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Intensive Care Management of Anaphylactic Shock Secondary to Wasp Stings: A Case Report I Made Eryana; Ni Luh Putu Winda Alpiniawati; Dewa Ayu Rina Wana; I Gede Putu Jarwa Antara
Open Access Indonesian Journal of Medical Reviews Vol. 4 No. 6 (2024): Open Access Indonesian Journal of Medical Reviews
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/oaijmr.v4i6.683

Abstract

Anaphylactic shock is a life-threatening allergic reaction that requires immediate medical intervention. Wasp stings are a common trigger for anaphylaxis, and rapid administration of epinephrine is crucial in preventing fatal outcomes. This case report describes the successful intensive care management of a patient who developed anaphylactic shock following multiple wasp stings. A 51-year-old female presented to the emergency department with anaphylactic shock after being stung by multiple wasps. She exhibited severe angioedema, hypotension, and tachycardia. Immediate treatment included intramuscular epinephrine, intravenous corticosteroids, antihistamines, and fluid resuscitation. The patient was transferred to the intensive care unit (ICU) for close monitoring and supportive care. In conclusion, this case highlights the importance of prompt recognition and treatment of anaphylactic shock, particularly the administration of epinephrine. It also emphasizes the role of ICU monitoring in managing severe allergic reactions and preventing complications.
Cerebral Toxoplasmosis with Preserved CD4 Count (>300 cells/µL) in the HAART Era: Unmasking Immune Reconstitution Inflammatory Syndrome and the Diagnostic Utility of Cotrimoxazole I Made Eryana; Made Nopriantha
Archives of The Medicine and Case Reports Vol. 6 No. 4 (2025): Archives of The Medicine and Case Reports
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/amcr.v6i4.830

Abstract

Cerebral toxoplasmosis (TE) typically presents in HIV-positive patients with severe immunosuppression (CD4 <100 cells/µL). However, in the era of Highly Active Antiretroviral Therapy (HAART), presentations have become atypical. We report a rare case of TE in a patient with a preserved CD4 count (>300 cells/µL), highlighting the phenomenon of unmasking immune reconstitution inflammatory syndrome (IRIS). A 22-year-old female, HIV-positive on a Tenofovir-Lamivudine-Efavirenz (TLE) regimen for one month, presented with subacute hemicrania, focal motor seizures, and complex visual hallucinations (zoopsia). Despite a CD4 count of 307 cells/µL and a suppressed viral load (<40 copies/mL), Contrast-Enhanced Computerized Tomography (CE-CT) revealed multiple ring-enhancing lesions with significant perilesional edema. The patient was diagnosed with TE-associated Unmasking IRIS. Due to the unavailability of Pyrimethamine, she was treated with high-dose Cotrimoxazole (960 mg q6h). Significant clinical improvement was observed by day 4, characterized by the cessation of seizures and hallucinations. Follow-up at two weeks confirmed sustained neurological recovery. In conclusion, a preserved CD4 count does not exclude opportunistic infections in the early post-HAART period. This case underscores the diagnostic pitfall of immune discordance and validates the efficacy of Cotrimoxazole as a primary therapeutic intervention in resource-limited settings.
Efficacy and Safety of CD19-Targeted Chimeric Antigen Receptor (CAR) T-Cell Therapy in Refractory Systemic Lupus Erythematosus: A Systematic Review of Clinical Outcomes and B-Cell Depletion Kinetics I Made Eryana; Ni Putu Ayu Windari Putri; Cokorda Agung Paramadika
Archives of The Medicine and Case Reports Vol. 7 No. 1 (2026): Archives of The Medicine and Case Reports
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/amcr.v7i1.831

Abstract

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune pathology characterized by a breakdown in self-tolerance, B-cell hyperactivity, and the production of pathogenic autoantibodies. While conventional B-cell depletion strategies utilizing monoclonal antibodies often fail to achieve deep tissue clearance, CD19-targeted chimeric antigen receptor (CAR) T-cell therapy has emerged as a transformative modality capable of inducing durable drug-free remission. This systematic review and meta-analysis evaluate the clinical efficacy, pharmacodynamics of B-cell depletion, and safety profile of both autologous and allogeneic CD19 CAR T-cell therapies in refractory SLE. We conducted a systematic literature review on manuscripts published between January 1st, 2014, and March 1st, 2025, focusing on interventional clinical trials and high-quality case series. Primary endpoints included the Definition of Remission in SLE (DORIS) and reduction in SLEDAI-2K scores. Secondary endpoints analyzed B-cell aplasia kinetics, seroconversion of anti-dsDNA, and adverse events, including cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and novel autoimmune-specific toxicities. Statistical synthesis utilized weighted averages for continuous variables and event rates for categorical outcomes. The analysis synthesized data from 20 distinct patients with refractory SLE across three pivotal cohorts. The pooled rate of DORIS remission at three months post-infusion was 100%. The mean SLEDAI-2K score decreased from a baseline of 12.5 to 0.8 at three months. Deep B-cell depletion was achieved in all patients, with a mean duration of aplasia of 112 days. Reconstitution of the B-cell compartment was characterized by a naïve phenotype (IgD+/CD27-), indicating a comprehensive immunological reset. Safety analysis revealed that while CRS occurred in 88% of patients, it was predominantly Grade 1 or 2. No high-grade ICANS occurred. Unique toxicity signals, including local immune effector cell-associated toxicity syndrome (LICATS), were identified. In conclusion, CD19-targeted CAR T-cell therapy induces rapid, profound, and sustained drug-free remission in patients with refractory SLE. The mechanism involves deep tissue depletion of B-cells and plasmablasts, facilitating a reset of the humoral immune system.