Unlike other adverse drug reactions, visceral organ involvement is a prominent feature of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome and correlates with mortality. The aim of this study was to systematically review cases published in PubMed-indexed, peer-reviewed journals in which patients had renal injury during the episode of DRESS syndrome (DS). We found 71 cases, of which 67 were adults and 56% were males. Female sex was associated with higher mortality. Chronic kidney disease (CKD) was present in 14% of patients who developed acute kidney injury (AKI) during DS. In 21% of cases, the kidneys were the only visceral organ involved, while 54% of patients had both liver and kidney involvement. Eosinophilia was absent in 24% of patients. The most common classes of medication associated with renal injury in DS were antibiotics in 34%, xanthine oxidase inhibitors in 15%, and anticonvulsants in 11%. Among antibiotics, vancomycin was the most common culprit in 68% of patients. AKI was the most common renal manifestation reported in 96% of cases, while isolated proteinuria or hematuria was present in only 4% of cases. In cases with AKI, 88% had isolated increase in creatinine and decrease in glomerular filtration (GFR), 27% had AKI concomitantly with proteinuria, 18% had oliguria, and 13% had concomitant AKI with hematuria. Anuria was the rarest manifestation, occurring in only 4% of patients with DS. Temporary renal replacement therapy was needed in 30% of cases, and all but one patient fully recovered renal function. Mortality of DS in this cohort was 13%, which is higher than previously reported. Medication class, latency period, or pre-existing CKD were not found to be associated with higher mortality. More research, particularly prospective studies, is needed to better recognize the risks associated with renal injury in patients with DS. The development of disease-specific biomarkers would also be useful so DS with renal involvement can be easier distinguished from other eosinophilic diseases that might affect the kidney.

Leukocytoclastic vasculitis (LCV) is a rare extraintestinal manifestation (EIM) of ulcerative colitis (UC). Observations about its association with UC stem from case reports and small case series. Due to its rarity, more rigorous cross-sectional studies are scarce and difficult to conduct. The aim of this systematic review was to synthetize the knowledge on this association by reviewing published literature in the form of both case reports and case series; and report the findings according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. In contrast to LCV in Chron disease (CD), which occurs secondary to biologic therapies used for its treatment, LCV in UC is a true reactive skin manifestation. Both genders are equally affected. Palpable purpura (41%) and erythematous plaques (27%) are the most common clinical manifestations. In 41% of patients, the rash is painful, and the lower extremities are most commonly involved (73%). Systemic symptoms such as fever, arthralgias, fatigue, and malaise are seen in 60% of patients. Unlike previous reports, we found that LCV more commonly occurs after the UC diagnosis (59%), and 68% of patients have active intestinal disease at the time of LCV diagnosis. Antineutrophil cytoplasmic antibody (ANCA) is positive in 41% of patients, and 36% of patients have other EIMs present concomitantly with LCV. The majority of patients were treated with corticosteroids (77%), and two (10%) required colectomy to control UC and LCV symptoms. Aside from one patient who died from unrelated causes, all others survived with their rash typically resolving without scarring (82%).

Background: Acute transverse myelitis (ATM) is an inflammatory disorder of the spinal cord with heterogeneous etiologies, including autoimmune, infectious, paraneoplastic, and drug-induced causes. Tumor necrosis factor-alpha (TNF-α) inhibitors have been infrequently associated with inflammatory central nervous system events, including transverse myelitis. TNF-inhibitor-associated myelitis typically presents with short-segment lesions, a normal brain MRI, and partial responsiveness to corticosteroids. Longitudinally extensive transverse myelitis (LETM) and steroid-refractory cases are uncommon. Case Presentation: A 39-year-old woman with psoriatic arthritis treated with etanercept for two years presented with subacute progressive bilateral lower-extremity sensory loss and weakness. MRI revealed a T2 hyperintense spinal cord lesion extending from T11 to L1 with gadolinium enhancement, consistent with transverse myelitis, while brain MRI was normal. Cerebrospinal fluid analysis showed lymphocytic pleocytosis, elevated protein, oligoclonal bands, and increased kappa free light chains. Extensive infectious, metabolic, paraneoplastic, and autoimmune testing, including aquaporin-4 and MOG antibodies, was negative. Despite high-dose intravenous corticosteroids and the discontinuation of etanercept, the patient experienced clinical worsening with lesion expansion, meeting criteria for LETM, and developed urinary retention. She subsequently underwent plasma exchange, resulting in radiologic improvement and moderate clinical recovery. Conclusions: This case highlights an atypical presentation of TNF-inhibitor-associated myelitis characterized by a biphasic course, longitudinally extensive spinal cord involvement, steroid refractoriness, and responsiveness to plasma exchange. These features suggest either an unusually severe TNF-inhibitor-related inflammatory phenotype or a TNF-inhibitor-triggered antibody-mediated demyelinating process. Reports of TNF-inhibitor-associated myelitis evolving into longitudinally extensive, steroid-refractory disease remain limited, and this presentation may broaden the recognized clinical spectrum of TNF-α-related CNS inflammatory events. Close neurologic follow-up and heightened awareness of severe CNS complications associated with TNF-α inhibitors are warranted.

