An epidemic of allergic contact dermatitis caused by a new allergen, caprylhydroxamic acid, in moisturizers.

BACKGROUND: In 2016, dermatologists in Finland suspected contact allergy in several patients using moisturizers under the trade name Apobase®. Following a formulation change, Phenostat™, which is a mixture of phenoxyethanol, caprylhydroxamic acid, and methylpropanediol, was used as a preservative in Apobase® moisturizers in Finland. OBJECTIVES: To confirm the suspected contact allergy to Apobase® cream, oily cream, and/or lotion, and to identify the specific contact allergen and define its optimal patch test concentration. METHODS: Thirty-nine patients with suspected contact allergy to Apobase® creams or lotion were patch tested in four Finnish dermatological clinics. The patch tests included old and new Apobase® formulas and their preservative agents: phenoxyethanol, methylpropanediol, and dilution series of Phenostat™ and caprylhydroxamic acid or its potassium salt. RESULTS: The patch tests showed positive reactions to the new Apobase® formulas, Phenostat™, and caprylhydroxamic acid or its potassium salt, but not to the old Apobase® formulas, methylpropanediol, or phenoxyethanol. CONCLUSIONS: We found a new contact allergen, caprylhydroxyamic acid, which caused an epidemic of allergic contact dermatitis in patients using moisturizers containing this preservative. Whether the sensitizing capacity of caprylhydroxamic acid depends on the other chemicals used in Apobase® moisturizers needs further investigation.

Contact sensitization to methylisothiazolinone in Finland--a multicentre study.

BACKGROUND: Antimicrobials constitute the second most common cause of contact allergy to cosmetics. Methylisothiazolinone (MI), previously always used together with methylchloroisothiazolinone (MCI), has recently been approved in the EU for use on its own in cosmetics and also various industrial products. MCI has been classified as an extreme-strong and MI as a strong-moderate sensitizer. OBJECTIVES: To study the frequency of positive patch test reactions to MI, and its relevance and relation to MCI/MI sensitivity, in Finland. METHODS: Over a period of 3 years (2006-2008), MI 0.1% (1000 ppm) and 0.03% (300 ppm) were patch tested in 10,821 patients at eight Finnish dermatological clinics. During 2008, patients with positive reactions to MI were asked to take part in a repeated open application test (ROAT). RESULTS: Of the patients tested, 1.4% and 0.6% showed positive patch test reactions to 0.1% and 0.03% MI, respectively. Sixty-six per cent of those who were MI-positive were also positive to 100 ppm MCI/MI. Thirty-three agreed to undergo the use test, and 10 of these gave positive results (30%). CONCLUSIONS: Our data show that MI used alone also potentially induces contact allergy. Careful monitoring is needed to determine whether or not this antimicrobial is safe to use in cosmetics.

Sensitization to thiourea derivatives among Finnish patients with suspected contact dermatitis.

BACKGROUND: Thiourea derivatives in rubber products may induce contact sensitization and allergic contact dermatitis. Sensitization is most often from neoprene rubber, but the multitude of possible sensitizing products has remained poorly characterized. OBJECTIVE: The aim of this study was to collect information on the occurrence of thiourea-related contact allergy and to show novel sources of sensitization. PATIENTS AND METHODS: A mixture of dibutyl-, diethyl-, and diphenylthiourea was included in patch test baseline series in five Finnish dermatology clinics during 2002-2007. In addition, an extended series of rubber chemicals was tested in patients with suspected rubber allergy. Sources of sensitization to thioureas were analysed in sensitized patients. RESULTS: Thiourea mix yielded positive patch test reactions in 59 of 15,100 patients (0.39%); 33/59 patients were also tested with individual rubber chemicals. Diethylthiourea was positive in 24/33, diphenylthiourea in 5, and dibutylthiourea in 1 patient. The most common sources of sensitization included various neoprene-containing orthopaedic braces, sports equipment, and foot wear. CONCLUSIONS: The sources of sensitization to thiourea chemicals were detected in most cases. These sources comprise a heterogenous group of products extending from orthopaedic materials to sports equipment.

Lactase-induced occupational protein contact dermatitis and allergic rhinoconjunctivitis.

Enzymes are high-molecular-weight proteins and highly sensitizing occupational allergens used widely in industrial processes. Lactase has been described to cause work-related respiratory and conjunctival immunoglobulin (Ig)-E-mediated sensitizations in workers in the pharmaceutical industry. In these previous reports, allergic rhinoconjunctivitis or asthma was confirmed with prick tests but not by challenge tests. Lactase previously has not been described as a cause of immediate or delayed contact skin reaction. Furthermore, there are no previous reports of lactase-specific IgE. We report a case of protein contact dermatitis and allergic rhinoconjunctivitis from occupational exposure to lactase in a pharmaceutical worker. The patient exhibited strong positive responses to lactase in prick tests. In an open application test, lactase elicited whealing, and in patch testing, lactase elicited an eczematous reaction. Serum lactase-specific IgE antibodies were demonstrated in immunospot and radioallergosorbent test assays, and lactase-IgE-binding fractions and their specificities were examined in immunoblot and immunoblot inhibition assays. The chamber challenge test was performed to detect the association between lactase sensitization and rhinoconjunctival symptoms. Our results have confirmed the previous observations that lactase can induce occupational IgE-mediated respiratory and conjunctival sensitizations, but they show that contact skin reactions caused by lactase may also occur.

Deer ked-induced occupational allergic rhinoconjunctivitis.

BACKGROUND: Deer keds (elk fly) have not previously been described as a cause of respiratory or conjunctival sensitization. OBJECTIVE: To report a case of IgE-mediated allergic rhinoconjunctivitis from occupational exposure to deer ked. METHODS: Skin prick testing (SPT) was performed with pollens, animal danders, mites, molds, and deer ked. The serum deer ked-specific IgE level was examined in ImmunoSpot and radioallergosorbent test assays, and deer ked IgE-binding fractions and their specificities were examined in immunoblot and immunoblot inhibition assays. Nasal provocation testing (NPT) and conjunctival provocation testing (CPT) were performed to detect the association between deer ked sensitization and rhinoconjunctival symptoms. Both SPT and NPT were performed with deer ked whole-body extract, whereas CPT was performed with deer ked wing. RESULTS: The results of SPT, NPT, and CPT were positive for deer ked. In laboratory tests, serum deer ked-specific IgE antibodies were demonstrated in radioallergosorbent test and ImmunoSpot assays. In immunoblot, IgE-binding bands were demonstrated at 17, 33, 70, and 85 kDa, which were clearly inhibited with deer ked extract but not with the control extract. CONCLUSIONS: Occupational IgE-mediated rhinoconjunctival allergy to deer ked was confirmed in this patient.