UltraPlasma™ Lupus Erythematosus (LE) Treatments
Targeting Discoid, Cutaneous, Systemic, and Comedonic Variants through UltraPlasma™ Therapies withOut! Drugs, Industrial Chemicals, Medicines, Surgery, Supplements, and Lasers.
TREATMENTS
MedicaLabs, Germany | https://medicalabs.de
10/24/20243 min read




UltraPlasma™ Multi-Platform Plasma Systems for Discoid Lupus Erythematosus (DLE) Treatment
Introduction
Discoid Lupus Erythematosus (DLE) is a chronic autoimmune skin condition characterized by inflamed, disc-shaped lesions, often resulting in scarring and pigmentation loss. Traditional therapies focus on immunosuppression and inflammation control. However, UltraPlasma™—a next-generation plasma therapy system integrating arc, argon, and helium plasmas—offers a novel non-invasive approach. This system utilizes a custom software-hardware spectrum controller to deliver precise reactive species, improve microcirculation, and support immune modulation directly at the skin interface.
1. Pathophysiology of Discoid Lesions (DLE)
DLE lesions typically involve:
Epidermis: Hyperkeratosis, basal cell degeneration, and interface dermatitis.
Dermis: Perivascular inflammation and lymphocytic infiltration.
Hypodermis: Involvement in deep scarring and tissue breakdown in chronic cases.
Blood functions: Reduced perfusion, oxygenation, and immune dysfunction.
Immune dysfunction: T-cell hyperactivation, autoantibody production (e.g., anti-Ro/SSA), and impaired resolution of inflammation.
2. UltraPlasma™ System Overview
The UltraPlasma™ device integrates three plasma sources and modulates them via a real-time spectrum controller:


3. Plasma-Induced Mechanisms in DLE Treatment
3.1 Epidermal Repair and Resurfacing
UltraPlasma™ arc plasma mode delivers UV-like excitation to reduce hyperkeratosis.
Ozone (O₃) and NO enhance local antioxidant defenses and DNA repair enzymes.
UltraPlasma™ argon plasma mode balances keratinocyte regeneration without thermal damage.
3.2 Dermal Microcirculation and Fibroblast Activation
UltraPlasma™ helium plasma mode modulates deep fibroblasts and endothelial cells.
Controlled NO release promotes vasodilation, tissue oxygenation, and healing.
3.3 Hypodermal Immunomodulation
Deep penetration of helium plasma aids lymphatic drainage and immune regulation.
RNS (Reactive Nitrogen Species) balance T-reg vs. Th17 cell ratios.




4. Role of Reactive Gases and Blood Interaction
⌘Conclusion⌘
UltraPlasma™ represents a paradigm shift in the treatment of Discoid Lupus Erythematosus (DLE), offering a multi-layered therapeutic approach that extends beyond surface-level symptom management. By integrating arc, argon, and helium plasma technologies into a harmonized output system, UltraPlasma™ delivers a precise spectrum of energy and reactive gas species tailored to the biological demands of each skin layer—epidermis, dermis, and hypodermis.
Through the synergistic effects of ozone (O₃), nitric oxide (NO), and other plasma-induced reactive species, the device not only reduces inflammatory lesions but also revitalizes microcirculation, repairs dermal architecture, and actively modulates dysfunctional immune responses. This positions UltraPlasma™ as both a regenerative and immune-regulatory therapy—an ideal match for the multifactorial nature of autoimmune skin conditions like DLE.
With customizable treatment protocols and non-invasive application, UltraPlasma™ provides dermatologists with a safe, versatile, and highly effective tool to manage chronic discoid lesions, reduce relapse rates, and enhance patients’ skin integrity and quality of life. As plasma medicine continues to evolve, UltraPlasma™ sets a new benchmark in combining advanced bioelectrical engineering with immuno-dermatological care.


5. Immune System Repair Strategy via UltraPlasma™
Targeted plasma pulses reduce autoreactive T-cell clusters.
NO and O₃ upregulate anti-inflammatory cytokines (IL-10, TGF-β).
Arc plasma’s ROS bursts help reset local immune cell metabolism.
Longitudinal treatments shift from inflammation to regeneration phase.
6. Suggested Treatment Protocol
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