Molecular Hydrogen Therapy in Aneurysmal SAH With RA and Newly-diagnosed SLE, Complicated With Acute Ischemic Infarction: A Case Report of Improved Immune Markers Including Tr1 Cells, Breg Cells and TIM3 Expression on Tc Cells

Abstract

Background/Aim: Most nontraumatic subarachnoid hemorrhages (SAHs) are caused by ruptured saccular aneurysms, often resulting in a devastating clinical event characterized by high mortality and significant morbidity among survivors. Numerous studies have confirmed the neuroprotective effects of the molecular hydrogen due to its unique biological properties. Case Report: We present the case of a 44-year-old female with aneurysmal SAH with rheumatoid arthritis (RA) and newly diagnosed systemic lupus erythematosus (SLE), complicated by acute ischemic infarction. Despite surgical, pharmacological and non-pharmacological interventions, including embolization of the aneurysm, immunosuppressant, non-vitamin K antagonist oral anticoagulant (NOAC), and plasmapheresis, loss of consciousness continued. The patient began daily treatment with hydrogen capsules, resulting in increased in Treg cells, Breg cells, increased TIM3+ expression on Tc cells, and the conversion of anti-dsDNA from positive to negative. Her clinical symptoms stabilized without adverse effects. Conclusion: This case highlights the potential benefits of molecular hydrogen therapy in managing aneurysmal SAH with underlying autoimmune disease, warranting further research.

Study details

Article type

Case Report

Disease / injury model

Aneurysmal subarachnoid hemorrhage (SAH) with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), complicated by acute ischemic infarction

Duration

6 months

Dose-dependent effect

No

Outcome

Positive

Findings

Hydrogen capsule therapy in a patient with aneurysmal subarachnoid hemorrhage (SAH), rheumatoid arthritis (RA), and newly diagnosed systemic lupus erythematosus (SLE) led to improved neurological condition, increased Treg, Breg, and Tr1 cells, increased TIM3+ expression on Tc cells, and conversion of anti-dsDNA from positive to negative, with no adverse effects and stable clinical symptoms.