Background and Clinical Significance: Thyroid cancer is increasing, particularly the differentiated type, with decreasing incidence of the anaplastic type. Anaplastic thyroid carcinoma (ATC) is a rare, aggressive, and often lethal form. It frequently presents with metastatic disease, regional and systemic, with common distant metastasis to the lung, bone, brain, and adrenal, and rarely to other places; Case presentation: A 74-year-old Arab male presented with symptomatic anemia and melena and was admitted for investigation of the cause. The patient was found to have a large retrosternal goiter and gastric tumor. CT scan showed a pedunculated, nonobstructive mass, suggestive of a GIST or leiomyoma. The neck mass presented with compressive symptoms. He underwent a combined neck and abdominal surgical resection based on a multidisciplinary team decision, as prior biopsies were not conclusive. The final pathology report identified similar tumors in the two specimens and suggested an anaplastic thyroid carcinoma as the primary tumor with metastasis to the stomach. Furthermore, the workup, including a PET scan 2 weeks post-surgery, revealed widespread metastases in the bone, lung, and liver, and the treatment was palliative. He was followed up in the outpatient clinic for 4 and a half months post-operatively. The patient developed sepsis and cardiopulmonary arrest and died; Conclusions: ATC can metastasize to many places in the body, including the stomach (as shown in our case), which can cause significant upper gastrointestinal bleeding and anemia. Metastatic ATC carries a poor prognosis; thus, physicians need to keep a high index of suspicion in approaching similar cases. A multidisciplinary approach for the management is of utmost importance for appropriate treatment. This disease's pathology, behavior, and targeted new treatment modalities must be explored further.

Background/Objectives: Sleep deprivation (SD) induces the accumulation of reactive oxygen species (ROS) in the intestine, causing inflammation in the intestine, thereby damaging the intestinal epithelial barrier function. As a traditional Chinese medicine, Dendrobium huoshanense (DHS) modulates intestinal flora, maintains the intestinal mucosal barrier, and promotes gastrointestinal motility and digestive secretion. However, the role and mechanism of DHS in improving SD-induced intestinal injury have not been fully studied. Methods: The SD model was established by subjecting rats to complete SD using a specialised SD instrument. Hematoxylin and eosin (HE) staining was performed to evaluate pathological injury in ileal tissues. Enzyme-linked immunosorbent assay (ELISA) and biochemical methods were used to quantify the main inflammatory cytokines, oxidative stress markers, and hypothalamic-pituitary-adrenal (HPA) axis activity. The expression levels of E-cadherin and Occludin proteins in the ileum tissue were analyzed by Western blotting. Additionally, the pH value of ileal mucus, unit secretion, water content, and dry matter weight were measured. Differential metabolites in rat ileum mucus were profiled using ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS). Results: DHS alleviated the pathological injury of the ileum induced by SD. DHS reduced the levels of serotonin (5-HT), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), while increasing interleukin-10 (IL-10) levels, thereby attenuating systemic inflammatory responses. Furthermore, DHS decreased malondialdehyde (MDA) content and elevated glutathione (GSH) and superoxide dismutase (SOD) levels in ileal tissues. DHS also upregulated the protein expression of E-cadherin and Occludin in intestinal tissues. In addition, DHS decreased the pH of ileal mucus, promoted intestinal mucus secretion, and increased dry matter content, facilitating the restoration of the mucus barrier. DHS may alleviate SD-induced ileal injury by modulating steroid hormone biosynthesis. DHS decreased the levels of adrenocorticotropic hormone (ACTH), cortisol (CORT), and corticotropin-releasing hormone (CRH), indicating that DHS suppresses the abnormal activation of the hypothalamic-pituitary-adrenal (HPA) axis. Conclusions: In this study, a comprehensive multi-index evaluation showed that DHS could significantly improve the ileal injury caused by SD in rats. The mechanism involved regulating the balance of serum neurotransmitters and inflammatory factors, reducing oxidative stress in tissues, and improving the physicochemical properties of intestinal mucus. Metabolomic analysis further revealed that these protective effects may be mediated via the regulation of steroid hormone biosynthesis pathways and are associated with the inhibition of abnormal HPA axis activation.

