Effect of Helicobacter pylori eradication therapy on clinical and laboratory biomarkers associated with gastric damage in healthy school-aged children: A randomized non-blinded trial.

OBJECTIVES: Helicobacter pylori (H. pylori) is the primary cause of gastric cancer and eradication in healthy adults has proven effective in decreasing cancer incidence. H. pylori is acquired largely in early childhood, however, the benefits of eradication in children are controversial. We aimed to determine the effect of H. pylori eradication on clinical and laboratory markers associated with gastric damage in apparently healthy school-aged children. METHODS: This was a pilot non-blinded trial including 61 children persistently infected with H. pylori who were randomized to eradication/no treatment and followed for at least 12 months, evaluating clinical and blood markers (Pepsinogen I (PGI) and II (PGII) determined by ELISA) associated with gastric damage. The treatment consisted of a sequential scheme including 7 days of omeprazole + amoxicillin followed by 7 days of omeprazole + clarithromycin + metronidazole; adherence and tolerance were surveyed. Eradication rates were assessed by stool antigen detection or urea breath test 1 month following treatment every 4 months thereafter to detect reinfection. RESULTS: Eradication occurred in 30/31 treated children (median age: 8.8, range: 7.9-10.8) and in 0/30 non-treated controls (median age: 8.6, range: 7.9-11) (p < .001). Treatment was associated with mild transient symptoms (altered taste, nocturnal upper abdominal pain, nausea, and diarrhea). Baseline frequency of symptoms was low and eradication did not change symptoms compared to controls. PGI, PGII, and anti-H. pylori seropositivity were similar in both groups at baseline and significantly decreased only in eradicated patients; PGI (92.5 vs. 74.4, p < .001), PGII (15.2 vs. 8.9, p < .001) levels, and frequency of anti-H. pylori seropositivity (100 vs. 68%, p < .001) respectively. Four eradicated children (13%) were reinfected during follow-up. CONCLUSIONS: H. pylori eradication therapy in apparently asymptomatic school-aged children was well tolerated and associated with decreased serum PGI and PGII levels. Future studies should expand on the middle-long-term effect of early H. pylori eradication, especially on preventing gastric cancer.

Helicobacter pylori, clinical, laboratory, and noninvasive biomarkers suggestive of gastric damage in healthy school-aged children: A case-control study.

BACKGROUND: Helicobacter pylori is acquired largely in early childhood, but its association with symptoms and indirect biomarkers of gastric damage in apparently healthy children remains controversial. We aimed to relate persistent H. pylori infection in apparently healthy school-aged children with clinical, laboratory, and noninvasive biomarkers suggestive of gastric damage using a case-control design. MATERIALS AND METHODS: We followed up 83 children aged 4-5 years with persistent H. pylori infection determined by stool antigen detection and/or a urea breath test and 80 noninfected matched controls from a low-income to middle-income, periurban city in Chile for at least 3 years. Monitoring included clinical visits every 4 months and annual assessment by a pediatric gastroenterologist. A blood sample was obtained to determine laboratory parameters potentially associated with gastric damage (hemogram and serum iron and ferritin levels), biomarkers of inflammation (cytokines, pepsinogens I and II, and tissue inhibitor metalloproteinase 1), and expression of cancer-related genes KLK1, BTG3, and SLC5A8. RESULTS: Persistently infected children had higher frequency of epigastric pain on physical examination (40% versus 16%; P = 0.001), especially from 8 to 10 years of age. No differences in anthropometric measurements or iron-deficiency parameters were found. Persistent infection was associated with higher levels of pepsinogen II (median 12.7 ng/mL versus 9.0 ng/mL; P < 0.001); no difference was observed in other biomarkers or gene expression profiles. CONCLUSIONS: H. pylori infection in apparently asymptomatic school-aged children is associated with an increase in clinical symptoms and in the level of one significant biomarker, pepsinogen II, suggesting early gastric involvement.

First Report of Tocilizumab Use in a Cohort of Latin American Patients Hospitalized for Severe COVID-19 Pneumonia.

Introduction/objectives: An interleukin-6 inhibition strategy could be effective in selected COVID-19 patients. The objective is to present our experience of tocilizumab use in patients with severe COVID-19. Methods: Observational retrospective cohort study. Hospitalized patients were evaluated by our multidisciplinary team for eventual use of tocilizumab. Patients with progressive ventilatory impairment and evidence of a hyperinflammatory state despite usual treatment received tocilizumab 8 mg/kg intravenous (maximum dose 800 mg), in addition to standard treatment. The use and time of use of mechanical ventilation (MV), the change of the Alveolar-arterial (A-a) gradient, of the ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2) and of inflammation laboratory parameters after 72 h of tocilizumab use was evaluated. Results: 29 patients received tocilizumab. 93.1% were men, 37.9% were obese, and 34.5% had hypertension. Of the 20 patients who were not on MV when receiving tocilizumab, 11 required non-invasive MV, for an average of 5 days, and one of them required intubation. A-a gradient, PaO2/FiO2, and inflammation parameters improved significantly. A better lymphocyte count, which improved significantly after tocilizumab use, was significantly associated with less use of MV. Five patients presented positive culture samples after tocilizumab, three being of clinical significance. A lower lymphocyte count was associated with having a positive culture. No other significant adverse events were seen. Conclusion: Our study suggests the utility and shows the safety of tocilizumab use in COVID-19 patients who have respiratory failure and evidence of hyperinflammation. Lymphocyte improvement was a predictor of good response.

