marker of mast cell degranulation in the FA mouse plasma. Moreover, the concomitant use of kakkonto significantly enhanced the effectiveness of OIT on the allergic symptoms, and the combination therapy further suppressed the Th2 immune responses and the mast cell degranulation. In addition, OIT significantly increased the population of Foxp3⁺ CD4⁺ regulatory T cells in the FA mouse colon, and this population was further increased by OIT in combination with kakkonto. Furthermore, the combined therapy with kakkonto reduced the expression of RA-degrading enzyme CYP26B1 mRNA in the FA mouse colon. These findings indicated that the combination of OIT with kakkonto represents a promising approach for FA treatment.</p></div

Differential gene expression of Th2 cell markers.

<p>(A) Heat map of the expression of genes associated with the Th2 response (subset mentioned in IPA dataset). (B) The IL-4, IL-5, IL-13, and GATA3 mRNA expression levels in the proximal colon. The segment of the proximal colon was obtained 1 h after the non-heated OVA challenge on day 49 (Normal n = 5, FA, OIT and OIT+kakkonto n = 14, *P<0.05, **P<0.01, ***P<0.001). (C) The OVA-specific IgE and IgG1 levels in the plasma was measured using an ELISA 1 h after the non-heated OVA challenge to assess the allergic symptoms on day 49 (Normal n = 5, FA, OIT and OIT+kakkonto n = 20).</p

Outline of the experimental design.

<p>OVA-sensitized BALB/c mice were challenged 3 times per week by oral administration of non-heated OVA solution. After day 40, mice were treated with kakkonto, OIT, OIT+kakkonto or placebo (MC: 0.5% methylcellulose solution and sterilized water) daily for 8 days. One hour before each oral heated OVA challenge, kakkonto or placebo (MC) was orally administrated. Before and after the OIT, mice received a non-heated OVA challenge to assess allergic symptoms (day 40 and day 49, respectively).</p

Association of retinoic acid with the combined therapy.

<p>(A) Association between our microarray result and the canonical pathway of “retinoid biosynthesis”. Each value is shown as a -log P value, which was calculated using the right-tailed Fisher’s exact test. The threshold line corresponds to the P value of 0.05. (B) CYP26B1, CRABP1 and ALDH1A1 mRNA expression level in the proximal colon. The segment of the proximal colon was obtained 1 h after the non-heated OVA challenge on day 49 (Normal n = 5, FA, OIT and OIT+kakkonto n = 14, *P<0.05, **P<0.01, ***P<0.001). (C) Dose dependency of RA on Foxp3⁺ CD4⁺ Treg differentiation. Naive CD4⁺ T cells from RAG-2^-/- DO11.10 mice were co-cultured with SpDCs with the presence of OVA peptide and RA (100 nM, 10 nM, 3.3 nM, 1 nM, 0.3 nM and vehicle) (n = 3, *P<0.05 vs vehicle).</p

Clinical symptoms in mice under different treatments.

<p>OVA-sensitized mice were treated with OIT, OIT and kakkonto combined therapy (OIT+kakkonto), kakkonto alone (kakkonto) or placebo (FA). One hour after the non-heated OVA challenge on day 49, the severity of allergic diarrhea was assessed (kakkonto n = 18, FA n = 46, OIT n = 48, OIT+kakkonto n = 48, **P<0.01, ***P<0.001).</p