Lactose breath test (LBT) is considered the gold standard for the diagnosis of lactose malabsorption. The test is considered positive for a peak of hydrogen (H2) ≥ 20 parts per million (ppm) above the baseline. Some patients (pts) showed a rapid peak between 30 and 90 minutes after lactose ingestion. The aim of this study was to evaluate the predictive value of an early peak during a LBT and an accelerated oro-cecal transit time (OCTT). We retrospectively analyzed all pts who referred to our Gastroenterology unit for Irritable Bowel Syndrome, from January to September 2012, who performed LBT, glucose and lactulose breath test. We consider a positive LBT for a peak of H2 > 20 ppm, a positive GHBT for a peak >12 ppm and we considered a normal OCCT a peak of H2 ≥ 10 ppm between 75 ± 105 min after lactulose load. The correlation between LBT and OCTT was evaluated by Pearson score. 93 pts (65 F/28 M mean age 47 ± 6 years) with a positive LBT, without small intestinal bacterial overgrowth were analyzed: 46 pts (32 F/14 M; mean age 48 ± 6 years) with an early peak (2 (≥20 ppm) were enrolled as case, and 47 pts matched for sex and age with a peak of H2 after 90 min were enrolled as controls. 72% (33/46) of the group with an early peak showed an accelerated, 17% (8/46) a normal and 11% (5/46) a delayed OCTT. Meanwhile, in control group 40.4% (19/47) showed a normal, 57.5% (27/47) a delayed and just 1 pts an accelerated OCTT. The specificity and sensibility of LBT for an accelerated OCTT were 97.9% and 71.7% respectively. The positive predictive value of LBT for an accelerated OCTT is 97.1%; the negative predictive value is 78%. There is a significant correlation between LBT and OCTT (p The presence of an early peak of H2 between 30 and 90 min after the ingestion of 25 gr of lactose could predict the presence of an accelerated OCTT in 97% of pts. If confirmed by further study, in this subset of pts, lactulose breath test for evaluating OCTT could be avoided.
The eosinophilic oesophagitis (EoE) is a chronic immune/antigen disorder of the oesophagus clinically characterized by dysphagia and pathologically by mucosa eosinophilic infiltration. Th2-type allergic reactions are considered having important roles in the aetiopathogenesis of EoE. Avoidance of food allergens, administration of steroidal anti-inflammatory medications and dilation of the oesophagus are the most important treatments. 'Systemic nickel allergy syndrome' (SNAS) interests about 20% of patients with nickel contact allergy which could present systemic cutaneous manifestations (urticaria, oedema, etc.) and also respiratory and digestive symptoms (meteorism, abdominal pain, diarrhoea, etc.). In the literature, it is demonstrated that nickel oral immunotherapy is effective in reducing symptoms of SNAS and in modulating inflammatory parameters. We describe the case of a 48-year-old woman suffering from EoE not responsive to the topical steroid administration and diagnosis of SNAS. The patient started nickel oral desensitization according to the literature protocol continuing nickel-free diet. After 1 year from the beginning of the treatment, during the maintenance dose (500 ng three times a week), she decreased gradually the dosage of immunotherapy and reintroduced all the culprit foods. After the immunotherapy interruption, during the free diet, she repeated the oesophagogastroscopy with a complete macroscopic and histological resolution. We showed the first case of an EoE in a patient affected by SNAS responsive to the nickel-free diet and the oral immunotherapy.
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