Glomus tumours are atypical in extracutaneous locations and very rarely located in reproductive organs. We present an unusual case of an incidentally discovered glomus tumour arising from the testis of a 47-year-old man. The testicular occurrence of this tumour type is not only exceptionally rare but also serves to highlight the debate regarding the optimal management of incidentally discovered small testicular lesions.

Background: Cell-free DNA (cfDNA) released during tissue damage has attracted interest as a marker of patient outcomes. However, limited research has examined its predictive utility in thermally injured patients. Methods: This study measured cfDNA concentrations across days 1, 3, 7, 14, and 28 post-burn in a total cohort of 98 adult patients with total body surface area (TBSA) burns ≥ 15% and healthy controls (HC). CfDNA concentrations in survivors (n = 79) versus non-survivors (n = 16) were compared and area under the receiver operating curve (AUROC) models generated to evaluate cfDNA as a predictor of mortality. Results: Patient cfDNA levels were significantly elevated at all time points compared to HC. Positive correlations were identified between day 1 cfDNA concentrations (n = 95) and %TBSA (r = 0.413, p < 0.0005), rBAUX (r = 0.365, p = 0.0005) and SOFA (r = 0.391, p = 0.0002). On day one, cfDNA levels showed good discriminatory ability for distinguishing between survivors and non-survivors (AUROC 0.778), with an optimal cut-off value of 446.37 pg/mL exhibiting a sensitivity of 0.80 and specificity of 0.70. Predictive models built on rBAUX, SOFA, interleukin(IL)-6 and IL-10 generated AUROC values of 0.733, 0.743, 0.472, and 0.688 respectively. Conclusions: Major burns result in immediate and persistent cfDNA elevation, with concentrations on day one higher in non-survivors. Plasma cfDNA concentrations on day one post-burn showed good performance as a prognostic marker for mortality. CfDNA therefore represents a rapid objective measure that may be useful during acute burn assessments to aid mortality predictions.

Despite Carpal Tunnel Syndrome (CTS) being the most common entrapment neuropathy, its pathophysiology remains debated. Sub-synovial connective tissues (SSCT) within the carpal tunnel are thought to play a role but are poorly characterised. MRI analysis offers potentially novel insights into SSCT characteristics. A pilot study of T2-weighted MRI was performed in healthy controls (n=7), and in CTS patients (n=16) pre- and 6 months post-surgical decompression. Image analysis was performed to quantify SSCT cross-sectional area, SSCT signal intensity ratio, and wrist index (depth/width) at distal, middle and proximal wrist landmarks. Median SSCT signal intensity was lower in the distal carpal tunnel of CTS patients pre-operatively (0.96) compared to controls (1.13; P = 0.008) and normalised post-operatively (1.13, P = 0.001). Median wrist index was also lower in CTS patients pre-operatively (0.60) compared to controls (0.67, P = 0.022), and again normalised post-operatively (0.74, P =0.001). This was attributed to changes in carpal depth in the antero-posterior axis with decompression surgery. This pilot study successfully demonstrated MRI assessment of SSCT in patients with CTS. The decreased SSCT signal intensities suggest predominant changes at the distal tunnel, potentially indicating reduced SSCT perfusion pre-surgery which normalised post-surgery. Our preliminary findings merit further investigation in a larger cohort.

Major trauma induces innate immune suppression, yet the underlying mechanisms are poorly understood. Resistin is an immunosuppressive molecule that is systemically elevated post-injury. However, its role in trauma-induced immune dysfunction and clinical outcomes is poorly defined. Here, we acquired blood samples from 147 adult trauma patients (≤1, 4–12, 48–72 h post-injury) and 95 burns patients (days 1, 3, 7, 14, 28 post-burn). We measured plasma resistin concentrations, studied resistin gene expression in peripheral blood mononuclear cells (PBMCs) and neutrophils, and measured resistin production by lipopolysaccharide (LPS)-challenged whole blood leukocytes. To identify potential novel triggers of resistin secretion by immune cells, we examined the effect that stimulation with mitochondrial-derived damage-associated molecular patterns (mtDAMPs) had on resistin production by neutrophils isolated from healthy donors. We also treated neutrophils, from healthy donors, and THP-1 cells with resistin prior to stimulation with Phorbol 12-myristate-13-acetate (PMA) or LPS to study its effects on reactive oxygen species (ROS) and cytokine production, respectively. Injured patients presented with significantly elevated circulating resistin concentrations and increased resistin gene expression in PBMCs and neutrophils. LPS and mtDAMP stimulation promoted resistin secretion by whole blood leukocytes and neutrophils. Plasma resistin concentrations were negatively associated with PMA-induced ROS generation by neutrophils, and LPS-induced cytokine production by monocytes. Resistin-treated THP-1 cells and neutrophils exhibited impaired functional responses upon secondary stimulation with LPS or PMA, respectively. Trauma patients who developed multiple organ dysfunction syndrome (MODS) presented with significantly elevated resistin concentrations, which at 48–72 h post-injury showed good performance as a predictor of post-traumatic MODS (AUROC, 0.796). Hyperresistinemia is an immediate and persistent feature of the inflammatory response to injury that may contribute to the development of innate immune dysfunction.