Serum concentrations of mast cell tryptase are reduced in heavy drinkers.

BACKGROUND: Baseline serum tryptase concentrations are commonly used in clinical practice as a marker of the body's mast cell burden. This study aimed to investigate serum tryptase concentrations in heavy drinkers. METHODS: Serum tryptase concentrations were determined in 126 heavy drinkers (75% males, median age 47 years) who were admitted to the hospital because of alcohol withdrawal syndrome (n = 60), general symptoms with abnormalities on biochemical tests that indicated acute liver disease (n = 19), complications of advanced liver disease (n = 33), and miscellaneous reasons (n = 14). Results were compared with those of 70 healthy controls (66% males, median age 40 years). RESULTS: Serum tryptase concentrations were lower in heavy drinkers than in healthy controls (median 2.23 µg/l vs. median 3.25 µg/l, p < 0.001). Ten heavy drinkers (7.9%) had undetectable (<1 µg/l) serum tryptase levels versus none of the healthy controls (p = 0.01). The association of low tryptase levels with heavy drinking was independent of age, gender, and smoking status. Among heavy drinkers, the lowest tryptase concentrations were observed in patients with alcohol withdrawal syndrome and patients with general symptoms with abnormalities on biochemical tests that indicated acute liver disease. Furthermore, serum tryptase concentrations were negatively correlated with markers of acute liver damage or alcohol consumption (serum aspartate aminotransferase and gamma-glutamyl transferase). Atopy (skin prick test positivity) was not associated with serum tryptase concentrations in heavy drinkers. CONCLUSIONS: Serum concentrations of mast cell tryptase are lower in heavy drinkers than in healthy controls.

The longitudinal relationship of changes of adiposity to changes in pulmonary function and risk of asthma in a general adult population.

BACKGROUND: Adiposity has been linked to both higher risk of asthma and reduced lung function. The effects of adiposity on asthma may depend on both atopic status and gender, while the relationship is less clear with respect to lung function. This study aimed to explore longitudinal weight changes to changes in forced expiratory volume in first second (FEV1) and forced vital capacity (FVC), as well as to incident cases of asthma and wheezing, according to atopy and gender. METHODS: A general population sample aged 19-72 years was examined with the same methodology five years apart. Longitudinal changes in weight, body mass index, waist circumference, and fat percentage (bio-impedance) were analyzed with respect to changes of FEV1 and FVC (spirometry), and incidence of asthma and wheezing (questionnaire). Gender, atopy (serum specific IgE-positivity to inhalant allergens) and adipose tissue mass prior to adiposity changes were examined as potential effect modifiers. RESULTS: A total of 2,308 persons participated in both baseline and five-year follow-up examinations. Over the entire span of adiposity changes, adiposity gain was associated with decreasing levels of lung function, whereas adiposity loss was associated with increasing levels of lung function. All associations were dependent on gender (p-interactions < 0.0001). For one standard deviation weight gain or weight loss, FEV1 changed with (+/-)72 ml (66-78 ml) and FVC with (+/-)103 ml (94-112 ml) in males. In females FEV1 changed with (+/-) 27 ml (22-32 ml) and FVC with (+/-) 36 ml (28-44 ml). There were no changes in the FEV1/FVC-ratio. The effect of adiposity changes increased with the level of adipose tissue mass at the start of the study (baseline), thus, indicating an aggregate effect of the total adipose tissue mass. Atopy did not modify these associations. There were no statistically significant associations between changes in adiposity measures and risk of incident asthma or wheeze. CONCLUSIONS: Over a five-year period, increasing adiposity was associated with decreasing lung function, whereas decreasing adiposity was associated with increasing lung function. This effect was significantly greater in males than in females and increased with pre-existing adiposity, but was independent of atopy.

Association between loss-of-function mutations in the filaggrin gene and self-reported food allergy and alcohol sensitivity.

BACKGROUND: Loss-of-function mutations of the filaggrin (FLG) gene cause an impaired skin barrier and increase the risk of atopic dermatitis. Interestingly, FLG mutations have also been found to be associated with a high risk of peanut allergy. OBJECTIVE: We investigated the association of FLG mutations with self-reported food allergy, symptoms of oral allergy syndrome (OAS), and alcohol sensitivity. METHODS: A total of 3,471 adults from the general population participated in a health examination. Information on food allergies, OAS and alcohol sensitivity was obtained by questionnaire. FLG mutation carriers were defined as having at least one null mutation allele of R501X or 2282del4. Primary lactose intolerance (PLI) was defined as the C/C genotype of the rs4988235 polymorphism. RESULTS: FLG mutations were associated with a higher risk of self-reported allergy to eggs (OR 3.22 and 95% CI 1.46-7.11), milk (OR 2.10 and 95% CI 1.12-3.92), fish (OR 4.54 and 95% CI 1.88-10.96) and wheat (OR 3.59 and 95% CI 1.61-8.02), but not with symptoms of OAS (OR 1.05 and 95% CI 0.73-1.51). Serum-specific IgE was measured in a subsample and confirmed the association between FLG and IgE to milk. A significant gene-by-gene interaction between FLG and PLI was observed in relation to self-reported allergy to milk. Furthermore, FLG mutations were associated with a higher risk of alcohol sensitivity. CONCLUSIONS: We found that loss-of-function mutations in the FLG gene were significantly associated with self-reported food allergy and alcohol sensitivity, but not with OAS. These findings, if confirmed, support the idea that skin barrier functions may be involved in the pathogenesis of food allergy.