SCF ENCYCLOPEDIA ENTRY

G6PD DEFICIENCY

SCF REDOX FAILURE & ERYTHROCYTE OXIDATIVE-RESILIENCE SYNCHRONIZATION COLLAPSE DOSSIER

I. OFFICIAL DISEASE CLASSIFICATION

G6PD deficiency belongs to SCF Clinical Domains C12 (Hematology), C6 (Metabolic Medicine), C1 (Genomic Medicine), C2 (Cellular Bioenergetics), and C13 (Systems Homeostasis Biology).

II. CLINICAL DEFINITION

G6PD deficiency is an inherited enzymatic disorder characterized by:

• Reduced antioxidant capacity
• Episodic hemolytic anemia
• Oxidative stress sensitivity
• Neonatal hyperbilirubinemia
• Red blood cell destruction
• Trigger-dependent hemolysis

Primary affected systems:

• Erythrocytes
• Pentose phosphate pathway
• NADPH generation systems
• Glutathione recycling pathways
• Oxidative defense networks

Associated conditions:

• Hemolytic anemia
• Neonatal jaundice

III. MAJOR CLASSIFICATIONS

A. Class I G6PD Deficiency

B. Class II G6PD Deficiency

C. Class III G6PD Deficiency

D. Class IV–V Variants

IV. CORE SCF ETIOPATHOGENIC THESIS

Within the Synergistic Compatibility Framework (SCF), G6PD deficiency represents a systems-level collapse of:

• Oxidative-defense harmonics
• Cellular redox equilibrium
• Antioxidant regeneration systems
• Erythrocyte resilience networks
• Bioenergetic protection mechanisms

SCF interprets G6PD deficiency as a decentralized redox communication disorder in which impaired antioxidant regeneration destabilizes erythrocyte survival during oxidative challenge.

V. G6PD FOUNDATION

Core Pathophysiologic Mechanisms

VI. MAJOR GENETIC CAUSES

Principal Gene

Genetic Characteristics

Associated condition:

• X-linked genetic disorder

VII. SCF FAULT ARCHITECTURE

VIII. MULTI-OMICS PATHOGENESIS

A. Genomics

Affected pathways:

• Pentose phosphate pathway
• NADPH generation
• Oxidative defense systems
• Redox homeostasis

B. Transcriptomics

Dysregulated pathways:

• Antioxidant response signaling
• Stress-response pathways
• Cellular detoxification systems

C. Proteomics

Observed abnormalities:

• Reduced G6PD enzyme activity
• Oxidized hemoglobin
• Damaged membrane proteins
• Antioxidant enzyme dysfunction

D. Metabolomics

Key dysfunction:

• NADPH depletion
• Reduced glutathione depletion
• ROS accumulation
• Oxidative metabolic stress

E. Redoxomics (SCF)

Observed abnormalities:

• Antioxidant failure
• Oxidative amplification loops
• Cellular detoxification collapse
• Erythrocyte oxidative injury

IX. SCF PATHOGENESIS FLOW

Stage 1 — G6PD Mutation

NADPH generation capacity declines.

Stage 2 — Oxidative Trigger Exposure

Cellular stress increases.

Stage 3 — Glutathione Depletion

Antioxidant defense collapses.

Stage 4 — Hemoglobin Oxidation

Heinz bodies form.

Stage 5 — Erythrocyte Destruction

Hemolysis develops.

Stage 6 — Hemolytic Crisis

Anemia and jaundice occur.

X. SYSTEMIC CONSEQUENCES

Associated conditions:

• Hyperbilirubinemia
• Hemoglobinuria
• Kernicterus

XI. RHENOVA INTERPRETATION

Project RHENOVA interprets G6PD deficiency as a redox-buffer destabilization syndrome.

RHENOVA Dynamics

• Oxidative amplification loops
• Antioxidant depletion cascades
• Erythrocyte fragility progression
• Hemolytic crisis initiation
• Redox synchronization collapse

RHENOVA Biomarkers

XII. DBI INTERPRETATION

The SCF Decentralized Biological Intelligence framework interprets redox systems as cellular defense networks coordinating:

• Oxidative protection
• Detoxification
• Metabolic resilience
• Cellular longevity
• Damage control

DBI Failure Features

• Antioxidant communication failure
• Detoxification overload
• Oxidative amplification
• Cellular defense collapse

This transforms coordinated oxidative protection into episodic hemolytic injury.

