Masermic (Spain)

Background: The pathophysiological mechanism of eosinophilic esophagitis (EoE) is complex and is still being investigated. We believe that there is a group of patients with eosinophilic esophagitis which could be differentiated as having an allergic phenotype who exhibit a sensitization profile (aeroallergens, panallergens, foods and specific IgG4 levels) with significant differences compared to patients with conventional allergic disease without associated eosinophilic esophagitis and healthy controls. Method: We measured the prevalence of sensitization to aeroallergens, foods and panallergens by means of molecular diagnostic techniques (ImmunoCAPTM ISAC) and determined the levels of specific IgG4 against foods and eosinophilic-derived neurotoxin (EDN) (ImmunoCAP technology) in patients with EoE of an allergic phenotype to study whether there are statistically significant differences with respect to the control groups (patients with different allergic pathologies without EoE and healthy patients without documented allergies). The total number of patients under study was 118, distributed among the different study groups. The case group (Allergic phenotype EoE patients) had 48 subjects. The food and respiratory allergy control groups had 30 subjects each. Finally, we included 10 in the healthy control group. Results: We were able to identify statistically significant differences when comparing levels of food-specific IgG4. Milk, egg, wheat, nuts, soy, cod, and Pru p3/LTP stood out. We did not observe significant differences in relation to sensitization to aeroallergens, foods, or panallergens. We also did not observe differences in EDN levels. Conclusions: We present a study in which statistically significant differences in IgG4 levels were observed in response to different types of food, comparing patients with eosinophilic esophagitis of allergic phenotype (case group) against subjects with allergic pathology without EoE and healthy subjects (control groups). Determining whether the detected foods are clinically relevant or not in these patients would be fundamental to establishing their usefulness as a treatment alternative in our patients.

Background/Objectives: Osteoporosis is considered a surgical indication in primary hyperparathyroidism (PHPT), regardless of menopausal status. This pilot study aimed to evaluate the impact of menopause and PHPT on bone mineral density (BMD) and to explore additional clinical factors that may influence bone health. Methods: We conducted an observational pilot study including 204 postmenopausal women with osteopenia or osteoporosis who underwent surgery for sporadic PHPT between 2009 and 2021 at Cruces University Hospital (Spain). Demographic data, anthropometric data, date of last menstrual period, years since menopause (YSM), and the clinical history of bone fragility were collected prior to parathyroidectomy. Biochemical parameters and months with hypercalcemia (MHCa)—as a surrogate for PHPT exposure—were analyzed. BMD results were expressed as a densitometric index, the T-Score. Results: Higher age (p = 0.043), greater body mass index (BMI) (p = 0.039), more YSM (p = 0.027), lower serum calcium levels (s-Ca) (p = 0.04), and glucocorticoid treatment antecedents (GcT) (p = 0.029) were all significantly associated with femoral osteoporosis. Similarly, higher weight (p = 0.004), greater MHCa (p = 0.01), lower height (p = 0.01) and s-Ca levels (p = 0.002) were significantly associated with spinal osteoporosis. Furthermore, logistic regression multivariate analysis determined that femur density was independently influenced by YSM (p < 0.001), s-Ca (p = 0.018), BMI (p = 0.002) and GcT (p = 0.006). Osteoporosis of the spine was also independently associated with YSM (p = 0.036), s-Ca (p = 0.031) and also with body weight (p = 0.003). Conclusions: The duration of menopause (YSM), rather than PHPT severity, is an independent predictor of osteoporosis in postmenopausal women.