Orofacial granulomatosis and diet therapy: a review of the literature and two clinical cases.

Orofacial granulomatosis is a nonspecific term that contains a wide variety of granulomatous entities, which share a clinical and histopathological presentation. It manifests as persistent or recurrent orofacial swelling, amongst other findings. Idiopathic orofacial granulomatosis, characterized by an absence of systemic granulomatous disease, is a diagnosis of exclusion. The main differential diagnosis is Crohn's disease. Its pathogenesis is unknown, however, it seems to be immune-mediated. Patch-test sensitivity to multiple allergens is well documented. Currently, therapeutic options consider restrictive diets, topical, intralesional, and systemic agents. First-line therapy is currently a matter of debate. We present a review of the value of diet therapy in this syndrome, along with two illustrative cases.

Orofacial granulomatosis and diet therapy: a review of the literature and two clinical cases

Abstract: Orofacial granulomatosis is a nonspecific term that contains a wide variety of granulomatous entities, which share a clinical and histopathological presentation. It manifests as persistent or recurrent orofacial swelling, amongst other findings. Idiopathic orofacial granulomatosis, characterized by an absence of systemic granulomatous disease, is a diagnosis of exclusion. The main differential diagnosis is Crohn's disease. Its pathogenesis is unknown, however, it seems to be immune-mediated. Patch-test sensitivity to multiple allergens is well documented. Currently, therapeutic options consider restrictive diets, topical, intralesional, and systemic agents. First-line therapy is currently a matter of debate. We present a review of the value of diet therapy in this syndrome, along with two illustrative cases.

[Prevalence of primary antiretroviral resistance among HIV infected patients in Chile]. / Prevalencia de resistencia primaria en pacientes con infección reciente por VIH-1 en Chile.

BACKGROUND: The main cause of virological failure during AIDS treatment is the resistance to antiretroviral medications (ARV). AIM: To search for mutations associated with ARV resistance in recently HIV-1 infected patients naïve to treatment, in Chile. MATERIAL AND METHODS: Patients over 18 years old with HIV-1 infection, naïve to anti-retroviral drugs before the study were included. Patients with CD4 cell counts less than 200 cells/mm3, viral load below 2000 copies/mL or any condition indicative of advanced AIDS were excluded. Criteria for diagnosis of recent infection (< 18 months) were a previous negative test for HIV antibodies or a history of an acute retroviral syndrome in the past 18 months. Resistance to drugs was analyzed using the TRUGENE HIV-1 assay from Bayer and the OpenGene DNA sequencing system. RESULTS: Ninety nine percent of patients had at least one mutation, 27% had 4 or more mutations, but high level resistance to ARV was found only in 2.7% of cases. Point mutations for non nucleoside reverse transcriptase inhibitors (NNRTI) were detected in 4.1% of cases (K103N in 1 patient, V179D in 2 patients), for nucleoside reverse transcriptase inhibitors (NRTI) in 8.1% of cases (T215S in 1 patient, V118I in 4 patients, M41L in 1 patient) and for protease inhibitors (PI) in 1.3% of cases. All mutations detected in the protease gene were secondary. Of these, the most common were L63P/T (38 patients), L10I/V (27 patients) and V77I (26 patients). Resistance to two or more antiretroviral classes was not detected. CONCLUSIONS: This study supports that, by now, primary resistance has a low prevalence in Chile. Therefore, a genotyping test before starting antiretroviral therapy is not necessary.

Novel recombinant norovirus causing outbreaks of gastroenteritis in Santiago, Chile.

Capsid and polymerase (RdRp) genes of 13 norovirus outbreak strains from Chile were compared. The genes sequences were discordant for five strains, and recombination was confirmed for two of them by amplification of a 1,360-bp gene segment containing a fragment of both genes. These strains belonged to a novel genogroup by RdRp sequence and to genogroup GII/3 by capsid sequence. Determining the clinical and epidemiological impact of human calicivirus recombination will require future studies.

Caliciviruses and foodborne gastroenteritis, Chile.

Human caliciviruses caused 45% of 55 gastroenteritis outbreaks occurring in Santiago, Chile, during 2000-2003. Outbreaks affected ?99 persons, occurred most commonly in the home, and were associated with seafood consumption. Thirteen outbreak strains sequenced were noroviruses, including 8 GII, 2 GI, and 3 belonging to a novel genogroup.