Evaluation of the change in glycated hemoglobin for patients in an employee health program formerly managed by a pharmacist-run ambulatory care clinic.

PURPOSE: To evaluate the change in mean glycated hemoglobin (HbA1c) for patients with diabetes in an employee health program after discontinuation of management by a clinical pharmacist. METHODS: This was a single-center, retrospective chart review of patients followed by a clinical pharmacist from January 1, 2020, through March 31, 2021. Patients included had type 2 diabetes, were 18 years of age or older, were not pregnant, and were not using an insulin pump. The baseline visit was defined as the last pharmacist visit within the study period. The follow-up visit was defined as the most recent visit upon chart review that occurred at least 5 months after the baseline visit. The primary and secondary endpoints were the mean change in HbA1c and number of antihyperglycemic agents from baseline to follow-up, respectively. Statistical analysis included descriptive statistics for baseline characteristics, a paired t test for the primary endpoint, and a McNemar test for the secondary endpoint. RESULTS: A total of 590 patients were screened, of whom 131 were included in the analysis. For the primary outcome, the mean baseline HbA1c was 7.3% while that at follow-up was 7.41% (mean change of 0.11%; SD, 1.22%; P = 0.326). For the secondary outcome, the baseline number of antihyperglycemic agents was 274 while the follow-up number was 276. There were no statistically significant differences for the primary and secondary outcomes. CONCLUSION: This study highlights a unique patient population with controlled HbA1c at baseline, for whom diabetes control may potentially be influenced by the patients' employment within a healthcare system and improved access to care. The lack of a significant difference in the primary endpoint implies that it may be appropriate to limit or have less frequent pharmacist visits for well-controlled patients. Further research should investigate how to identify patients who would benefit from continued follow-up with a clinical pharmacist vs those who can be managed with minimal resources.

Cutting edge: A critical functional role for IL-23 in psoriasis.

Interleukin-23 is a key cytokine involved in the generation of Th17 effector cells. Clinical efficacy of an anti-p40 mAb blocking both IL-12 and IL-23 and disease association with single nucleotide polymorphisms in the IL23R gene raise the question of a functional role of IL-23 in psoriasis. In this study, we provide a comprehensive analysis of IL-23 and its receptor in psoriasis and demonstrate its functional importance in a disease-relevant model system. The expression of IL-23 and its receptor was increased in the tissues of patients with psoriasis. Injection of a mAb specifically neutralizing human IL-23 showed IL-23-dependent inhibition of psoriasis development comparable to the use of anti-TNF blockers in a clinically relevant xenotransplant mouse model of psoriasis. Together, our results identify a critical functional role for IL-23 in psoriasis and provide the rationale for new treatment strategies in chronic epithelial inflammatory disorders.

Hyperglycemia management using insulin in the acute care setting: therapies and strategies for care in the non-critically ill patient.

BACKGROUND: Hyperglycemia is prevalent in hospitalized non-critically ill patients and is associated with higher morbidity and mortality. Poor glycemic control is related to elevated costs due to longer hospital stays and higher rates of complications. OBJECTIVE: To review current literature evaluating treatment strategies for management of hyperglycemia in the non-critically ill hospitalized patient and to discuss the role of pharmacists in glycemia management. DATA SOURCES: A literature review (January 2000-January 2010) was conducted via PubMed, Web of Science, Cumulative Index to Nursing and Allied Health, the Cochrane Library, Combined Health Information Database, and Education Resources Information Center. MeSH terms for diabetes were used along with stress hyperglycemia, insulin therapy, and insulin analogs in combination with non-critically ill, hospitalized, acute care, or inpatient. STUDY SELECTION AND DATA EXTRACTION: All articles identified from the data sources were reviewed for inclusion. Clinical trial reports, practice guidelines, and reviews involving insulin therapies and/or quality improvement initiatives for hyperglycemia in the acute care setting were evaluated. A total of 133 citations were reviewed and an additional 11 citations were identified from reference lists. DATA SYNTHESIS: The association between hyperglycemia and increased mortality is recognized in the acute care setting among critically ill patients; however, data to support glycemia management in non-critically ill patients continue to be established. National consensus guidelines support strategies for glycemia control that focus on insulin therapy and treatment-driven protocols. These initiatives can result in quality improvement when led by multidisciplinary teams, including pharmacists. Literature supports a pharmacist role in glucose monitoring and insulin dosing. CONCLUSIONS: Management of hyperglycemia is a critical component of acute care. Insulin treatment regimens and protocols for non-critically ill patients in the acute care setting are evolving with recognition of ideal glucose targets to prevent adverse outcomes. Glycemia management can be complex and presents opportunities for pharmacist involvement.

IL-1 receptor accessory protein and ST2 comprise the IL-33 receptor complex.

IL-33 (IL-1F11) is a recently described member of the IL-1 family of cytokines that stimulates the generation of cells, cytokines, and Igs characteristic of a type 2 immune response. IL-33 mediates signal transduction through ST2, a receptor expressed on Th2 and mast cells. In this study, we demonstrate that IL-33 and ST2 form a complex with IL-1R accessory protein (IL-1RAcP), a signaling receptor subunit that is also a member of the IL-1R complex. Additionally, IL-1RAcP is required for IL-33-induced in vivo effects, and IL-33-mediated signal transduction can be inhibited by dominant-negative IL-1RAcP. The implications of this shared usage of IL-1RAcP by IL-1(alpha and beta) and IL-33 are discussed.

IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines.

Cytokines of the interleukin-1 (IL-1) family, such as IL-1 alpha/beta and IL-18, have important functions in host defense, immune regulation, and inflammation. Insight into their biological functions has led to novel therapeutic approaches to treat human inflammatory diseases. Within the IL-1 family, IL-1 alpha/beta, IL-1Ra, and IL-18 have been matched to their respective receptor complexes and have been shown to have distinct biological functions. The most prominent orphan IL-1 receptor is ST 2. This receptor has been described as a negative regulator of Toll-like receptor-IL-1 receptor signaling, but it also functions as an important effector molecule of T helper type 2 responses. We report a member of the IL-1 family, IL-33, which mediates its biological effects via IL-1 receptor ST 2, activates NF-kappaB and MAP kinases, and drives production of T(H)2-associated cytokines from in vitro polarized T(H)2 cells. In vivo, IL-33 induces the expression of IL-4, IL-5, and IL-13 and leads to severe pathological changes in mucosal organs.

Immune surveillance and effector functions of CCR10(+) skin homing T cells.

Skin homing T cells carry memory for cutaneous Ags and play an important sentinel and effector role in host defense against pathogens that enter via the skin. CCR10 is a chemokine receptor that is preferentially expressed among blood leukocytes by a subset of memory CD4 and CD8 T cells that coexpress the skin-homing receptor cutaneous lymphocyte Ag (CLA), but not the gut-homing receptor alpha(4)beta(7). Homing and chemokine receptor coexpression studies detailed in this study suggest that the CLA(+)/CCR10(+) memory CD4 T cell population contains members that have access to both secondary lymphoid organ and skin compartments; and therefore, can act as both "central" and "effector" memory T cells. Consistent with this effector phenotype, CLA(+)/CCR10(+) memory CD4 T cells from normal donors secrete TNF and IFN-gamma but minimal IL-4 and IL-10 following in vitro stimulation. Interactions of CCR10 and its skin-associated ligand CC ligand 27 may play an important role in facilitating memory T cell entry into cutaneous sites during times of inflammation.