Potential conflict of interest: Nothing to report. To the Editor: We have read with great interest the article by Lainé et al.1 They concluded that in dysmetabolic iron overload syndrome patients, iron depletion by phlebotomy did not improve metabolic and hepatic features, was not well tolerated, and was associated with weight gain. In their study, dysmetabolic iron overload syndrome patients had a liver iron concentration (LIC) >50 μmol/g by magnetic resonance imaging.2 Our group3 has published a study that provides further evidence that LIC is not raised in patients with hyperferritinemia and metabolic syndrome. Patients with dysmetabolic hyperferritinemia (metabolic syndrome and hyperferritinemia) have a mean LIC within normal values, and LIC in patients with dysmetabolic hyperferritinemia have no significant differences from patients with hyperferritinemia and without metabolic syndrome. This points toward the importance of ferritin as a marker of inflammation rather than clinically important hepatic iron deposition and provides caution when interpreting these values and making subsequent clinical management decisions, for example, whether to perform a phlebotomy.4 The LIC determination in Lainé et al.'s study1 was performed by magnetic resonance imaging, using Rennes University's calculation model.2 This method has a tendency to overestimate LIC, which limits the diagnostic performance and accuracy for clinical practice.5 In a study with 171 biopsied patients, 43% of patients with no iron overload were diagnosed using MRI as having liver iron overload and 45% of patients with moderate iron overload were diagnosed as having high iron overload. The specificity for the absence of liver iron overload was 57%.5 We can expect that an important group of Lainé et al.'s 274 patients may have been overestimated for LIC values. Probably, the real LIC values were lower than those published.

ABSTRACTBackground:Celiac disease (CD) is an autoimmune enteropathy that develops in genetically susceptible individuals exposed to gliadin. Early diagnosis of CD may reduce the risk of complications, and several studies have related the duration of gluten exposure to the risk of other autoimmune diseases. It has been proposed that silent CD be diagnosed as soon as possible to avoid potential complications.Objectives:The purpose of this study was to determine the prevalence of CD among children less than 3 years and to provide treatment to those patients diagnosed with CD.Patients and Methods:Parents of 1100 healthy children born between October 1998 and December 1999 were asked at the time of delivery to enroll their children in a program for the early diagnosis of CD. The parents of 830 children agreed to participate. Patients in the study were examined and anti–tissue transglutaminase antibody was first measured at about 1.5 years of age. A second antibody titer was obtained at about 2.5 years of age. Patients with detectable autoantibodies underwent intestinal biopsy for confirmation of CD.Results:Of the 830 children initially enrolled, 613 and 484 returned for the first and second visits, respectively. None had anti–tissue transglutaminase antibodies at the first visit, but 9 had anti–tissue transglutaminase immunoglobulins at the second visit. In 7 of these 9, intestinal biopsy confirmed the diagnosis of CD which suggests a minimum prevalence of CD of 1 per 118 healthy newborns.Conclusions:The authors observed a very high prevalence of CD, comparable to that observed in other European populations, which might even be higher if all of the children initially examined had returned for their second visit. If general screening for CD were accepted, the authors would recommend age 2–3 years as the best time for measuring tissue transglutaminase antibodies.

Helicobacter pylori is the major cause of peptic ulcer disease, but the proportion of H. pylori-negative peptic ulcers seems to be increasing in developed countries. We investigated the frequency of H. pylori-negative peptic ulcer without intake of nonsteroidal anti-inflammatory drugs (NSAIDs) in a Mediterranean European country. We prospectively collected consecutive patients with an endoscopically verified active peptic ulcer over 6 months from different areas of Spain. Helicobacter pylori infection was assessed by rapid urease test and histologic examination (corpus and antral biopsies). A (13)C-urea breath test was performed if H. pylori was not detected with the invasive test. Patients were considered H. pylori-negative if all three tests were negative. NSAID use was determined by structured data collection. Of 754 consecutive peptic ulcer patients, 16 (2.1%) were H. pylori-negative and had not used NSAIDs before the diagnosis. Of the 472 patients who had duodenal ulcers, 95.7% (n = 452) were H. pylori-positive and only 1.69% (n = 8) were negative for both H. pylori infection and NSAID use; 193 patients had benign gastric ulcers and 87% (n = 168) of them were infected by H. pylori (p <.001 vs. duodenal ulcers). NSAID intake was more frequent in gastric ulcer patients (52.8%) than in duodenal ulcer patients (25.4%; p <.001). Consequently, the frequency of H. pylori-negative gastric ulcer in patients not using NSAID was 4.1% (n = 8). Peptic ulcer disease is still highly associated with H. pylori infection in southern Europe, and only 1.6% of all duodenal ulcers and 4.1% of all gastric ulcers were not associated with either H. pylori infection or NSAID use.