Ibuprofen in the treatment of UV-B-induced inflammation

Stern, R. S.

doi:10.1001/archderm.121.4.508

Cited by 6 publications

(6 citation statements)

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“…Finally, topically applied NF-κB decoy ODN resulted in local inhibition of sunburn reactions, without affecting inflammation in nontreated skin sites, with the implication that NF-κB decoy ODN acted primarily on cells that reside in skin. Our conclusion is further supported, albeit indirectly, by the clinical observation that sunburn reactions can be treated successfully by nonsteroidal antiinflammatory agents (44), which are now known to block NF-κB activation by interfering with IkB kinase-2 (IKK2) activity (45). Moreover, two groups reported independently that mice lacking the IkBα gene developed spontaneously widespread severe dermatitis with leukocyte infiltration, suggesting a pathway through which NF-κB activation directly leads to skin inflammation (46,47).…”

Section: Figuresupporting

confidence: 60%

A role for NF-κB–dependent gene transactivation in sunburn

Abeyama¹,

Eng²,

Jester³

et al. 2000

J. Clin. Invest.

156

116

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Section: Figuresupporting

confidence: 60%

A role for NF-κB–dependent gene transactivation in sunburn

Abeyama¹,

Eng²,

Jester³

et al. 2000

J. Clin. Invest.

156

116

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“…However, most investigators concentrated on measurements of superficial blood flow using reflectance instruments, laser Doppler flowmetry or scaling of skin redness. Hyperalgesia was either not tested or was reported casually based on complaints of patients (Snyder, 1975;Stern & Dodson, 1985). A systematic study about time course of thermal and mechanical hyperalgesia after UVB irradiation in humans has been reported only in abstract form before (Benrath et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Time course of UVA‐ and UVB‐induced inflammation and hyperalgesia in human skin

Hoffmann

Schmelz

1999

European Journal of Pain

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Dose-dependency and time course of hyperalgesia and erythema following UVA (16.8 and 36 J/cm(2)) and UVB (one and three times the minimum erythema threshold) irradiation was investigated in 10 healthy human subjects. Skin patches (1.5 cm in diameter) on the ventral side of the upper leg were irradiated with UVA or UVB light. Hyperaemia (Laser Doppler flowmetry, infrared thermography), thermal hyperalgesia to radiant heat stimuli, and mechanical hyperalgesia to controlled impact stimuli were tested at 1, 6, 12, 24, 48 and 96 h after irradiation. Dose-dependent delayed hyperaemia and hyperalgesia was induced only by UVB irradiation. UVB-induced increase in blood flow peaked at 12 h after irradiation and normalized by 96 h. Although superficial blood flow, as measured by Laser Doppler flowmetry, increased up to eight-fold, no significant increase of skin temperature was detected using infrared thermography. Development of mechanical and thermal hyperalgesia was delayed and reached a plateau between 24 and 48 h. In contrast to UVB, UVA irradiation of up to 36 J/cm(2), sufficient to produce intense tanning of the skin, did not induce significant hyperalgesia or delayed hyperaemia. It is concluded that UVB- but not UVA-irradiation is a suitable experimental model of subacute thermal and mechanical hyperalgesia. The different time courses of erythema and hyperalgesia indicate that inflammatory mediators responsible for vasodilatation are not identical with those inducing hyperalgesia. Copyright 1999 European Federation of Chapters of the International Association for the Study of Pain.

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“…In this study of patients that showed a benefit of meloxicam ingestion, the factor of benefit was not more than 3. In the literature, an increase in sun protection of about 2.4-fold is the highest protection described concerning the NSAIDS indomethacin, acetylsalicylic acid (COX-1 antagonists), diclofenac and ibuprofen (COX-1 and COX-2 antagonists) after topical or systemic administration (3)(4)(5)(6)(7)(8).…”

Section: Discussionmentioning

confidence: 99%

“…The COX-1 antagonists, acetylsalicylic acid and indomethacin, lead to a delay in UV erythema, when applied topically or orally (3)(4)(5)(6). Ibuprofen, which blocks COX-1 and COX-2, additionally shows an effect on the cellular level in reducing the number of sunburn cells (SBCs), apoptotic keratinocytes of the epidermis, appearing after UV irradiation (7)(8)(9).…”

mentioning

confidence: 99%

Meloxicam in acute UV dermatitis — a pilot study

Bayerl

Pagung

Jung

1998

Photoderm Photoimm Photomed

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The non-steroidal anti-inflammatory drug (NSAID) meloxicam is a preferential cyclooxygenase-2 (COX-2) antagonist. The UV protective potential of this drug was studied to compare it with the reported beneficial effects of such preferentially COX-1 specific NSAIDs as indomethacin and acetylsalicylic acid in the literature. In a pilot study (open-label, non-randomized, non-controlled, unblinded), 10 patients received UV irradiation with the minimal erythema dose (MED), first with meloxicam (7.5 mg/die) to reduce post-operative pain and second without ingestion of meloxicam. The factor of UV protection was evaluated. In six of ten patients meloxicam showed no benefit, whereas four of ten patients had a 1.3- up to 3-fold UV protection. In this study, the benefit in UV protection of meloxicam as a preferential COX-2 antagonist was not above the reported benefit of the "old" COX-1 inhibiting NSAIDS.

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Ibuprofen in the treatment of UV-B-induced inflammation

Cited by 6 publications

References 0 publications

A role for NF-κB–dependent gene transactivation in sunburn

A role for NF-κB–dependent gene transactivation in sunburn

Time course of UVA‐ and UVB‐induced inflammation and hyperalgesia in human skin

Meloxicam in acute UV dermatitis — a pilot study

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