Background/Objectives: Chronic pain conditions are common among older residents in long-term care facilities (LTCFs), often leading to increased demand for analgesic drugs. Despite this, pain is frequently underdiagnosed and undertreated, especially in individuals with cognitive impairments such as dementia. Both underuse and overuse of analgesics remain a challenge in LTCFs, affecting patient outcomes and quality of life. This systematic review aimed to identify patient- and facility-level factors associated with variation in analgesic use in LTCFs. Methods: This review followed PRISMA guidelines. A comprehensive literature search was conducted in PubMed, CINAHL, Cochrane Library, and Scopus for studies published between 2013 and 2024. Eligible studies were focused on adults aged ≥ 60 years in LTCFs and examined patient and facility factors related to analgesic prescription. Risk of bias was assessed independently by two reviewers using STROBE, JBI, and MMAT tools. Disagreements were resolved by a third reviewer. Results: A total of 6266 studies were retrieved; 13 papers met the eligibility criteria after screening. Dementia was the most frequently reported factor associated with lower analgesic prescribing, largely due to difficulties in assessing pain and communication barriers. Other patient-related factors included pain severity and comorbidities. Facility-level factors such as staffing levels, staff qualifications, and facility size were also associated with variation in prescribing practices. Conclusions: Dementia highly impacts pain management due to assessment and communication challenges. Improved pain assessment tools and staff training are needed to recognize pain in cognitively impaired residents and ensure appropriate analgesic use in LTCFs.
Background/Objectives: Colorectal cancer (CRC) is complicated by cachexia, a wasting syndrome with muscle and fat loss that worsens survival and treatment outcomes. Evidence suggests the gut microbiome may contribute to CRC cachexia, but its role remains unclear. This systematic review synthesized evidence to identify microbial signatures linked to cachexia hallmarks. Methods: The protocol was pre-registered with PROSPERO and following PRISMA guidelines. PubMed, Web of Science, and Scopus were searched for studies on CRC patients and preclinical models. Eligible studies compared microbiota compositions between cachectic and non-cachectic groups to identify alterations linked to cachexia progression. Study quality was assessed using the Newcastle–Ottawa Scale and CAMARADES checklist. Results: Of 2,456 records, 15 studies met inclusion criteria; Study quality was moderate for pre-clinical studies and high for clinical cohort studies. Murine CRC cachexia models showed reduced alpha diversity and beta diversity shifts. Butyrate-producing taxa were depleted, whereas, Enterobacteriaceae and other pathobionts were enriched. Some microbial changes were independent of food intake and linked to inflammation, metabolic dysregulation, and muscle wasting. Clinical evidence was limited to two reports from the same cohort, in which higher pre-surgical abundance of Fusobacterium nucleatum and lower Porphyromonas and Actinomyces spp. were associated with cachexia onset. Conclusions: Overall, current evidence suggests that CRC-associated cachexia is accompanied by gut microbiome alterations, but causality and clinical relevance remain uncertain.
Background/Objectives: Colorectal cancer (CRC) is complicated by cachexia, a wasting syndrome with muscle and fat loss that worsens survival and treatment outcomes. Evidence suggests that the gut microbiome may contribute to CRC cachexia, but its role remains unclear. This systematic review synthesizes evidence to identify microbial signatures linked to cachexia hallmarks in CRC. Methods: The protocol was pre-registered with PROSPERO and followed PRISMA guidelines. PubMed, Web of Science, and Scopus were searched for studies on CRC patients and preclinical models with cachexia. Eligible studies compared microbiota composition between cachectic and non-cachectic groups to identify alterations linked to cachexia progression. Study quality was assessed using the Newcastle–Ottawa Scale and CAMARADES checklist. Results: Of 2456 records, 15 studies met inclusion criteria, including 13 preclinical studies and 2 clinical studies. Study quality was moderate for preclinical studies and high for clinical cohort studies. Murine CRC cachexia models showed reduced alpha diversity and beta diversity shifts. Butyrate-producing taxa were depleted, whereas Enterobacteriaceae and other pathobionts were enriched. Some microbial changes were independent of food intake and linked to inflammation, metabolic dysregulation, and muscle wasting. Clinical evidence was limited to two reports from the same cohort, in which higher pre-surgical abundance of Fusobacterium nucleatum and lower Porphyromonas and Actinomyces spp. were associated with cachexia onset. Conclusions: Current evidence suggests an association between CRC-associated cachexia and gut microbiome alterations, but causality, directionality, and clinical relevance remain uncertain.