Matrix-assisted laser desorption/ionization mass spectrometry (MALDI/MS) imaging enables spatially resolved molecular analysis; however, its sensitivity depends strongly on matrix uniformity and ionization efficiency, which pose challenges for low-abundance compounds such as steroid hormones. In this study, we developed a platinum (Pt) thin film-based surface-assisted laser desorption/ionization mass spectrometry (SALDI/MS) and matrix-enhanced SALDI/MS (ME-SALDI/MS) method to increase ion yields and improve steroid imaging with minimal sample pretreatment. Using sputter-deposited Pt films, 20 endogenous steroids were comprehensively detected without chemical derivatization. Furthermore, derivatized steroids analyzed by ME-SALDI/MS exhibited significantly higher ion yields than those obtained by conventional MALDI/MS or SALDI/MS, demonstrating a synergistic enhancement of desorption and ionization efficiency. ME-SALDI/MS imaging of porcine adrenal gland tissue enabled visualization of multiple derivatized steroids with high ion yields-including progesterone, corticosterone, and cortisol-reflecting their biosynthetic localization across cortical zones. Collectively, these results highlight the potential of Pt thin film-based SALDI and ME-SALDI/MS as robust tools that provide high ion yields for imaging of steroids and other biomolecules with inherently low desorption and ionization efficiency.

Adrenal lymphoma is a rare clinical entity, classified as either primary adrenal lymphoma (PAL) or secondary adrenal lymphoma. PAL is a highly aggressive malignancy with an extremely low incidence rate. To date, <250 cases have been reported in the English literature. The clinical manifestations of PAL are diverse and non-specific, often resulting in a delayed diagnosis or a misdiagnosis. In patients with comorbid hypertension, the differential diagnosis of an adrenal mass typically emphasizes functional tumors, such as aldosterone-producing tumors (which cause primary aldosteronism) and pheochromocytoma. Due to the usual absence of characteristic hormonal abnormalities, PAL is frequently overlooked in clinical practice. The present report describes the cases of 3 male patients with PAL, aged 83, 73 and 63 years. The first 2 patients had pre-existing hypertension prior to the confirmation of PAL. The present report summarizes the diagnostic strategies for PAL and relevant differential diagnoses, and describes the treatment responses observed in each case. Diagnosing PAL is challenging, and its prognosis is generally poor. PAL should be considered in the differential diagnosis of adrenal masses, particularly in patients with a history of hypertension. Once diagnosed, management should be guided by a multidisciplinary team specialized in adrenal and hematological disorders.

Medical treatment of Cushing syndrome (CS) with steroidogenesis inhibitors or ACTH-directed agents is typically given using a titration strategy to achieve "normal" exposure to cortisol, as determined by a 24-hour urine free cortisol (UFC) measurement. This approach generally achieves similar serum cortisol levels across the day and fails to provide a normal diurnal pattern of cortisol. Chronotherapy addresses this problem through weighted afternoon/evening dosing of cortisol-lowering drugs. Additionally, because of day-to-day variability of cortisol production, patients may be undertreated on days of higher cortisol production and overtreated on days of lower cortisol production. A "block and replace" strategy is an alternative approach in which consistent biochemical glucocorticoid deficiency is the goal, with added glucocorticoid replacement to provide physiologic diurnal exposure to cortisol. Recently, the term mild autonomous cortisol secretion (MACS) has been used to describe patients without clinical features of CS who fail to suppress cortisol after 1 mg dexamethasone. MACS includes individuals with an adrenal mass(es) who may have hypertension, type 2 diabetes mellitus, and/or osteoporosis. The role of medical vs surgical treatment of MACS is currently debated. We here review the advantages and disadvantages of each approach to medical treatment of CS and MACS, concluding that "block and replace" deserves wider consideration, especially in patients who have severe disease, and to avoid adrenal insufficiency in those with highly variable UFC, or are taking agents that may cause adrenal insufficiency. Conversely, in those with mild disease, chronotherapy normalizes nighttime cortisol exposure while reducing drug burden.

X-linked adrenoleukodystrophy (ALD) is a progressive neurometabolic disorder caused by pathogenic variants in the ABCD1 gene, resulting in the systemic accumulation of very-long-chain fatty acids (VLCFAs). C26:0-lysophosphatidylcholine (LPC(26:0)) is the primary biochemical marker of ALD and the basis for newborn screening programs worldwide. LPC(26:0) arises from the accumulation of VLCFA-CoA species that are incorporated into phosphatidylcholine via the lysophospholipid acyltransferase LPLAT10, followed by phospholipase A2-mediated hydrolysis. Compared to conventional plasma VLCFA analysis, measurement of LPC(26:0) by liquid chromatography or flow injection tandem mass spectrometry in plasma or dried blood spots offers superior sensitivity and specificity, even in female patients, for whom VLCFA analysis yields false-negative results in 15-20% of cases. Beyond diagnosis, accumulating evidence indicates that LPC(26:0) and the broader landscape of VLCFA-containing lipids correlate with disease severity. Higher levels are associated with cerebral ALD, adrenal insufficiency, and severe spinal cord disease, and data from newborn screening cohorts suggest that neonatal LPC(26:0) levels may also stratify risk for early-onset disease manifestations. LPC(26:0) accumulates in CNS lipoproteins and exhibits direct neurotoxic and proinflammatory properties in experimental models. This implicates LPC(26:0) not only as a biomarker, but also as a potential mediator of ALD pathology. Furthermore, LPC(26:0) shows promise as a pharmacodynamic biomarker of biochemical correction across therapeutic strategies, from hematopoietic stem cell transplantation to emerging approaches including ELOVL1 inhibition. However, key questions remain regarding the cell type and tissue origin of circulating LPC(26:0), its precise contribution to neuroinflammation, and the threshold levels that reliably predict clinical outcomes in individual patients.

