Reversal of brain dysfunction with UV-A1 irradiation in a patient with                 systemic lupus

Menon, Yamini; McCarthy, Karen; McGrath, H

doi:10.1191/0961203303lu374oa

Cited by 12 publications

(16 citation statements)

References 15 publications

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“…UVA-1 radiation in lupus-prone MRL-lpr mice also prevented development of CLE-like skin lesions (45). Based on these findings, UVA-1 was tested in SLE patients in varying dosing regimens in case report, open-label and randomized control trial settings ( Table 2) (37)(38)(39)(40)(41)(46)(47)(48)(49)(50). In these trials, UVA-1-treated patients demonstrated decreased systemic symptoms and disease activity scores (e.g.…”

Section: Uva-1 Therapy For Lupus Patientsmentioning

confidence: 99%

Photosensitivity in cutaneous lupus erythematosus

Kim

Chong

2013

Photoderm Photoimm Photomed

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Cutaneous lupus erythematosus (CLE) encompasses several different forms including acute, subacute, and chronic manifestations that may or may not occur in the setting of systemic lupus erythematosus (SLE). Ultraviolet radiation (UVR) is a well-known exacerbating factor for CLE, with photosensitivity comprising one of the American College of Rheumatology (ACR) diagnostic criteria for SLE. However, discerning true photosensitivity in this population is difficult due to the broad language utilized by the ACR and the delayed-onset nature of photosensitive lupus lesions. Photoprovocation testing provides a more objective method to measure photosensitivity, but photoprovocation trials demonstrate significantly varying results due to protocol variations. Despite UVR’s deleterious effect on lupus patients, UVA-1 may have therapeutic benefits as shown by some observations on murine and human lupus subjects. Accurately discerning photosensitivity has diagnostic implications for SLE and provides motivation for greater patient adherence to photoprotective measures.

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Section: Uva-1 Therapy For Lupus Patientsmentioning

confidence: 99%

Photosensitivity in cutaneous lupus erythematosus

Kim

Chong

2013

Photoderm Photoimm Photomed

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“…The effects of HO-1 and its products in the CNS add further to their therapeutic potential in lupus. 6 , 8 , 12 For a start, full-body UV-A1 irradiation mitigates “brain fog,” a common and often major complaint in patients with lupus. 6 , 12 This cognitive dysfunction, which presents as decreased attentiveness, memory deficits, diminished problem-solving capability, and decreases in information organization, is frequently the most immediate and gratifying effect of UV-A1 irradiation therapy.…”

Section: Ho-1 and The Central Nervous System (Cns)mentioning

confidence: 99%

Ultraviolet-A1 irradiation therapy for systemic lupus erythematosus

McGrath

2017

Lupus

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Systemic lupus erythematosus (lupus, SLE) is a chronic autoimmune disease characterized by the production of autoantibodies, which bind to antigens and are deposited within tissues to fix complement, resulting in widespread systemic inflammation. The studies presented herein are consistent with hyperpolarized, adenosine triphosphate (ATP)-deficient mitochondria being central to the disease process. These hyperpolarized mitochondria resist the depolarization required for activation-induced apoptosis. The mitochondrial ATP deficits add to this resistance to apoptosis and also reduce the macrophage energy that is needed to clear apoptotic bodies. In both cases, necrosis, the alternative pathway of cell death, results. Intracellular constituents spill into the blood and tissues, eliciting inflammatory responses directed at their removal. What results is “autoimmunity.” Ultraviolet (UV)-A1 photons have the capacity to remediate this aberrancy. Exogenous exposure to low-dose, full-body, UV-A1 radiation generates singlet oxygen. Singlet oxygen has two major palliative actions in patients with lupus and the UV-A1 photons themselves have several more. Singlet oxygen depolarizes the hyperpolarized mitochondrion, triggering non-ATP-dependent apoptosis that deters necrosis. Next, singlet oxygen activates the gene encoding heme oxygenase (HO-1), a major governor of systemic homeostasis. HO-1 catalyzes the degradation of the oxidant heme into biliverdin (converted to bilirubin), Fe, and carbon monoxide (CO), the first three of these exerting powerful antioxidant effects, and in conjunction with a fourth, CO, protecting against injury to the coronary arteries, the central nervous system, and the lungs. The UV-A1 photons themselves directly attenuate disease in lupus by reducing B cell activity, preventing the suppression of cell-mediated immunity, slowing an epigenetic progression toward SLE, and ameliorating discoid and subacute cutaneous lupus. Finally, a combination of these mechanisms reduces levels of anticardiolipin antibodies and protects during lupus pregnancy. Capping all of this is that UV-A1 irradiation is an essentially innocuous, highly manageable, and comfortable therapeutic agency.

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“…Apart from the short term benefit following UVA1 phototherapy, Molina et al were also able to describe a long term benefit following low-dose UVA1 treatment (once/twice per week, 6–15 J/cm 2 ) for a mean impressive period of 3.4 years in six patients of their former study [77]. Additionally, recent data of a case report suggest that UVA1 might contribute to a reversal of brain dysfunction and may also improve covered discoid lupus lesions via unknown systemic pathways [78]. As to our knowledge, no positive effects of PUVA treatment have been reported so far.…”

Section: Resultsmentioning

confidence: 99%