Two patients with isoniazid-induced photosensitive lichenoid eruptions confirmed by photopatch test

Causative agents of drug eruptions are frequently unknown, and skin tests with candidate drugs would be useful before systemic challenge. It remains to be clarified how phostosentive lichenoid drug eruptions are induced, but allergy, including delayed type allergy, has been suggested. Two patients who had taken anti-tuberculous drugs developed a lichenoid drug eruption, primarily on sun-exposed skin. Patch and photopatch tests were performed with each of the ingested drugs (10% in petrolatum). Photopatch tests to isoniazid (INH) were positive. These were confirmed by oral challenge followed by irradiation with UVA. In conclusion, photopatch tests facilitated identification of the causative drug in two patients with photosensitive lichenoid eruptions to INH.     

Drug Eruption (Erythema Multiforme Type) Due to a Digestive Enzyme Drug

An 84-year-old Japanese male had pruritic indurated erythema on his upper limb and left lower abdomen, which had developed abruptly two months before visiting our hospital. Hematological examination showed eosinophilia, 550/mm³. Histopathological findings were suggestive of erythema multiforme in response to a drug. By means of patch tests and a p.o. challenge test, Aczym^®, a digestive enzyme drug, was shown to be the cause of his condition. Further study revealed that the specific ingredients involved were pancreatin and Taka-diastase. An eruption resulting from ingestion of a digestive enzyme drug has not previously been reported.     

Eczematous drug eruption from carbamazepine: coexistence of contact and photocontact sensitivity

We report a 46-year-old patient with an eczematous eruption on sun-exposed areas which we believe was caused by carbamazepine intake. Oral provocation with the drug produced papulo-vesicular eruptions that were greatly potentiated by long-wave ultraviolet irradiation. Positive reactions to carbamazepine were elicited by patch and photopatch tests and by lymphocyte stimulation tests 6 months after cessation of the intake of carbamazepine.     

Cross-reactivity among p-amino group compounds in sulfonamide fixed drug eruption: diagnostic value of patch testing

We studied 28 patients with fixed drug eruption (FDE) caused by sulfonamide antibiotics to investigate cross-reactivity between sulfonamide derivatives and p-amino compounds and to explore the usefulness of patch testing, as an alternative to controlled oral challenge testing (COCT), in diagnosis within this clinical area. COCT with sulfamethoxazole (SMX), sulfadiazine (SDZ), sulfamethizole (SMZ), furosemide (FU), procaine (PRO) and glipizide (GPZ) was performed. Patch testing (PT) with SMX and SDZ was carried out. In all patients, the diagnosis of FDE was confirmed by positive COCT and allergy to trimethoprim ruled out by COCT. 42.8 and 31.8% of the SMX-induced FDE patients reacted to SMZ and SDZ, respectively. All patients (n = 28) tolerated FU, PRO and GPZ. COCT performed with the 3 sulfonamide antibiotics in 12 patients was positive in 2 subjects with the 3 drugs, in 2 patients only with SMX and SMZ and in the remaining 8, SMX was the only causative drug. PT was positive in 5 of 25 patients positive on COCT. The probability of obtaining a positive PT was higher among patients who had a residual lesion than that among those who lacked this. Cross-reactivity between different sulfonamide antibiotics is thus variable, being most likely between SMX and SMZ. We have found no cross-reactivity between sulfonamide antibiotics and other sulfonamide derivatives or p-amino drugs in FDE. PT is a useful tool in the diagnosis of FDE, especially if there are residual lesions, because it avoided the need for COCT in 20% of patients.     

Mucha-Habermann disease-like eruptions due to Tegafur

The first case of Mucha-Habermann disease-like drug eruptions due to Tegafur is reported. A 59-year-old man noticed various skin lesions after he had taken 300 mg of Tegafur daily for about 200 days. The patient had papulonecrotic eruptions on his trunk and extremities. The histology from a papular lesion revealed epidermal necrosis surrounded by spongiosis, perivascular inflammatory infiltrations composed of lymphocytes and erythrocytes, and endothelial swelling. The etiology of Mucha-Habermann disease is not known, but an immune mechanism may be supported by our case.     

