QJM: An International Journal of Medicine最新文献

Background: The role of muscle strength in cancer prevention and the impact of modifiable factors on this association remain unclear.

Aim: This study investigated the association between relative handgrip strength and cancer risk while also examining the role of lifestyle factors on this association in adults aged 50+.

Design: Prospective cohort study using data from 16 countries across three surveys.

Methods: Relative handgrip strength was the dominant-hand maximum grip divided by body mass index (BMI) and sex-standardized. Cancer cases were self-reported physician diagnoses. Cox proportional hazards models assessed the association between realtive handgrip strength and cancer risk. Restricted cubic splines assessed potential nonlinear associations, with dose-response curves illustrating the relationship stratified by three lifestyle factors.

Results: Of 29,924 participants, 2,614 developed cancer over 8.3 years of follow-up. Each one-unit increase in relative handgrip strength was associated with a 7% lower cancer risk [HR (95% CI): 0.93 (0.89; 0.97)]. Cancer risk declined progressively across strength quartiles, with quartile 4 showing a 16% lower risk [HR (95% CI): 0.84 (0.74; 0.95)] compared to quartile 1, while quartile 1 had a 20% higher risk [HR (95% CI): 1.20 (1.06; 1.35)] than quartile 4. Drinkers, smokers, and physically inactive individuals consistently exhibited higher cancer risk than their healthier counterparts. A sex-specific tool was developed to estimate relative handgrip strength from BMI and absolute grip strength.

Conclusion: Higher relative handgrip strength was linearly associated with a lower cancer risk, with a stronger protective effect in individuals with healthy lifestyles.

Background: Herpes Zoster (HZ) reactivation following COVID-19 suggests immune dysregulation, posing a risk for long-term neuro-ophthalmic sequelae. This study investigates the relationship between post-COVID HZ and the subsequent hazard of uveitis and optic neuritis.

Methods: This retrospective analysis used the TriNetX Research Network, following patients for 3 years. Propensity Score Matching (PSM) was performed on COVID-19 survivors, comparing the HZ-exposed group (n = 11,172) against a matched HZ-unexposed control group (n = 11,173). Cox proportional hazards models calculated the 3-year Hazard Ratios (HRs) for incident uveitis and optic neuritis.

Results: Post-COVID HZ reactivation was associated with a significantly elevated and persistent risk of both outcomes. HZ was consistently related to a 3.06-fold increase in the hazard of uveitis (HR = 3.06; 95% CI, 2.56-3.65; p < 0.001) and a 2.10-fold increase in the hazard of optic neuritis (HR = 2.10; 95% CI, 1.62-2.71; p < 0.001). The relationships remained significant across sensitivity analyses, and the risk remained high even in the vaccinated subgroup.

Conclusions: HZ reactivation after COVID-19 is related to a higher instantaneous risk of subsequent uveitis and optic neuritis, even among immunocompetent individuals. HZ may serve as a clinical marker for neuro-immune injury, supporting the consideration of targeted ophthalmic surveillance and timely antiviral intervention to prevent vision loss.

Background: Alzheimer's disease (AD) is a neurodegenerative disorder with lipid metabolism implicated in its pathogenesis. The potentially causal relationship between specific lipid subtypes and AD remains unclear due to confounding factors. This study employs Mendelian randomization (MR) to investigate the genetic associations between plasma lipid subtypes and AD risk.

Methods: A MR method was employed utilizing genetic instruments derived from a genome-wide association study (GWAS) involving 7,174 Finnish participants who were assessed for 179 lipid species. Summary statistics for AD were sourced from the European Alzheimer & Dementia Biobank, which included 39,106 cases and 46,828 controls. Primary estimates were calculated through inverse-variance weighted (IVW) regression, and sensitivity analyses were performed to confirm reliability.

Results: MR analysis identified phosphatidylinositol (PI) (16:0_20:4), phosphatidylcholine (PC) (16:0_22:4), and sterol ester (SE) (27:1/15:0) as risk factors for AD. Conversely, PI (16:0_18:1), PI (18:0_18:1), PI (18:1_18:1), and several triacylglycerol (TAG) subtypes were protective. Sensitivity analyses confirmed the robustness of these associations.

Conclusion: This study provides genetic evidence supporting a potential causal association between lipid metabolism and AD, identifying specific PI, PC, SE, and TAG subtypes as risk or protective factors. These findings offer insights into AD pathogenesis and highlight potential lipid-based therapeutic targets.

A 58-year-old woman from a TB-endemic area presented with fever and dyspnea. Imaging revealed large pericardial and bilateral pleural effusions. Initial misdiagnosis as pneumonia and heart failure led to ineffective treatment. Pericardial fluid analysis showed elevated adenosine deaminase (ADA, 47 U/L) and a positive interferon-gamma release assay (IGRA). Mycobacterium tuberculosis was later isolated from the fluid culture. This case illustrates a pragmatic diagnostic triad (ADA, IGRA, culture) for tuberculous pericarditis in settings lacking advanced molecular tools, enabling timely initiation of antitubercular therapy.

Acute pancreatitis (AP) is most commonly associated with gallstones or alcohol use, while hypercalcemia due to primary hyperparathyroidism (PHPT) represents a less frequent but clinically relevant etiology. We present the case of a 61-year-old man who was admitted with acute epigastric pain and elevated serum pancreatic enzymes. Imaging revealed diffuse pancreatic edema with small peripancreatic fluid collections but no gallstones or biliary abnormalities. Further evaluation demonstrated significant hypercalcemia with elevated parathyroid hormone levels, consistent with PHPT. Neck ultrasound and Technetium-99m sestamibi scintigraphy identified a right inferior parathyroid adenoma. The patient was treated with intravenous fluids, bisphosphonates, diuretics, and supportive therapy for AP, resulting in rapid clinical and biochemical improvement. Definitive management with parathyroidectomy led to normalization of calcium levels and a significant intraoperative PTH decrease. At 1-month follow-up, the patient remained asymptomatic without recurrence of hypercalcemia or pancreatitis. This case highlights the pathophysiological link between hypercalcemia and pancreatic injury, where elevated calcium promotes premature activation of digestive enzymes and inflammatory pathways in acinar cells. Although PHPT accounts for a minority of AP cases, recognizing this association is crucial, particularly in patients without typical risk factors. Routine assessment of serum calcium in unexplained pancreatitis facilitates early diagnosis of PHPT and timely surgical intervention, preventing recurrent episodes and improving long-term outcomes.

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder characterized by synovial joint inflammation, leading to progressive joint damage, deformity, and disability. The lungs are the most common site for extra-articular manifestation, and significant Interstitial lung disease can occur in one in ten RA patients, leading to a significant increase in disability and mortality. This puts a substantial strain on patients and healthcare resources. The current understanding of RA and its manifestations remains limited. This review article explores the currently available data and literature.