Analysis of antibody reactivity against cysteine sulfinic acid decarboxylase, a pyridoxal phosphate-dependent enzyme, in endocrine autoimmune disease

The structurally related group II pyridoxal phosphate (PLP)-dependent amino acid decarboxylases glutamic acid decarboxylase (GAD), aromatic L-amino acid decarboxylase (AADC), and histidine decarboxylase (HDC) are known autoantigens in endocrine disorders. We report, for the first time, the prevalence of serum autoantibody reactivity against cysteine sulfinic acid decarboxylase (CSAD), an enzyme that shares 50% amino acid identity with the 65- and 67-kDa isoforms of GAD (GAD-65 and GAD-67), in endocrine autoimmune disease. Three of 83 patients (3.6%) with autoimmune polyendocrine syndrome type 1 (APS1) were anti-CSAD positive in a radioimmunoprecipitation assay. Anti-CSAD antibodies cross-reacted with GAD-65, and the anti-CSAD-positive sera were also reactive with AADC and HDC. The low frequency of anti-CSAD reactivity is in striking contrast to the prevalence of antibodies against GAD-65, AADC, and HDC in APS1 patients, suggesting that different mechanisms control the immunological tolerance toward CSAD and the other group II decarboxylases. Moreover, CSAD may be a useful mold for the construction of recombinant chimerical antigens in attempts to map conformational epitopes on other group II PLP-dependent amino acid decarboxylases.     

Permeability of different types of medical protective gloves to acrylic monomers

Dental personnel and orthopedic surgeons are at risk when manually handling products containing methyl methacrylate (MMA). Dental products may also contain cross-linking agents such as ethylene glycol dimethacrylate (EGDMA) or 1,4-butanediol dimethacrylate (1,4-BDMA). Skin contact with monomers can cause hand eczema, and the protection given by gloves manufactured from different types of material is not well known. The aim of this study was to determine the breakthrough time (BTT, min) as a measure of protection (according to the EU standard EN-374-3) for a mixture consisting of MMA, EGDMA and 1,4-BDMA. Fifteen different gloves representing natural rubber latex material, synthetic rubber material (e.g. nitrile rubbers), and synthetic polymer material were tested. The smallest monomer MMA permeated within 3 min through all glove materials. A polyethylene examination glove provided the longest protection period to EGDMA and 1, 4-BDMA (> 120 min and 25.0 min), followed by the surgical glove Tactylon (6.0 min and 8.7 min) and the nitrile glove Nitra Touch (5.0 min and 8.7 min). This study showed that the breakthrough time (based on permeation rate) cannot be regarded as a 'safe limit'. When the permeation rate is low, monomers may have permeated before BTT can be determined. Using double gloves with a synthetic rubber inner glove and a natural rubber outer glove provided longer protection when the inner glove was rinsed in water before placing the outer glove on top.     

Mutational analysis of the autoimmune regulator (AIRE) gene in sporadic autoimmune Addison's disease can reveal patients with unidentified autoimmune polyendocrine syndrome type I

OBJECTIVE: To investigate whether patients with Addison's disease and polyendocrine syndromes have undiagnosed autoimmune polyendocrine syndrome type I (APS I). MATERIALS AND METHODS: Forty patients with clinical manifestations resembling APS I and with autoantibodies typical of this condition were screened for Norwegian autoimmune regulator (AIRE) gene mutations. RESULTS: A 30-year old man who had developed Addison' s disease at the age of 12, but had no other components of APS I, was homozygous for the 1094-1106 deletion mutation in exon 8 of the AIRE gene, the most common mutation found in Norway. CONCLUSIONS: APS I patients with milder and atypical phenotypes are difficult to diagnose on clinical grounds. Autoantibody analysis and mutational analysis of AIRE may therefore be helpful modalities for identifying these individuals.     

Sleep disturbances in patients with Addison's disease

OBJECTIVE: The standard replacement therapy in Addison's disease does not restore normal nocturnal levels of the hormones of the hypothalamic-pituitary-adrenal axis. The aim of the study was to describe the prevalence and characteristics of sleep disturbances in patients with Addison's disease. METHODS: Sixty patients completed a self-administered sleep questionnaire and the Epworth Sleepiness Scale (ESS) questionnaire. Activity-based monitoring (actigraph recordings) and sleep diaries were obtained from eight patients. RESULTS: Thirty-four percent reported weekly sleep disturbances (difficulties falling asleep in 13%; repeated awakenings in 14%; early morning awakenings in 20%). The sleep need was 8.21 h (s.d. 1.34; range 6-14 h), and sleep onset latency was 29 min (s.d. 29, range 2-150 min). Forty percent of the patients were tired during daily activities more than once a week, but the scores of the ESS were 6.0 (s.d. 3.5), which is not higher than normal. The actigraph recordings showed higher sleep efficiency than the subjective recordings. CONCLUSION: We did not identify specific sleep disturbances which were characteristic for patients with Addison's disease. Patients with Addison's disease have increased daytime fatigue, but no more daytime sleepiness than normal.