We reported a rare case of disseminated diffuse large B-cell lymphoma (DLBCL) initially presenting as refractory orbital cellulitis in a 53-year-old male. The patient presented with acute periorbital swelling, pain, and restricted ocular motility, unresponsive to broad-spectrum antibiotics. Magnetic resonance imaging (MRI) revealed extensive sinusitis with a peripherally enhancing medial extraconal orbital mass and adjacent bony erosions. A prompt functional endoscopic sinus surgery and histopathology revealed a poorly differentiated malignant neoplasm. Immunohistochemistry confirmed DLBCL, non-germinal center B-cell subtype. Systemic evaluation with whole-body MRI and fluorodeoxyglucose-positron emission tomography demonstrated widespread dissemination involving the lungs, gastrointestinal tract, adrenal glands, and skeleton. The patient was initiated on required chemoimmunotherapy with central nervous system prophylaxis and remains under oncology follow-up. This case highlights the diagnostic challenge posed by orbital lymphoma mimicking infectious orbital cellulitis and underscores the need for early imaging and tissue diagnosis in culture-negative, non-resolving cases. A high index of suspicion and multidisciplinary collaboration are essential for timely diagnosis and effective management.

Pheochromocytoma crisis, a rare yet life-threatening endocrine emergency, is characterized by acute hemodynamic instability that can lead to severe cardiovascular collapse, including cardiac arrest. Systemic glucocorticoid administration has been shown to trigger such crises in patients with pheochromocytoma. This report describes a 38-year-old female who developed symptoms including chest tightness, dyspnea, and vomiting shortly after receiving a methylprednisolone injection for urticaria, suggesting a possible association between glucocorticoid administration and the subsequent crisis. On admission, she suffered cardiac arrest and was managed with extracorporeal membrane oxygenation (ECMO). Coronary angiography, blood microbial RNA analysis, and metagenomic testing revealed no abnormalities. Despite comprehensive pharmacological treatment, the patient's symptoms persisted, with recurrent ventricular fibrillation detected on electrocardiogram, prompting further investigations. A computed tomography (CT) scan identified an adrenal mass, and biochemical tests confirmed the diagnosis of pheochromocytoma. Following successful laparoscopic adrenalectomy, the patient experienced significant clinical improvement. This case demonstrates the potential for methylprednisolone to trigger or contribute to a pheochromocytoma crisis. However, it is important to acknowledge that other concurrent factors, such as use of medication, systemic inflammatory response, and physiological stress of resuscitative interventions, may have also played a role. The challenges posed by the diagnosis of this condition underscore the need for caution when administering glucocorticoids to patients with suspected pheochromocytoma.

Renal hilar Castleman disease is a rare lymphoproliferative disorder characterized by non-specific radiological manifestations. It is easily misdiagnosed as primary renal or adrenal malignant tumors in clinical practice, which may consequently lead to unnecessary radical nephrectomy. A 51-year-old female with a history of right breast cancer treated with mastectomy and adjuvant endocrine therapy 7 years prior presented with right nipple erosion. Biopsy confirmed Paget's disease, and preoperative staging with contrast-enhanced computed tomography (CT) incidentally revealed a solitary soft-tissue mass adjacent to the left renal hilum and abdominal aorta, with a maximum diameter of 8.5 cm × 6.2 cm and moderate heterogeneous enhancement. Strip-like and punctate calcifications were observed within the lesion, accompanied by reactive lymph nodes at the periphery and compression as well as displacement of the left renal vessels. The patient presented no specific clinical symptoms related to the retroperitoneal mass. According to comprehensive preoperative assessment and multidisciplinary consultation, the patient underwent complete radical resection of the renal hilar mass combined with left nephrectomy. Postoperative histopathological examination and immunohistochemical staining confirmed the diagnosis of hyaline-vascular type Castleman disease. The patient recovered uneventfully after surgery, and no local recurrence or distant metastasis was observed during the 12-month follow-up, with a favorable long-term prognosis. This case highlights the radiological difficulties in differentiating renal hilar Castleman disease from malignant renal tumors and emphasizes the necessity of standardized preoperative multimodal evaluation, which helps avoid excessive surgical intervention such as blind radical nephrectomy for unexplained retroperitoneal masses.