Decatur Memorial Hospital (DMH), is a Decatur, Illinois affiliate of Memorial Medical Center (Springfield, Illinois) and is a 300-bed, not-for-profit, community hospital that has been providing medical care since 1916 to residents of Central Illinois. Today, DMH has more than 2,300 dedicated employees, 300 physicians, and is a designated Level II Trauma Center. DMH has been recognized nine years as a 50 Top Cardiovascular Hospital by IBM Watson Health. On October 1, 2019, a merger with Memorial Medical Systems of Springfield was announced with Memorial Medical Center listed as the "parent company" in the Decatur Herald-Review.
Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare but emerging central nervous system demyelinating disorder that can mimic other neurological conditions. The use of TNF-alpha inhibitors in patients with autoimmune diseases has been linked to central nervous system demyelinating events, but the relationship remains poorly understood. Case description: We present a 64-year-old male with a history of ankylosing spondylitis previously treated with a TNF-alpha inhibitor who developed progressive dizziness, ataxia, visual disturbances and cognitive changes. Despite extensive workup, including imaging and cerebrospinal fluid analysis, initial evaluations were inconclusive. MRI was non-diagnostic, and cerebrospinal fluid lacked oligoclonal bands. Ultimately, a serum MOG antibody titre of 1:1,000 confirmed the diagnosis of MOGAD. The patient improved with intravenous corticosteroids and was discharged on a tapering dose of oral prednisone. This case highlights an MRI-negative presentation of MOGAD with strong serologic findings. Conclusion: This case emphasises the diagnostic challenge of MOGAD in patients with autoimmune backgrounds and neurologic symptoms without clear imaging findings. Clinicians should consider MOGAD in the differential diagnosis when evaluating such patients, particularly those with prior TNF-alpha inhibitor exposure. Early recognition and treatment with immunotherapy can lead to significant clinical improvement.
BACKGROUND Cytomegalovirus (CMV) infection is typically asymptomatic in immunocompetent individuals but can cause severe complications, such as immune thrombocytopenic purpura (ITP). This case report describes an uncommon instance of CMV-induced ITP in a 36-year-old immunocompetent man who was refractory to steroids and intravenous immunoglobulin (IVIG) and responded to antiviral therapy. CASE REPORT A previously healthy 36-year-old White man presented with flu-like symptoms, including subjective fevers, anorexia, nausea, cough, and a 6.8-kg weight loss over 2 weeks. Initial laboratory test results revealed severe thrombocytopenia (platelet count 4×10⁹/L) alongside elevated lymphocyte counts and mild splenomegaly. Additional serology confirmed a positive CMV IgM antibody. The patient was identified as having ITP and was treated with high-dose methylprednisolone and platelet transfusion, leading to initial platelet recovery. However, he returned within a week with severe epistaxis and a critical drop in platelet count to 0×10⁹/L. Subsequent testing confirmed CMV infection, with a viral load of 8790 copies/mL viral load. After unsuccessful IVIG treatment, antiviral therapy with valganciclovir was initiated, leading to a sustained increase in platelet count and eventual symptom resolution. CONCLUSIONS CMV-induced ITP, although rare in immunocompetent individuals, should be considered in cases of refractory thrombocytopenia unresponsive to standard therapies. Prompt diagnosis and the initiation of targeted antiviral therapy are crucial for effective recovery, as they address the underlying viral etiology and can significantly improve patient outcomes. This case underscores the importance of including CMV in the differential diagnosis for persistent thrombocytopenia to ensure timely and appropriate treatment.
Patients with KRAS wild-type (wt) metastatic colorectal cancer (mCRC) treated with single-agent cetuximab (C) or panitumumab (P), have improved progression-free survival (PFS) and overall survival (OS) compared to best supportive care but an objective response rate (ORR) of only 13–17
BACKGROUND Viral infections can cause a spectrum of muscle involvement, from mild myalgia to severe conditions like rhabdomyolysis. While benign muscle pain is common, viral myositis complicated by rhabdomyolysis and acute kidney injury is an uncommon but serious occurrence. If not promptly recognized and treated, these complications can result in significant morbidity and even mortality. Timely diagnosis and intervention are crucial to mitigating the risks. CASE REPORT We present the case of a 47-year-old man with a history of recent flu-like symptoms, who developed generalized muscle pain and weakness. Upon further evaluation, he was diagnosed with acute viral myositis. His condition was complicated by severe rhabdomyolysis, as evidenced by a markedly elevated creatine phosphokinase (CPK) level of 880 300 U/L, which subsequently led to acute kidney injury. Despite immediate intervention with aggressive intravenous fluid resuscitation, he required emergency hemodialysis secondary to electrolyte imbalances. Over the course of several weeks, he required ongoing dialysis, but with continued treatment his renal function gradually improved, and dialysis was discontinued after 1 month. CONCLUSIONS This case highlights the importance of early recognition and treatment of viral myositis complicated by rhabdomyolysis and acute renal failure. Aggressive management, including fluid resuscitation and hemodialysis, is crucial in preventing life-threatening complications.
BackgroundDespite advances in cancer care and detection, >65% of patients with squamous cell cancer of the head and neck (HNSCC) will develop recurrent and/or metastatic disease. The prognosis for these patients is poor with a 5-year overall survival of 39%. Recent treatment advances in immunotherapy, including immune checkpoint inhibitors like pembrolizumab and nivolumab, have resulted in clinical benefit in a subset of patients. There is a critical clinical need to identify patients who benefit from these antiprogrammed cell death protein 1 (anti-PD-1) immune checkpoint inhibitors.MethodsHere, we report findings from a multicenter observational study, PREDicting immunotherapy efficacy from Analysis of Pre-treatment Tumor biopsies (PREDAPT), conducted across 17 US healthcare systems. PREDAPT aimed to validate OncoPrism-HNSCC, a clinical biomarker assay predictive of disease control in patients with recurrent or metastatic HNSCC treated with anti-PD-1 immune checkpoint inhibitors as a single agent (monotherapy) and in combination with chemotherapy (chemo-immunotherapy). The test used RNA-sequencing data and machine learning models to score each patient and place them into groups of low, medium, or high.ResultsThe OncoPrism-HNSCC prediction significantly correlated with disease control in both the monotherapy cohort (n=62, p=0.004) and the chemo-immunotherapy cohort (n=50, p=0.01). OncoPrism-HNSCC also significantly predicted progression-free survival in both cohorts (p=0.015 and p=0.037, respectively). OncoPrism-HNSCC had more than threefold higher specificity than programmed death-ligand 1 combined positive score and nearly fourfold higher sensitivity than tumor mutational burden for predicting disease control.ConclusionsHere, we demonstrate the clinical validity of the OncoPrism-HNSCC assay in identifying patients with disease control in response to anti-PD-1 immune checkpoint inhibitors.Trial registration numberNCT04510129.