XIII. CLINICAL MANIFESTATIONS

Hematologic Manifestations

• Acute hemolytic anemia
• Pallor
• Fatigue
• Weakness

Hepatic Manifestations

• Jaundice
• Elevated bilirubin
• Neonatal hyperbilirubinemia

Urinary Manifestations

• Dark urine
• Hemoglobinuria

Trigger-Associated Manifestations

Common triggers include:

• Certain infections
• Oxidative medications
• Fava bean exposure

Associated condition:

• Fava bean

XIV. DIAGNOSTICS

Diagnostic Hallmarks

Metabolic principle:

G6PD\ Deficiency \Rightarrow NADPH\ Depletion

Redox relationship:

NADPH\ Depletion \Rightarrow Glutathione\ Failure

Clinical consequence:

Oxidative\ Stress \Rightarrow Hemolysis

XV. SCF SYSTEMIC AXIS INVOLVEMENT

XVI. STANDARD OF CARE

Trigger Avoidance

Primary management:

• Avoid oxidant drugs
• Avoid known triggers
• Prompt treatment of infections

Acute Hemolytic Crisis Management

Associated procedure:

• Red blood cell transfusion

Neonatal Management

XVII. SCF-PCR THERAPEUTIC ARCHITECTURE

A. Preventative (PCR-P)

Goals:

• Prevent oxidative injury
• Preserve erythrocyte survival
• Maintain redox balance

B. Curative (PCR-C)

Goals:

• Restore G6PD activity
• Normalize NADPH production
• Correct genetic defects

C. Restorative (PCR-R)

Goals:

• Restore antioxidant resilience
• Improve redox communication
• Reduce oxidative injury
• Rebuild erythrocyte synchronization harmonics

XVIII. ETHNOBIOPROSPECTING TARGETS

Traditional Chinese Medicine

• Astragalus membranaceus
• Schisandra chinensis

Ayurveda

• Emblica officinalis
• Withania somnifera

Vietnamese Thuốc Nam

• Phyllanthus amarus
• Moringa oleifera

XIX. SCF API DISCOVERY TARGETS

High-Priority Molecular Targets

• G6PD restoration technologies
• NADPH-regeneration pathways
• Glutathione-recycling systems
• Antioxidant amplification platforms
• Redox-buffer stabilization systems
• Oxidative stress suppressors
• Erythrocyte synchronization restoration platforms

XX. SCF LAYMAN’S SUMMARY

G6PD deficiency is one of the most common inherited enzyme disorders worldwide. Because red blood cells cannot produce enough NADPH, they struggle to maintain their antioxidant defenses. When exposed to oxidative stress from infections, medications, or certain foods such as fava beans, red blood cells can rapidly break apart, causing anemia, jaundice, and dark urine. SCF interprets G6PD deficiency as a systems-level redox communication disorder involving impaired NADPH generation, glutathione depletion, oxidative injury, and loss of synchronized erythrocyte defense mechanisms.

XXI. STRATEGIC RESEARCH PRIORITIES

1. G6PD gene-restoration technologies
2. NADPH-regeneration therapeutics
3. Glutathione recycling enhancement systems
4. AI-driven hemolytic crisis forecasting platforms
5. Oxidative stress suppression technologies
6. Erythrocyte resilience optimization systems
7. Redox synchronization restoration platforms

MASTER REGISTRY INDEX

SCF-G6PD-0001 — G6PD Deficiency Master Registry

SCF-G6PD-REDOX-0002 — Oxidative Defense Failure Layer

SCF-G6PD-NADPH-0003 — NADPH Regeneration Dysfunction Layer

SCF-G6PD-RHENOVA-0004 — Redox Buffer Destabilization Layer

SCF-G6PD-DBI-0005 — Antioxidant Communication Failure Layer

SCF-G6PD-PCR-0006 — Preventative–Curative–Restorative Layer