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. 2026 Apr 28;40(3):1832–1841. doi: 10.21873/invivo.14337

Adjunctive Molecular Hydrogen Capsule Therapy in Empyema Complicated by Chronic Inflammatory Demyelinating Polyneuropathy: A Case Report

GUAN-LONG LI 1,2, JENG-WEI LU 3,4,5, YI-JUNG HO 6,7, SHAN-WEN LUI 8, TING-YU HSIEH 9, KUANG-YIH WANG 10,11, FENG-CHENG LIU 10
PMCID: PMC13133804  PMID: 42049414

Abstract

Background/Aim

The management of Stage II empyema complicated by chronic inflammatory demyelinating polyneuropathy (CIDP) presents a formidable clinical challenge due to the precarious balance required between aggressive infection control and the modulation of immune-mediated neurological frailty. We report a complex case of comorbid empyema and CIDP successfully managed with a multidisciplinary approach and adjuvant molecular hydrogen (H2) therapy.

Case Report

A 76-year-old male with CIDP presented with acute respiratory failure secondary to Stage II empyema. Following video-assisted thoracoscopic surgery (VATS) decortication, the patient exhibited systemic hyperinflammation and immune exhaustion. Adjuvant oral molecular hydrogen therapy was initiated during the critical phase. Longitudinal immunophenotyping was performed to monitor the therapeutic response. Clinical recovery coincided with profound immunological remodeling. We observed a cell-specific up-regulation of fas cell surface death receptor (Fas) expression in hyper-activated naïve and effector cytotoxic T cells (Tc), suggesting a H2-facilitated apoptotic clearance of pro-inflammatory lineages. Conversely, the helper T-cell (Th) reservoir was preserved. Recovery was further characterized by the consistent restoration of intermediate and post-germinal center memory B-cell populations, coupled with a substantial augmentation of suppressive T and B-cell subsets (Tregs and Bregs). This shift toward immune homeostasis prevented secondary autoimmune flares and facilitated successful discharge.

Conclusion

Molecular hydrogen may act as a systemic bioregulator that fosters immune homeostasis by selectively targeting hyper-activated effector cells while promoting regulatory cell recovery. This dual antioxidant and immunomodulatory capacity positions H2 as a promising adjuvant therapy for complex infectious and neuroinflammatory conditions.

Keywords: Case report, empyema, chronic inflammatory demyelinating polyradiculoneuropathy, molecular hydrogen

Introduction

Empyema is characterized by the accumulation of purulent fluid within the pleural space, most frequently manifesting as a complication of bacterial pneumonia and the progression of parapneumonic effusion. Optimal clinical outcomes rely on a multimodal therapeutic strategy: systemic antimicrobial therapy combined with timely pleural evacuation, typically achieved via tube thoracostomy. In cases involving loculated collections where primary drainage is insufficient, the administration of intrapleural fibrinolytics may be employed to enhance clearance. However, surgical intervention specifically video-assisted thoracoscopic surgery (VATS) or open decortication remains the definitive indication for patients with advanced stage disease or those refractory to conservative medical management (1).

Chronic inflammatory demyelinating polyneuropathy (CIDP) an uncommon immunological disorder defined by escalating muscular paralysis and somatosensory impairment persisting beyond eight weeks (2) significantly complicates the management of empyema. The condition exacerbates clinical instability through a triad of mechanisms: systemic immunosuppression, respiratory muscle impairment, and profound immune dysregulation (3, 4). At the cellular level, CIDP is driven by a complex interplay of autoreactive T and B cells, inflammatory cytokines, and autoantibodies that precipitate macrophage-induced demyelination (3). While standard CIDP management focuses on individualized immunomodulatory therapies predominantly intravenous immunoglobulin (IVIG), corticosteroids, and plasmapheresis (2) the presence of concurrent empyema introduces a critical therapeutic paradox. Clinicians must navigate a precarious balance between necessary immunosuppression and aggressive infection control. Given that conventional interventions often yield suboptimal outcomes in such complex presentations, there is a compelling need for adjunctive therapies capable of simultaneously modulating systemic inflammation and mitigating neurological frailty.

