Spontaneous pneumothorax is a potentially life-threatening condition. Its occurrence during pregnancy is exceedingly rare, with fewer than 100 cases reported. Early diagnosis is crucial in preventing respiratory compromise that could affect both the mother and fetus. We present a case of recurrent spontaneous pneumothorax in a 28-year-old patient at 6-week gestation again in the second trimester. The patient's presentation includes dyspnea and chest pain. Plain chest radiograph revealed large right-sided pneumothorax in both instances was managed by chest tube insertion.
Background Primary Immune Regulatory Disorders (PIRDs) are caused by genetic defects resulting in diverse clinical manifestations. We aimed to present the spectrum of PIRDs in children in Kuwait. Methods The data was obtained from the Kuwait National Primary Immunodeficiency Disorders Registry (KNPIDR), and the patients were followed prospectively. Results 59 patients with PIRDs, constituting 14% of all patients registered in the KNPIDR, were included in this study. Most of the patients belonged to familial hemophagocytic lymphohistiocytosis syndromes (42.4%), followed by regulatory T cell defects subcategories (15.3%). The median ages at the onset of symptoms and diagnosis were 4 and 18 months, respectively. Parental consanguinity was documented in 88.1% of cases while family history of PIRDs in 45.7%. The most common clinical features were lymphoproliferation, hematologic manifestations, and infections, affecting 71.2%, 67.8%, and 47.5%, respectively. Genetic diagnosis was reached in 84.9% of the tested patients and the most common genes affected were STXBP2 followed by PRF1 and LYST. Most patients (88.8%) had autosomal recessive disease. 35.6% of the patients underwent hematopoietic stem cell transplantation and a similar percentage received immunosuppressive and/or immunomodulating therapies. There was a total of 21 deaths (35.6%) with a median age at death of 36 months while the median time from diagnosis to death was 5 months. Conclusions PIRDs are heterogenous group of disorders with complex disease phenotypes. Genetic testing should be done as soon as possible when these diseases are suspected since early diagnosis is crucial for proper therapeutic interventions.
BACKGROUND:Total hip arthroplasty (THA) and total knee arthroplasty (TKA) are commonly performed procedures, but post-operative recovery is often complicated by significant pain, opioid-related side effects, and psychological distress. Esketamine has been proposed as an adjunct due to its analgesic and antidepressant properties, but its efficacy and safety remain unclear. Methods: A systematic review and meta-analysis of randomized controlled trials (RCTs) was performed by searching PubMed, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials (CENTRAL) up to July 2025. Dichotomous and continuous outcomes were synthesized using risk ratios (RRs) and standardized or mean differences, each reported with 95% confidence intervals (CIs). Results: Seven RCTs involving 1,101 patients were included. Esketamine did not significantly reduce pain at rest at 12 or 24 hours. Low-certainty evidence suggested that esketamine may reduce pain during activity at 12 hours (standardized mean difference (SMD): -0.28; 95% CI: -0.45, -0.12; p < 0.001), although this effect was not sustained at 24 hours. Very low-certainty evidence suggested a possible reduction in anxiety scores at post-operative day 7, with no significant effect observed at day 1. No clear effect on depression was observed at any time point. Esketamine was associated with a higher incidence of hallucinations (RR: 4.36; 95% CI (1.48, 12.88); p = 0.01), with no significant differences in delirium, nightmares, or post-operative nausea and vomiting. CONCLUSIONS:Low- to very low-certainty evidence suggests that esketamine may provide modest short-term improvement in activity-related pain and delayed anxiety reduction following THA and TKA. However, findings should be interpreted cautiously given the limited number of studies, clinical heterogeneity, and instability observed in sensitivity analyses. Esketamine was also associated with an increased risk of hallucinations.