Background: Anti–3‐hydroxy‐3‐methylglutaryl–coenzyme A reductase (anti‐HMGCR) antibody–positive immune‐mediated necrotizing myopathy (IMNM) is a rare autoimmune myopathy characterized by progressive proximal muscle weakness and markedly elevated creatine kinase levels. Although commonly associated with prior statin exposure, statin‐naïve cases and atypical presentations are well described. Patients with idiopathic inflammatory myopathies are also at increased risk for venous thromboembolism (VTE), though data specific to IMNM remain limited. Case Presentation: An 83‐year‐old man with brief, remote statin exposure presented with progressive proximal muscle weakness and a three‐year history of oropharyngeal dysphagia preceding limb involvement. Laboratory evaluation revealed markedly elevated creatine kinase and transaminases. Anti‐HMGCR antibodies were positive, and muscle biopsy confirmed necrotizing myopathy. During evaluation for occult malignancy, bilateral pulmonary emboli were incidentally identified. The patient required high‐dose corticosteroids, mycophenolate mofetil, and intravenous immunoglobulin for refractory disease. With aggressive immunosuppressive therapy and rehabilitation, he demonstrated substantial clinical recovery at 6 months. Conclusion: This case highlights oropharyngeal dysphagia as an early and, for a prolonged period, isolated manifestation of anti‐HMGCR antibody–positive IMNM; here, it preceded the onset of limb weakness by approximately 3 years. It underscores the importance of comprehensive diagnostic evaluation in patients with unexplained oropharyngeal dysfunction, in whom an inflammatory myopathy may otherwise be overlooked for years. Clinicians should maintain awareness of thrombotic risk in inflammatory myopathies, particularly during active disease. Early recognition and prompt immunosuppressive therapy remain critical to optimize outcomes and prevent irreversible muscle damage.

To evaluate predictors of falls in the hospital-at-home (HaH) setting from a single institution in 3 US states. In this retrospective study of HaH patients residing in Florida, Wisconsin, and Arizona, we identified 51 patients who fell and were matched to 153 patients without fall, between July 2020 and July 2023. Patient demographics and clinical characteristics were collected, including age, sex, race, Charlson Comorbidity Index, geographic location, body mass index, Hester Davis Scale, admission diagnosis, continuous intravenous infusion, polypharmacy, marital status/life partnership, area deprivation index, and use of supplemental oxygen. Association of patient characteristics were examined using unadjusted and multivariable logistic regression models (July 29, 2020 to July 5, 2023). The rate of falls was 6.8 per 1,000 patient bed-days. In multivariable analysis, we found that older age (odds ratio [OR; per each 10-year increase], 1.37; P=.043), higher Charlson Comorbidity Index (OR [per each 5-unit increase], 1.80; P=.012), and supplemental oxygen use (OR, 2.05; P=.045) were independent predictors of falls in the HaH setting. Although not statistically significant, an increased risk of falls was observed in patients with a diagnosis of respiratory disorder (OR, 2.07; P=.075). In patients hospitalized at home, the risk of falls may increase with older age, higher Charlson Comorbidity Index, and supplemental oxygen use. Mitigation strategies to prevent falls in patients with these risk factors should be considered in the HaH setting.