Molecular hydrogen (H2) functions as a potent immunomodulatory and neuroprotective agent, primarily through its targeted antioxidant, anti-inflammatory, and anti-apoptotic properties. In infectious states, H2 mitigates pathological hyperinflammation by selectively scavenging reactive oxygen species (ROS) in particular, the highly unstable hydroxyl moieties (OH) (5). This reduction in oxidative stress inhibits downstream inflammatory signaling cascades, resulting in the attenuated synthesis of pro-inflammatory signaling molecules [such as tumor necrosis factor-alpha (TNF-α)] alongside the simultaneous induction of anti-inflammatory factors like interleukin 10 (IL-10) (6). These mechanisms collectively facilitate immune homeostasis and attenuate infection-induced tissue damage. Within the central nervous system, H2 exerts neuroprotection by modulating microglial dynamics, specifically promoting a functional remodeling of cells from a cytotoxic M1 profile toward a regenerative M2 phenotype, an effect driven by the antagonism of the toll-like receptor 4 (TLR4)/ nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) regulatory axis, thereby reducing neuroinflammation and neuronal apoptosis. In preclinical models of sepsis-associated encephalopathy and vascular dementia, H2 administration has demonstrated significant efficacy in improving cognitive outcomes. These benefits are largely attributed to the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, which bolsters endogenous antioxidant defenses and suppresses inflammatory gene expression (7). In summary, H2 acts as a pleiotropic modulator that targets the intersection of oxidative stress, inflammatory cascades, and programmed cell death (8). Its ability to simultaneously address systemic inflammation and neurological frailty underscores its significant translational potential for treating complex infectious and neuroinflammatory pathologies.

This clinical account details a presentation of pleural empyema in an individual complicated by CIDP, managed through a novel therapeutic approach incorporating adjunctive H2 capsule therapy. The study protocol was reviewed and approved by the Institutional Review Board (IRB) of the Tri-Service General Hospital, National Defense Medical Center, Taiwan (IRB No. C202405129; approved on July 31, 2024). The clinical protocol was executed in rigorous compliance with institutional standards and the ethical tenets established by the Declaration of Helsinki and its successive revisions. Written informed consent for the dissemination of clinical data and this case report was secured from the patient.

Case Report

An eminent 76-year-old male academic specializing in psychiatric medicine, presented with abrupt, involuntary episodes of crying and occasional laughter in the absence of congruent emotional stimuli, clinical manifestations consistent with pseudobulbar affect (PBA) (9). Concurrently, the patient exhibited progressive generalized motor weakness, predominantly affecting the lower extremities, alongside hypoesthesia within the T5-L2 dermatomes. Notable signs of autonomic dysfunction, specifically urinary retention and constipation, were also present. Given the complexity of the neurological and psychiatric presentation, he was admitted to the psychiatric inpatient unit from October 10 to October 16, 2025. During this hospitalization, pharmacological intervention was initiated with a combination of dextromethorphan/quinidine and duloxetine (9), while a comprehensive diagnostic evaluation was conducted to further elucidate the underlying etiology.

Magnetic resonance imaging (MRI) of the entire spine revealed no evidence of significant nerve root compression (10). Subsequent electrophysiological studies provided objective evidence of neurological deficit. Electrophysiological assessment revealed protracted distal latencies of the right peroneal compound muscle action potential (CMAP), coupled with attenuated CMAP amplitudes across the right ulnar, peroneal, and tibial distributions. Subsequent sensory neurophysiological evaluation revealed protracted distal latencies and decelerated conduction velocities of the right sural sensory nerve action potentials (SNAPs), with reduced SNAP amplitudes observed across the right median, ulnar, and sural nerves. Additionally, electromyography (EMG) showed no spontaneous activity (fibrillation or positive sharp waves) at rest; however, decreased volitional recruitment was noted in the right vastus lateralis, left vastus medialis, and bilateral tibialis anterior muscles (11, 12). These findings are highly suggestive of a sensorimotor polyaxonopathy (12). A lumbar puncture was performed on October 14, 2025. Cerebrospinal fluid (CSF) analysis revealed findings consistent with CIDP, exhibiting albuminocytologic dissociation (13). Therapeutic intervention commenced on October 15, 2025, with an initial five-day course of IVIG therapy (2). For continuity of specialized care, the patient was transferred to the neurology department from October 16 to October 30, 2025, for the completion of the IVIG regimen, followed by readmission to the psychiatric ward from October 30 to November 5, 2025, for stabilized monitoring.

