Fluorescence remission spectroscopy of psoriatic lesions and the effect of topical anthralin therapy

Wollina, Uwe; Wd, Schmidt; Koch, Andrè; Scheibe, Armin; Erfurth, F; Faßler, D.

doi:10.1111/j.1468-3083.2009.03323.x

Cited by 11 publications

(10 citation statements)

References 21 publications

(18 reference statements)

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“…It seems reasonable since the proliferation of psoriatic keratinocytes requires consumption of NADH during oxidative phosphorylation and ATP synthesis. In the study of Wollina et al the NADH fluorescence was found to be reduced in psoriatic lesions [15]. In the search for new antipsoriatic agents NAD(+) used topically was found to be as effective as 0.1% anthralin [16].…”

Section: Wykorzystuje Dinukleotyd Nikotynoamidoadeninowymentioning

confidence: 99%

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UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis

Bernacka¹,

Liszewska²,

Robak³

et al. 2018

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Narrow band (311 nm) UVB phototherapy is established treatment for psoriasis. DNA is a target for UVB via formation of cyclobutane pyrimidine dimers, which trigger loss of dendritic cells and macrophages, and inhibit CD4+ and CD8+ T cells. UV causes the formation of thymine dimers, which activate nuclear enzyme poly(ADP-ribose) polymerase. The fact that poly(ADP-ribose) polymerase utilizes nicotinamide-adenine dinucleotide (NAD) explains NAD decreases after UV irradiation. NADH regulates transcriptional repressor carboxyl-terminal binding protein, whereas NAD(+) is a co-substrate in deacylation reactions, engaged in genomic silencing. Hyperproliferation of psoriatic keratinocytes requires NADH during oxidative phosphorylation. In one study the NADH fluorescence (reflecting NADH amount) was reduced in psoriatic lesions. NAD(+) used topically was as effective as 0.1% anthralin. Spectrophotometry enables real-time measurements of NADH fluorescence in vivo in the epidermis and points out a new direction for application of biophysics in medicine. streszczenie Fototerapia wąskim pasmem UVB (311 nm) jest uznaną metodą leczenia łuszczycy. Molekularnym punktem uchwytu fototerapii UVB jest DNA poprzez tworzenie się dimerów cyklobutanopirymidynowych, które wyzwalają utratę komórek dendrytycznych i makrofagów oraz hamują komórki CD4+ i CD8+. Promieniowanie UV powoduje wytwarzanie dimerów tymidynowych aktywujących jądrową polimerazę poli(ADP-rybozy) (PARP). Zużywanie przez PARP dinukleotydów nikotynoamidoadeninowych (NAD) wyjaśnia zjawisko zmniejszania się zawartości NAD po naświetlaniu UV. NADH reguluje represorowe białko transkrypcji wiążące koniec karboksylowy, natomiast NAD(+) służy jako kosubstrat w reakcjach deacylacji, które mają udział w wyciszaniu genomu. Hiperproliferacja keratynocytów w łuszczycy wymaga zużywania NADH podczas fosforylacji oksydacyjnej. W jednym z badań stwierdzono obniżoną fluorescencję NADH (odzwierciedlającą zawartość NADH) w zmianach łuszczycowych. Stwierdzono, że NAD(+) stosowany miejscowo jest równie skuteczny co 0,1% antralina. Spektrofotometria umożliwia pomiar fluorescencji NADH w naskórku

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Section: Wykorzystuje Dinukleotyd Nikotynoamidoadeninowymentioning

confidence: 99%

“…Wollina i wsp. wykazali, że fluorescencja NADH zmniejsza się w zmianach łuszczycowych [15]. Przy poszukiwaniu nowych leków przeciwłuszczycowych stwierdzono, że stosowany miejscowo NAD(+) jest równie skuteczny jak 0,1% antralina [16].…”

Section: Wykorzystuje Dinukleotyd Nikotynoamidoadeninowyunclassified

UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis

Bernacka¹,

Liszewska²,

Robak³

et al. 2018

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“…On the one hand, one can speculate that increased proliferation and inflammation in a psoriatic lesion result in NADH rapid consumption. Wollina et al revealed that indeed the NADH fluorescence, which reflects NADH amount in the skin, was reduced in psoriatic lesions [15]. Unfortunately, this is the only existing study devoted to determining the NADH level in psoriatic skin in vivo [15].…”

Section: Nicotinamide-adenine Dinucleotide In Psoriasismentioning

confidence: 99%

“…Wollina et al revealed that indeed the NADH fluorescence, which reflects NADH amount in the skin, was reduced in psoriatic lesions [15]. Unfortunately, this is the only existing study devoted to determining the NADH level in psoriatic skin in vivo [15]. An opposite hypothesis links increased cellular metabolism to the increased NADH/NAD + ratio.…”

