Piroxicam-induced Photosensitivity Research Articles

Topical Provocation in Fixed Drug Eruption from Nonsteroidal Anti-Inflammatory Drugs

Objective: Evaluate the importance of topical lesional provocation in the study of fixed drug eruption (FDE) from nonsteroidal anti-inflammatory drugs (NSAID). Patients and Results: We studied 14 patients with FDE imputed with high probability to piroxicam (8 patients), nimesulide (5) and feprazone (1). One patient with FDE from piroxicam suffered lesion reactivation after intravenous tenoxicam. The suspected drug and related compounds were patch tested on residual lesional skin and on the normal back skin. Positive results were obtained, only in affected areas, in 13 out of 14 patients (92.9%): in all cases due to feprazone and nimesulide and in 7/8 cases of FDE due to piroxicam. The 7 patients reactive to piroxicam also had positive tests to tenoxicam, and 1 out of 5 reacted to meloxicam. None reacted to thiosalicylic acid. Comments and Conclusions: Topical lesional provocation is a safe, sensible and specific complementary method for drug imputation in FDE from these NSAID, namely for nimesulide, as it reproduced a positive test in the 5 patients. In the case of FDE from piroxicam, our studies confirm cross-reactivity with tenoxicam whereas in piroxicam-induced photosensitivity tenoxicam can be used safely. In photosensitivity the responsible moiety is a UVA photoproduct of piroxicam antigenically and structurally similar to thiosalicylic acid, a moiety which is not involved in FDE.

Oxicam-induced photosensitivity: Patch and photopatch testing studies with tenoxicam and piroxicam photoproducts in normal subjects and in piroxicam-droxicam photosensitive patients

The mechanism of piroxicam-induced photosensitivity is unknown. It was first attributed to metabolites of the drug produced in vivo but further photochemical studies disclosed that piroxicam was not stable to light, forming at least two photoproducts. Photosensitivity reactions to droxicam and tenoxicam have been not reported. The aim of this study was to determine whether piroxicam photoproducts contribute to the light reactions induced by this drug, to describe a case of droxicam-induced photosensitivity and to study the in vivo photosensitizing potential of tenoxicam. Patch and photopatch tests with two major photoproducts of piroxicam, with different preparations of UVA-preirradiated piroxicam, and with low and high concentrations of tenoxicam were performed in normal volunteers and in piroxicam-photosensitive patients. Phototesting studies were also performed before and after the oral administration of tenoxicam in both groups of subjects. Positive patch test responses were obtained in piroxicam-photosensitive patients only with the preirradiated piroxicam preparations. Phototesting studies with tenoxicam were normal in both groups. Minor or intermediate piroxicam photoproducts are more likely to be responsible for the photosensitivity reactions induced by this drug.

Sensitivity to thimerosal and photosensitivity to piroxicam

17 patients allergic to thimerosal, with no previous history of photosensitivity or piroxicam ingestion, 2 patients with piroxicam-induced photosensitivity, and 10 controls were patch or photopatch tested, with 1 or more of the following: thimerosal, thiosalicylic acid, irradiated and non-irradiated solutions of piroxicam alone, L-cysteine alone and piroxicam plus L-cysteine, and piroxicam in petrolatum., The results of the tests supported the hypothesis that there are cross-reactions between thiosalicylic acid and prioxicam, a photosensitizer. The mechanism of the cross-reactions may involve photoproducts of piroxicam and L-cysteine, as patients allergic to thiosalicylic acid, who have positive photopatch tests to piroxicam, also had positive patch tests to the irradiated solution of piroxicam plus L-cysteine.

Piroxicam-induced photosensitivity and contact sensitivity to thiosalicylic acid

A photocontact dermatitis developed in three patients after the application of gel containing 0.5% piroxicam. Patch tests were positive to thiomersal and thiosalicylic acid. Photopatch tests with piroxicam at several concentrations were positive in the three patients but negative in 62 normal volunteer subjects. Patch tests performed on 14 patients with proved systemic photosensitivity to piroxicam were positive for thiomersal and thiosalicylic acid. Nine of 12 patients previously sensitized to thiosalicylic acid and with no history of exposure to piroxicam showed positive photopatch test reactions to this chemical. These results support a relation between piroxicam-induced photosensitivity and contact sensitivity to thiosalicylic acid. Contact allergic sensitivity to the latter is a marker for patients with a high risk of developing photosensitivity reactions to piroxicam. These reactions may be due to photoproducts of the drug rather than metabolites.

Patients with piroxicam-induced photosensitivity are sensitive to thimerosal

Patients with piroxicam-induced photosensitivity are sensitive to thimerosal

Piroxicam-induced photosensitive dermatitis

Eleven patients had piroxicam-induced photosensitivity when first seen. Six were photopatch-tested to piroxicam (2%, 5%, 20% concentrations); all tests were positive. This same group were patch test-positive to thimerosal. Three of the eleven patients became persistent light reactors. Two additional patients developed persistent hand dermatitis.

Possible mechanism of piroxicam-induced photosensitivity

† The therapeutic use of piroxicam as a nonsteroidal anti-inflammatory agent is associated with the development of photosensitivity in less than 1% of patients. The eruption usually occurs within a few days of commencing treatment with the medication. This time course suggests a phototoxic reaction. Attempts to demonstrate the phototoxic effects of piroxicam in humans, laboratory animals, and in in vitro cell assays were unsuccessful. At high concentration, however, one metabolite of piroxicam was phototoxic in animal studies and in in vitro assays. A second metabolite was mildly phototoxic in laboratory animals. These results suggest a mechanism whereby piroxicam photosensitivity may be due to a metabolite preferentially formed or accumulated in affected patients. (<i>Arch Dermatol</i>1986;122:1283-1287)

Possible Mechanism of Piroxicam-Induced Photosensitivity

The therapeutic use of piroxicam as a nonsteroidal anti-inflammatory agent is associated with the development of photosensitivity in less than 1% of patients. The eruption usually occurs within a few days of commencing treatment with the medication. This time course suggests a phototoxic reaction. Attempts to demonstrate the phototoxic effects of piroxicam in humans, laboratory animals, and in in vitro cell assays were unsuccessful. At high concentration, however, one metabolite of piroxicam was phototoxic in animal studies and in in vitro assays. A second metabolite was mildly phototoxic in laboratory animals. These results suggest a mechanism whereby piroxicam photosensitivity may be due to a metabolite preferentially formed or accumulated in affected patients.

Piroxicam-induced photosensitivity: In vivo and in vitro studies of its photosensitizing potential

A 36-year-old woman developed a photolocalized erythematous papulovesicular eruption while taking piroxicam. Histologic study revealed a superficial and deep spongiotic dermatitis. Phototesting with ultraviolet B (UVB) and ultraviolet A (UVA) was abnormal at the time the patient was seen and after oral challenge with the drug for 5 days. A modified lymphocyte transformation test was positive. The photosensitizing potential of the drug was evaluated in vivo and in vitro. In vivo studies consisted of phototesting twelve medical students before and after intake of piroxicam during 5 consecutive days. No lowering of the minimal erythema dose (MED) values or abnormal reactions to UV and visible light were observed in these students. In vitro studies by the Candida plate method and by photohemolysis showed negative results. Our studies suggest a systemic photoallergy mechanism requiring wavelengths in the UVA range for the reaction. This drug should be avoided in patients receiving photochemotherapy.