The Sunburn Pain Model: The Stability of Primary and Secondary Hyperalgesia Over 10 Hours in a Crossover Setting

Gustorff, Burkhard; Anzenhofer, Sebastian; Sycha, Thomas; Lehr, Stephan; Kress, Hans G.

doi:10.1213/01.ane.0000093224.77281.a5

Cited by 73 publications

(81 citation statements)

References 14 publications

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“…Comparisons across individual trials can be questionable. For example, inflammatory reactions induced by three times the minimal erythema dose of UVB in healthy subjects measured by laser Doppler flowmetry, as well as the presence and/or magnitude of secondary hyperalgesia, have shown quite different results in trials of apparently similar design [16,25,37]. However, comparative studies with several skin models may be relevant in the search for pivotal mediators of hyperalgesia in the skin during the life cycle of inflammation.…”

Section: Discussionmentioning

confidence: 99%

A novel model of inflammatory pain in human skin involving topical application of sodium lauryl sulfate

2010

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Section: Discussionmentioning

confidence: 99%

A novel model of inflammatory pain in human skin involving topical application of sodium lauryl sulfate

2010

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“…This contrasts with the situation in individuals with injuries such as sunburn and other dermatological conditions where heat pain threshold drops substantially, for whom peripherally acting COX2 inhibitors may be more effective (62,63).…”

Section: Figurementioning

confidence: 92%

COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice

Vardeh

Wang²,

Costigan³

et al. 2009

J. Clin. Invest.

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A cardinal feature of peripheral inflammation is pain. The most common way of managing inflammatory pain is to use nonsteroidal antiinflammatory agents (NSAIDs) that reduce prostanoid production, for example, selective inhibitors of COX2. Prostaglandins produced after induction of COX2 in immune cells in inflamed tissue contribute both to the inflammation itself and to pain hypersensitivity, acting on peripheral terminals of nociceptors. COX2 is also induced after peripheral inflammation in neurons in the CNS, where it aids in developing a central component of inflammatory pain hypersensitivity by increasing neuronal excitation and reducing inhibition. We engineered mice with conditional deletion of Cox2 in neurons and glial cells to determine the relative contribution of peripheral and central COX2 to inflammatory pain hypersensitivity. In these mice, basal nociceptive pain was unchanged, as was the extent of peripheral inflammation, inflammatory thermal pain hypersensitivity, and fever induced by lipopolysaccharide. By contrast, peripheral inflammation-induced COX2 expression in the spinal cord was reduced, and mechanical hypersensitivity after both peripheral soft tissue and periarticular inflammation was abolished. Mechanical pain is a major symptom of most inflammatory conditions, such as postoperative pain and arthritis, and induction of COX2 in neural cells in the CNS seems to contribute to this.

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“…The sunburn model uses UVB irradiation to induce stable primary and secondary hyperalgesia. [16] The primary area…”

Section: Pharmacodynamics Assessmentmentioning

confidence: 99%

“…[13] The sunburn model is used in a simplified way as previously described [18] for assessing the central and peripheral analgesic effect of paracetamol and ketorolac, respectively. The sunburn model has been characterized and validated by another research group; [16] however it has not been fully characterized when used in a simplified way, [18] that is by estimating the dose of UVB according to the volunteers' skin type. Moreover this model has never been used for assessing the effect of a combination of analgesics that act on different targets.…”

Section: Pharmacodynamics Assessmentmentioning

confidence: 99%

Validation of the Simplified UVB Model to Assess the Pharmacodynamics of Analgesics in Healthy Human Volunteers

Lorenzini

Besson²,

Daali³

et al. 2012

Chimia

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A pharmacokinetic/pharmacodynamic, randomized, crossover, placebo-controlled study was conducted in healthy human volunteers with the primary objective of exploring the existence of a positive interaction between paracetamol 1 g and ketorolac 20 mg intravenously on experimental pain models. Further, the simplified UVB model was validated as a screening tool for analgesics or a combination of analgesics in clinical drug development. It was observed that the UVB irradiation induced primary hyperalgesia, evidenced by significant decreases of the heat pain threshold from (mean ± SD) 46.9 ± 1.1°C to 40.1 ± 1.7°C (p<0.001) and of the mechanical pain threshold (62% decrease). A small intra-and inter-individual variability was observed as well as consistent intra-day stability for the heat pain threshold. The UVB irradiation also resulted in the development of an area of secondary hyperalgesia of 21.3 ± 11.3 cm 2 . The mechanical pain threshold and area of secondary hyperalgesia showed small intra-individual variability and consistent intra-day stability. However, a greater variability was observed between subjects, which suggests that a crossover design would allow limiting the number of subjects.

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The Sunburn Pain Model: The Stability of Primary and Secondary Hyperalgesia Over 10 Hours in a Crossover Setting

Abstract: The sunburn pain model provides a long time course of stable hyperalgesia with a high within-day stability and between-day repeatability for primary and secondary hyperalgesia.

Cited by 73 publications

References 14 publications

A novel model of inflammatory pain in human skin involving topical application of sodium lauryl sulfate

A novel model of inflammatory pain in human skin involving topical application of sodium lauryl sulfate

COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice

Validation of the Simplified UVB Model to Assess the Pharmacodynamics of Analgesics in Healthy Human Volunteers

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