Development of salient medication reminders to facilitate information transfer during transition from inpatient to primary care: the Delphi process.

OBJECTIVE: Transitional care is important to successful hospital discharge. Providing patients with a clear and concise summary of medication-related information can help improve outcomes, in particular, among older adults. The present study aimed to propose a framework for the development of salient medication reminders (SMR), which include drug-related risks and precautions, using the Delphi process. DESIGN: Identification of potential SMR statements for 80% of medication types used by older adult patients discharged from geriatric medicine departments, followed by a Delphi survey and expert panel discussion. SETTINGS: Medical and geriatric departments of public hospitals in Hong Kong. PARTICIPANTS: A panel of 13 geriatric medical experts. OUTCOME MEASURE: A Likert scale ranging from 1 (strongly disagree) to 5 (strongly agree) points, scoring item relevance, importance and clarity. The minimum of 70% consensus was required for each statement to be included. RESULTS: The expert panel achieved consensus through the Delphi process on 80 statements for 44 medication entities. Subsequently, the SMR steering group endorsed the inclusion of these statements in the SMR to be disseminated among older adults at the time of discharge from geriatric medicine departments. CONCLUSIONS: The Delphi process contributed to the development of SMR for older adult patients discharged from public hospitals in Hong Kong. Patient experience with and staff response to the SMR were assessed at four hospitals before implementation at all public hospitals.

Association of metformin use with vitamin B12 deficiency in the institutionalized elderly.

Elderly people living in long term care institutions are particularly at risk of vitamin B12 deficiency. The prevalence of vitamin B12 deficiency was 34.9% among the 1996 institutionalized elderly residents in our previous study. The present retrospective study evaluated the association of metformin use with vitamin B12 deficiency in the same group of patients. Of 1996 patients, 507 (25.4%) had diabetes, of which 188 received metformin treatment. The prevalence of vitamin B12 deficiency in diabetic patients taking metformin was 53.2% compared with 31% (P < 0.001) of diabetic patients not taking metformin and 33.3% (P < 0.001) of those without diabetes. Among the vitamin B12 deficient patients, diabetic patients taking metformin had lower serum vitamin B12 concentration (97 pmol/L) than the diabetic patients not taking metformin (113 pmol/L, P < 0.001) and those without diabetes (111 pmol/L, P < 0.001). Subanalysis of 174 metformin users found that dose and duration of metformin use were significantly associated with vitamin B12 deficiency. Adjusted odds ratio for those taking metformin ≥1500 mg /day was 2.72 (95% CI 1.11-6.7, P = 0.029) compared with those using metformin <1000mg/day. Adjusted odds ratio for those taking metformin>4 years was 3.00 (95% CI 1.35-6.68, P = 0.007) compared with those taking metformin <2 years. Prevalence of vitamin B12 deficiency among those taking metformin ≥1500 mg/day for >2 years was 75.9% and was more than 2 times that of patients taking metformin <1500 mg/day for ≤2 years (35.3%). In conclusion, metformin use is associated with increased risk and severity of vitamin B12 deficiency in the institutionalized elderly residents. Patients taking metformin ≥1500 mg/day for >2 years are particularly at risk. Testing for vitamin B12 status before and regularly after the start of metformin may be considered.

Distinct profiles of critically short telomeres are a key determinant of different chromosome aberrations in immortalized human cells: whole-genome evidence from multiple cell lines.

Chromosomal aberrations are common in cancers. However, the search for chromosomal aberrations leading to development of specific solid tumors has been severely hindered because the majority of solid tumors have complex chromosomal aberrations that differ within the same tumor types. A similar phenomenon exists in immortalized cell lines. The underlying mechanisms driving these diverse aberrations are largely unknown. Telomeres play crucial roles in protecting the integrity of eucaryotic chromosomes and maintaining genomic stability of human cells. Telomere lengths on individual chromosomes in normal human somatic cells are heterogeneous and undergo progressive shortening with aging process. In this study, for the first time, a molecular cytogenetic method using sequential telomere quantitative fluorescence in situ hybridization and spectral karyotyping on the same human metaphases was applied successfully to examine the dynamic profiles of individual telomere shortening and their relationship to chromosome aberrations in multiple human cell lines undergoing immortalization. Human ovarian surface epithelial cells and esophageal epithelial cells were immortalized by the expression of HPV16 E6 and E7, which drive cells to proliferate by inactivating p53 and Rb genes. In these cell lines, we consistently detected large-scale differences in telomere signal intensities not only among nonhomologous chromosome arms but also between some homologous chromosome arms. The cell lines derived from different donors had different profiles of critically short telomeres (lacking telomere signals). Strikingly, the different profiles of chromosomal structural aberrations in multiple immortalized cell lines were highly significantly associated with the distinct distributions of critically short telomeres in whole-genome. Since cellular immortalization is one of the hallmarks of cancer, our findings suggest that distinct profiles of critically short telomeres in different human individuals might play an essential role in determining the complex and individual-specific chromosomal structural aberrations in human solid tumors.