On November 2, 2025, the patient developed acute dyspnea, chest tightness, and pyrexia. Clinical examination revealed an oxygen saturation (SpO2) of 90% and coarse crackles upon pulmonary auscultation. Biochemical analysis revealed a markedly increased C-reactive protein (CRP) concentration, measured at 11.3 mg/dl, while chest radiography demonstrated progressive bilateral infiltrates consistent with hospital-acquired pneumonia (HAP) (14). Empirical broad-spectrum antibiotic therapy was promptly initiated (15). By November 5, the patient’s respiratory status further declined, with arterial blood gas (ABG) analysis confirming acute hypoxemic respiratory failure (16), necessitating urgent intensive care unit (ICU) admission. During the peak of clinical and radiographic severity on November 10, 2025, adjuvant oral H2 therapy was introduced (8). The regimen consisted of one capsule daily, each containing 170 mg of hydrogen-enriched calcium, capable of releasing approximately 1.7×1021 molecules of H2. Concurrently, lymphocyte surface markers were analyzed to monitor immune status (Figure 1). Due to persistent oropharyngeal dysphagia and choking episodes, a nasogastric tube was inserted on November 14 for nutritional and pharmacological administration. Contrast-enhanced computed tomography (CT) of the chest on November 15 revealed a loculated right-sided pleural effusion with adjacent consolidation (Figure 2B), findings pathognomonic for Stage II empyema (17, 18). Following a multidisciplinary consultation, the patient received VATS for decortication and right-sided tube thoracostomy on November 17, 2025.

Figure 1.

Figure 1

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Timeline of the patient’s clinical course, illustrating hospitalizations, symptom onset, major diagnostic milestones, therapeutic interventions, and longitudinal lymphocyte phenotyping. Shaded bars denote admissions to psychiatry (PSY), neurology (NEU), intensive care (ICU), and chest medicine (CHE). Key events, including chronic inflammatory demyelinating polyneuropathy (CIDP) diagnosis and surgical intervention (VATS + decortication), are indicated by date. The lower bar represents the period of adjunctive oral molecular hydrogen therapy, initiated on November 11, 2025.

Figure 2.

Figure 2

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Imaging findings of right-sided encapsulated empyema before and after surgical decortication. (A) Chest radiograph (November 9, 2025) demonstrating extensive opacification of the right middle and lower lung zones, consistent with a large pleural effusion or consolidation. (B) Coronal contrast-enhanced chest computed tomography (November 15, 2025) showing a lenticular, loculated pleural fluid collection with pleural thickening in the right hemithorax (arrow), compatible with encapsulated empyema prior to surgery. (C) Follow-up chest radiograph (December 15, 2025) after video-assisted thoracoscopic surgery (VATS) decortication demonstrating marked re-expansion of the right lung and resolution of the pleural collection.

Intraoperative findings and subsequent histopathology confirmed the diagnosis of empyema (19). Postoperatively, the chest tube was maintained under controlled suction. The clinical course was characterized by a steady resolution of pyrexia, a decline in CRP levels, and radiographic evidence of lung re-expansion (Figure 2C). Oxygen requirements gradually diminished, allowing for the patient’s transfer to the thoracic ward on November 20. The chest tube was successfully removed on November 24, and the patient remained stable until discharged from the thoracic unit on December 11, 2025. Upon resolution of the acute empyema, the patient was readmitted to the psychiatric unit on December 11, 2025, for the continued management of behavioral and psychological symptoms (BPSD). To monitor the immunological trajectory alongside clinical recovery, sequential lymphocyte surface marker analyses were performed. The “resolving phase” markers were assessed on December 17, 2025, providing a baseline for the second phase of IVIG therapy, which was administered on December 30, 2025. A final “resolution phase” immunological profile was obtained on January 13, 2026, confirming the achievement of clinical and biochemical stabilization. The patient remained under inpatient psychiatric observation until achieving discharge criteria on January 20, 2026 (Figure 1).