Section: Nicotinamide-adenine Dinucleotide In Psoriasismentioning

confidence: 99%

Methotrexate use and NAD+/NADH metabolism in psoriatic keratinocytes

Liszewska

Robak

Bernacka

et al. 2020

pdia

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A b s t r a c tMethotrexate inhibits tetrahydrofolic acid production and influences mitochondrial oxygen uptake and activity of several enzymes in the respiratory chain reactions, which utilize nicotinamide adenine dinucleotide-linked (NAD-linked) substrates. Hyperproliferation of keratinocytes in psoriasis requires oxidative phosphorylation, in which the reduced form of nicotinamide adenine dinucleotide (NADH) is an electron donor. One hypothesis links increased cellular metabolism to the increased NADH/NAD + ratio; as expected, the topical application of NAD + (oxidized form of nicotinamide-adenine dinucleotide) resulted in a clinical improvement of psoriatic lesions in one study. Nevertheless, another report revealed reduced fluorescence of NADH in psoriatic plaques. The biological activity of NADH is not limited only to serving as the electron donor. It was also found to regulate gene transcription.

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“…The average total energy applied was 2.05 J, with 1.13 J in the UVB med range. We used the fluorescence‐remission imaging (FRIS) as described before 7 for non‐invasive objective measurements.…”

Section: Clinical Outcome Lesion a – 307 Nm‐excimer Light; Lesion Bmentioning

confidence: 99%

Targeted 307 nm UVB‐excimer light vs. topical dithranol in psoriasis

Wollina

Koch

Scheibe

et al. 2011

Acad Dermatol Venereol

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EditorPhoto(chemo)therapy is a well established psoriasis therapy. As demonstrated by Parrish and Jaenicke, the action spectrum for psoriasis clearing is 300-313 nm. 1 In recent years, targeted UVB phototherapy with 308 nm-excimer laser and excimer light has been developed. It avoids unnecessary UV-exposure of non-lesional skin and allows higher dosages for lesional skin what results in a more rapid clearing. Both seem to achieve comparable efficacy with lower investment costs for excimer light. [2][3][4][5] We report a pilot trial in moderate plaque-type adult psoriasis patients using a newly developed 307 nm-excimer lamp compared to topical dithranol.This is an open clinical pilot trial with permission from the local ethical committee. Every patient served as his ⁄ her own control. Systemic therapy was not allowed. Two target lesions of comparable size and plaque-modified Psoriasis Activity and Severity Index (PSI) scores 6 were selected for monitoring. Lesion A was treated with 307 nm-excimer light only. Lesion B was treated with dithranol.Targeted UVB treatment was performed with a new device three times starting with the minimal erythema dose (MED). The mean 307 nm-excimer light exposure per session was 20 s resulting in a mean total irradiation time of 37 s. With the support of a quartz bar targeted treatment with a focus area of 3 cm 2 is realized. The average UVB med irradiance was 18 mW ⁄ cm 2 , maximum 20 mW ⁄ cm 2 . The average total energy applied was 2.05 J, with 1.13 J in the UVB med range. We used the fluorescence-remission imaging (FRIS) as described before 7 for non-invasive objective measurements.A total of 21 patients were recruited with 19 patients completing the investigation [15 men, six women]. The mean age was 51 years (range 26-84 years). All patients had a Fitzpatrick skin phototype II or III. The mean improvement of the PSI score was 3.0 for lesion A (three times excimer light) and for lesion B (twice daily dithranol) (P = 0.965; Mann-Whitney U-test). The results clearly demonstrate an equipotency of the targeted phototherapy to topical dithranol (Table 1).Tolerance was superior with targeted phototherapy. The most common adverse effect in excimer light-treated lesions was a mild to moderate erythema (n = 11), temporary blistering (n = 3), but there was no scarring or oozing. The NADH-fluorescence is reduced in psoriatic lesions. Excimer light treatment results in a normalization of NADH-fluorescence in contrast to dithranol.The UVB-excimer lamps are an alternative for targeted UVBtherapy in psoriasis. They seem to be as effective as non-targeted narrow-band UVB and 308 nm-excimer laser therapy. 4,5 There has been no study comparing targeted UVB phototherapy with topical treatments. In this study for the first time 307 nm-excimer light therapy was compared to topical dithranol therapy. Dithranol is one of the most potent topical antipsoriatic drugs. 8 We used a newly developed 307 nm-excimer light for targeted UVB-therapy and compared its efficacy and safety to topical dithranol twice d...

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Fluorescence remission spectroscopy of psoriatic lesions and the effect of topical anthralin therapy

Abstract: Vascular perfusion is increased in psoriatic lesions as demonstrated by remission spectroscopy. NADH-fluorescence is reduced in lesional psoriatic skin and in anthralin-induced erythema. FRIS is a suitable tool for objective evaluation of the cutaneous response to antipsoriatic treatment.

Cited by 11 publications

References 21 publications

UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis

UVB-311 nm phototherapy and NAD(+)/NADH metabolism in keratinocytes in patients with psoriasis

Methotrexate use and NAD+/NADH metabolism in psoriatic keratinocytes

Targeted 307 nm UVB‐excimer light vs. topical dithranol in psoriasis

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