Cutaneous Reactions Induced by Calcium Channel Blocker: High Frequency of Psoriasiform Eruptions

Fifteen cases with cutaneous reactions to calcium channel blockers (Ca-antagonist), dihydropiridine (including nicardipine, nifedipine, nisoldipine), verapamil, and diltiazem are reported. The patients from Yokohama City University Hospital and affiliated hospitals included 4 males and 11 females with cardiovascular diseases. Their average age was 64.7 (54 to 82) years. They had been taking Ca-antagonists for an average of 95 days (7 days to 10 years) before they developed dermatitis. The frequency of reactions to Ca-antagonists was high with diltiazem (5/16: 31.25%) and dihydropyridine (7/16: 43.75%), including nifedipine (4/7), nisoldipine (1/7), and nicardipine (2/7). Stevens-Johnson syndrome (MCOS) was associated only with verapamil. A notable type of eruption was the psoriasiform type, including exacerbation of psoriasis, which was resolved or easily controlled after discontinuation of the drug. Provocation tests verified the Ca-antagonist as the cause in 7 cases of psoriasiform eruption. The frequency of positive patch tests to Ca-antagonists was low except for diltiazem. Patch tests with diltiazem showed positive reactions in 54% (7 of 13 patients), based on our experience and papers published in Japan. Ca-antagonists are occasional causes of a wide spectrum of cutaneous reactions and should also be considered as causative factors in patients who develop psoriasiform eruptions or in patients whose psoriasis is exacerbated while using these drugs.     

Drug eruption caused by ranitidine hydrochloride (Zantac) which showed a strong reaction in a drug-induced lymphocyte stimulation test

An 80-year-old male who developed a generalized papular erythema-type drug eruption after being treated with ranitidine hydrochloride is herein reported. The duration from the intake of the medicine to the onset of the eruption was 3 days, and the eruption remained unchanged for a week after withdrawal of the medicine and even after the eruption itself was treated. A diagnosis of drug eruption by ranitidine hydrochloride was confirmed based on a strongly-positive reaction of a drug-induced lymphocyte stimulation test (DLST).     

破伤风抗毒素所致药疹42例临床特点分析

目的：明确破伤风抗毒素所致药疹的临床特点。方法：对42例破伤风抗毒素所致药疹的临床资料进行回顾性分析。结果：42例患者中破伤风抗毒素皮试阴性40例,阳性2例。发疹潜伏期6 ~12天,平均为6.5天,皮疹表现为注射局部红斑2例,全身泛发性皮疹40例(发疹型6例,荨麻疹型32例,多型红斑型2例)。42例患者中伴发热5例,呕吐5例,关节痛12例。糖皮质激素治疗有效。结论：破伤风抗毒素所致药疹最常见类型为荨麻疹型,可伴发热、消化道症状及关节痛。药疹的发生与皮试结果无关。     

Lichenoid drug eruptions due to nandrolone furylpropionate (Demelon)

A case of lichenoid drug eruption due to nandrolone furylpropionate (Demelon) is reported. A 71-year-old man with aplastic anemia developed widespread erythema and reticulation with violaceous papules and pigmentation after receiving intramuscular injections of Demelon weekly for 2 months. The eruption gradually resolved after drug withdrawal, leaving reticular pigmentation. A biopsy specimen of the skin lesion showed lichenoid-type reactions including hydropic or colloid degeneration of the basal cells, sometimes with satellite necrosis, and a band-like subepidermal lymphocytic infiltrate. Most of the mononuclear cells stained strongly for helper/inducer T lymphocytes (Leu 3a).     

A Case of Eosinophilic Pustular Folliculitis (Ofuji's Disease) Induced by Patch and Challenge Tests with Indeloxazine Hydrochloride

A 73-year-old male developed disseminated erythema over his entire body after exposure to indeloxazine hydrochloride, a cerebral activator. Patch testing with indeloxazine hydrochloride showed a positive reaction, and plaques, vesicles and pustules developed on the face after the patch test. These had the pathologic feature of eosinophilic pustular folliculitis (EPF, Ofuji's disease). A challenge test also provoked eruptions on the face, trunk, arms and legs, which were compatible with EPF. Moreover, both the patch and challenge tests with indeloxazine hydrochloride induced eosinophilia. This is the first report of drug allergy-induced EPF, where drug sensitivity induced an abnormal eosinophilic response mimicking EPF.