The patient’s clinical course necessitated an extensive 102-day hospitalization, spanning from October 10, 2025, to January 20, 2026. Management required a highly coordinated, multidisciplinary approach involving the departments of Psychiatry, Neurology, Critical Care Medicine, and Pulmonology. This comprehensive care strategy successfully addressed the complex interplay between CIDP and the severe respiratory complications arising from stage II empyema.

Discussion

This case underscores a complex clinical trajectory in which acute neurological distress, secondary to CIDP, was exacerbated by severe pulmonary infection, ultimately culminating in stage II empyema and acute hypoxemic respiratory failure (Figure 1 and Figure 2). The clinical management of such multifaceted cases necessitates a precise equilibrium between suppressing pathological hyperinflammation and preventing detrimental immune exhaustion. Following surgical decortication via VATS, the implementation of adjunctive H2 therapy offered a strategic therapeutic window. The subsequent radiographic resolution of the empyema (Figure 2C) suggests that H2 may function as a systemic bioregulator. Beyond its established antioxidant capacity, H2 has been demonstrated to modulate macrophage polarization, potentially facilitating a phenotypic shift from the pro-inflammatory M1 state toward the neuroprotective and anti-inflammatory M2 state. This transition not only mitigates acute neuroinflammation but also promotes tissue repair and prevents the progression of chronic fibrotic remodeling (7).

A pivotal finding in this study is the cell-specific modulation of Fas expression within distinct T-cell compartments. Fas is a canonical death receptor that mediates activation-induced cell death (AICD), a homeostatic process essential for the elimination of hyper-activated lymphocytes to mitigate collateral tissue damage (20). We identified a profound surge in Fas expression specifically within the naïve and effector cytotoxic T-cell (Tc) subpopulations (Figure 3A and C). This up-regulation peaked concurrently with maximal CRP levels and peak clinical severity (Figure 4), likely reflecting the heightened susceptibility of Tc cells to apoptosis during the empyema-induced systemic hyperinflammatory state.

Figure 3.

Figure 3

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Fas-positive (Fas⁺) cells in T-cell subsets measured using flow cytometry: (A) effector cytotoxic T cells (Tc), (B) effector helper T cells (Th), (C) naïve Tc cells, and (D) naïve Th cells. Healthy controls (HC) served as reference. Fas expression was markedly elevated in effector and naïve Tc cells during the acute phase (November 10, 2025), then progressively declined after initiation of molecular hydrogen therapy, reaching below HC levels in naïve Tc cells at final follow-up (January 12, 2026). Minimal longitudinal changes were observed in Th subsets.

Figure 4.

Figure 4

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Longitudinal C-reactive protein (CRP) levels from October 2025 to January 2026. CRP rose sharply in early November, peaking at 14.51 mg/dl on November 5, 2025, concurrent with pneumonia and acute respiratory failure. Following video-assisted thoracoscopic surgery decortication and initiation of adjunctive molecular hydrogen therapy, CRP progressively declined, returning to below the upper limit of normal (ULN, 0.8 mg/dl; red line) by early December and remaining stable thereafter.

Mechanistically, H2 has been reported to attenuate the TLR4/NF-κB signaling pathway, a primary driver of the pro-inflammatory cytokine cascade, including TNF-α release (7). By suppressing this signaling axis, H2 may facilitate the selective apoptotic clearance of hyper-activated Tc cells via Fas-mediated pathways while preserving the helper T (Th) cell reservoir (Figure 3B and D). This divergent response suggests that H2 acts as a selective immunomodulator, preferentially targeting pro-inflammatory cytotoxic lineages for apoptotic clearance while maintaining the helper T-cell population, thereby preventing a protracted and maladaptive inflammatory state.