Fracture healing is a complex biological process determined by mechanical stability, vascular supply, and systemic physiological factors. Despite advances in fracture management, nonunion remains an important clinical challenge. Emerging evidence indicates that the gut microbiome is a key regulator of bone metabolism and fracture repair through immune modulation, nutrient digestion, and microbial signaling pathways. We conducted a narrative review synthesizing experimental and clinical evidence on the impact of gut microbiome alterations on fracture healing and nonunion. Literature searches were performed in PubMed, Google Scholar, and Scopus for studies published between 2013 and 2026. A total of 107 records were initially screened by title and abstract, and 11 studies meeting inclusion criteria were included in the final synthesis. Many screened articles focused on osteoporosis, general bone metabolism or outcomes related to microbiome that didn’t evaluate fracture healing, non-union, delayed union, or complications related to fractures, therefore they were excluded. The gut microbiome emerges as an important regulator of bone metabolism and fracture repair. Microbial metabolites, particularly short-chain fatty acids, are associated with enhanced osteoblast activity, suppressed osteoclast-mediated bone resorption, and improved calcium absorption, collectively supporting bone mineral density and trabecular integrity. Dysbiosis impairs fracture healing by promoting gut barrier dysfunction, increasing intestinal permeability, and elevating systemic inflammation. Elevated pro-inflammatory cytokines, including IL-17a, are linked to reduced callus mineralization and delayed bone regeneration. Evidence also suggests a reciprocal interaction, where fracture events can alter gut microbiome composition and function. Microbiome-targeted interventions, such as probiotic and prebiotic supplementation, show therapeutic potential by improving bone microarchitecture, stimulating osteogenic signaling, and mitigating inflammation. Clinically, microbial dysregulation, particularly in infection-associated states, correlates with prolonged healing times and increased bone loss. The gut microbiome is an emerging systemic regulator of bone metabolism and may influence fracture healing and nonunion risk through mechanisms that include immune modulation, microbial metabolites, and nutrient metabolism. Dysbiosis may impair bone regeneration and increase the risk of delayed union or nonunion. Microbiome-targeted therapies are promising, but more human studies are needed to confirm their clinical relevance. These findings highlight the interconnected roles of the microbiome, immune function, and metabolism in bone healing, underscoring the need for further research.
ABSTRACT Introduction Whether obstructive sleep apnea (OSA) severity is independently associated with sarcopenia, beyond the effects of age, obesity and sex, has not been established in a single‐centre cohort using standardised ultrasound‐based assessment. We examined sarcopenia prevalence and its components across OSA severity strata in a Kuwaiti cohort using the ISarcoPRM sarcopenia algorithm. Methods Cross‐sectional within‐cohort analysis of 110 adults aged 50 years or older with confirmed OSA (apnea‐hypopnea index [AHI] 5 or more events/h by Level 3 portable monitoring; SomnoTouch, Somnomedics, Germany), stratified as mild (AHI 5–14.99, n = 28), moderate (AHI 15–29.99, n = 39) or severe (AHI 30 or more, n = 43). Sarcopenia was assessed using the ISarcoPRM algorithm: quadriceps muscle thickness by ultrasound, Sonographic Thigh Adjustment Ratio (STAR), handgrip strength (Jamar dynamometer) and chair stand test (CST). Results Demographic and comorbidity profiles were balanced across severity groups (all p > 0.05). Quadriceps muscle thickness, STAR and handgrip strength did not differ significantly across severity strata (all Kruskal–Wallis p > 0.05). CST time showed a significant gradient across severity strata (Kruskal–Wallis p = 0.047), and both AHI and ODI correlated modestly with CST time (r = +0.209, p = 0.029 and r = +0.203, p = 0.034, respectively). Sarcopenia prevalence was 21.4%, 30.8% and 34.9% in mild, moderate and severe OSA, respectively, with no significant trend (Cochran–Armitage p = 0.237). Age (OR 1.12 per year, 95%CI 1.05–1.19, p < 0.001) and BMI (OR 1.10 per kg/m2, 95%CI 1.02–1.18, p = 0.009) were the independent predictors of sarcopenia; OSA severity was not (adjusted OR 1.19, 95%CI 0.65–2.18, p = 0.577). Low STAR prevalence was 83.6%, driven by the high‐obesity burden in this cohort and the origin of STAR cut‐offs in a lower BMI Turkish reference population. Conclusion In this Kuwaiti OSA cohort, age and BMI are the dominant determinants of sarcopenia, with no independent contribution from OSA severity. A modest association between OSA severity indices and CST time suggests that physical function may be more sensitive to OSA‐related changes than muscle mass per se. The near‐universal low STAR prevalence points to the need for population‐specific normative data in high‐obesity cohorts.