The B-cell compartment underwent profound remodeling throughout the clinical course, transitioning from acute exhaustion to functional recovery. At the peak of the infection, a marked depletion of transitional B cells and class-switched memory B cells was identified (Figure 5A and B). Transitional B cells serve as the critical developmental link between bone marrow output and peripheral maturation (21); their systemic reduction likely signifies either intensive recruitment to inflammatory sites or the exhaustion of the early B-cell pool under severe inflammatory pressure. Concurrently, the decline in class-switched memory B cells reflects a transient disruption of established adaptive immune memory during the acute septic crisis (22). Following the initiation of H2 therapy, we observed a steady reconstitution of these B-cell populations, indicating the effective recovery of B-cell lymphopoiesis and the restoration of systemic immune surveillance. This regenerative pattern suggests that H2 therapy does not exert broad, non-selective immunosuppression. Instead, it appears to facilitate a functional “resetting” of the adaptive immune system, ensuring the preservation and recovery of long-term immune memory following a major clinical insult.

Figure 5.

Figure 5

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Longitudinal changes in lymphocyte subsets from October 2025 to January 2026. Healthy control (HC) values are shown as reference lines. (A) Transitional B cells declined after peak systemic illness (December 17, 2025) and subsequently recovered toward HC levels. (B) Class-switched memory B cells markedly decreased during the acute respiratory crisis (November 10, 2025) and progressively reconstituted thereafter. (C) Regulatory T cells (Treg) increased over time, exceeding HC levels during the recovery phase (January 2026). (D) Regulatory B cells (Breg) remained below HC values, with suppression during acute inflammation followed by partial recovery. Data are expressed as percentages of parent populations (CD19+ B cells for A, B, D; CD4+ T cells for C).

The restoration of immune homeostasis was further evidenced by a dynamic increase in regulatory T-cell (Treg) and regulatory B-cell (Breg) populations. Tregs are indispensable for suppressing autoinflammatory cascades via the secretion of inhibitory cytokines, such as IL-10 and transforming growth factor beta (TGF-β) (23). Concurrently, Bregs provide a critical checkpoint for maintaining B-cell tolerance and suppressing the production of pathogenic autoantibodies (Figure 5C and D) (24, 25). In the present case, these regulatory subsets demonstrated a progressive upward trajectory, eventually reaching or exceeding reference levels during the resolution phase. This late-stage enrichment likely established a robust immunomodulatory buffer, effectively preventing secondary autoimmune flares a frequent and debilitating complication in complex overlap syndromes. The synchronous expansion of both Treg and Breg populations underscores a holistic enhancement of the host’s regulatory landscape. This shift is potentially driven by the pro-homeostatic effects of H2, which appear to foster an environment conducive to regulatory cell proliferation and functional stabilization.

Conclusion

This case demonstrates that adjunctive H2 therapy, combined with VATS decortication, was associated with immune rebalancing in stage II empyema complicated by CIDP. Longitudinal profiling suggested selective Fas-mediated clearance of hyperactivated cytotoxic T cells, preservation of helper T cells, and expansion of regulatory lymphocyte subsets. Rather than nonspecific immunosuppression, H2 appeared to promote immune homeostasis and tissue repair while potentially limiting autoimmune exacerbation. These observations warrant prospective investigation into the immunomodulatory mechanisms of H2 therapy in complex inflammatory disorders.

Conflicts of Interest

The Authors declare no conflicts of interest or competing interests related to this study.

Authors’ Contributions

HLT: Conceptualization, methodology, writing-original draft, writing review and editing. JWL: Conceptualization, methodology, writing-original draft, writing review and editing. YJH: Conceptualization, methodology, project administration, writing-review and editing. SWL: Conceptualization, methodology, writing-review and editing. TYH: Conceptualization, methodology, writing-review and editing. KYW: Conceptualization, methodology, writing-review and editing. FCL: Conceptualization, investigation, supervision, writing-review and editing.

Acknowledgements

This study was funded by the National Science and Technology Council, Taiwan (grants NSTC 112-2314-B-016-033, NSTC 113-2314-B-016-052, NSTC 114-2314-B-016-052-MY3, NSTC 114-2313-B-019-012) and Tri-Service General Hospital, Taiwan (grants TSGH-E-112218 and TSGH-E-113238).

Artificial Intelligence (AI) Disclosure

During manuscript preparation, a large language model (Microsoft Copilot, by OpenAI) was used only for language editing and stylistic improvements in selected paragraphs. All research data generation, analysis, and interpretation were performed solely by the authors. No figures or visual data were created or modified using generative AI or machine learning-based tools.

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