P176 A case of lupus enteritis successfully treated with anti-TNF alpha inhibitor

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COVID-19 vaccine immunogenicity in 16 patients with autoimmune systemic diseases. Lack of both humoral and cellular response to booster dose and ongoing disease modifying therapies

Patients with autoimmune systemic diseases (ASDs) represent a frail population during the ongoing COVID-19 pandemic. The vaccination is the major preventive measure; however, a significant number of ASD patients show an impaired production of anti-COVID-19 neutralizing antibodies (NAb), possibly counterbalanced by adequate T-cell response. The present study aimed at evaluating both humoral and cellular response to COVID-19 vaccine booster dose in this particular setting

Covid-19 And Rheumatic Autoimmune Systemic Diseases: Role of Pre-Existing Lung Involvement and Ongoing Treatments

The Covid-19 pandemic may have a deleterious impact on patients with autoimmune systemic diseases (ASD) due to their deep immune-system alterations

Recensiones

Manuel José Pedraza Gracia = Incunabula universitatis: los incunables de las bibliotecas universitarias españolas. Edición a cargo de Ramón Rodríguez Álvarez. Oviedo, Universidad de Oviedo, 2015. 313 p. ISBN: 978-84-16046-82-9.  Maria Gioia Tavoni = Atti del convegno Incunabula. Printing, Trading, Collecting, Cataloguing, 10-12 settembre 2013, La Bibliofilia, 116, n. 1/3 (2014). ISSN 0006-0941. Nicolás Bas Martín = Rosa M. GREGORI ROIG, La impressora Jerònima Galés i els Mey (València, segle XVI), Valencia, Biblioteca Valenciana, 2012. 611 p. ISBN 978-84-482-5722-4. Nicolás Bas Martín = Juan GOMIS COLOMA, Menudencias de imprenta. Producción y circulación de la literatura popular (Valencia, siglo XVIII), Valencia, Institució Alfons el Magnànim, 2015. 557 p. ISBN 978-84-7822-2015. Antonio Carpallo Bautista = José Luis GONZALO SÁNCHEZ-MOLERO, Leyendo a Edo. Madrid, Consejo Superior de Investigaciones Científicas, 2013, 163 p. ISBN: 978-84-00-09660-1

Salivary gland pathology in IgG4-related disease: A comprehensive review

IgG4-related disease (IgG4-RD) is a rare fibroinflammatory condition that can affect almost any organ, characterized by swollen lesions and often by eosinophilia and elevated serum IgG4 concentrations. The diagnosis of IgG4-RD is a challenging task: in fact, single or multiple organs can be affected and clinical, serological, and histological findings can be heterogeneous. In IgG4-RD, the involvement of salivary glands is observed in 27% to 53% of patients. Several organ-specific conditions, now recognized as different manifestations of IgG4-related sialadenitis (IgG4-RS), were viewed in the past as individual disease entities. The study of salivary glands may sometimes be complex, because of the number of pathological conditions that may affect them, often with overlapping clinical pictures. Integration of different imaging techniques is often required in the case of swelling of salivary glands, even though biopsy remains the gold standard for a definite diagnosis of IgG4-RS. Thus, in this review, we discuss new insights in the pathogenesis of IgG4-RD, focusing on its clinical aspects and the tools that are currently available for a correct differential diagnosis when the salivary glands are involved

IL-1 family cytokines and receptors in IgG4-related disease

BACKGROUND/AIM: The IgG4-related disease (IgG4-RD) is a fibroinflammatory condition that can affect almost any organ, often associated with eosinophilia and increased levels of IgE and IgG4. Overexpression in tissues of Th2-related cytokines but also of IFN-γ has been reported. Given the major role of Il-1 family cytokines in inducing and regulating inflammation, and the paucity of data so far available in IgG-RD, we performed a comprehensive analysis of IL-18, related IL-1 family cytokines and soluble receptors in these patients. PATIENTS AND METHODS: Fifteen patients fulfilling the criteria for the diagnosis of IgG4-RD and 80 blood donors as control were recruited. Cytokines of the IL-1 family (IL-1α, IL-1β, IL-33, IL-18), soluble receptors (sIL-1R1, sIL-1R2, sIL-1R3, ST2/sIL-1R4) and antagonists (IL-1Ra, IL-18 binding protein -IL-18BP-) were measured in sera by multiarray ELISA assay. Free IL-18 was calculated as the amount of IL-18 not inhibited by IL-18BP. RESULTS: Half of the patients had a multiorgan disease, mainly affecting retroperitoneum, lymph nodes and pancreas. sIL-1R1 (p=0.0001), sIL-1R2 (p=0.0024), ST2/sIL-1R4 (p=0.002) were significantly increased in IgG4-RD sera compared with healthy controls; sIL-R3 was significantly lower in patients vs controls (p=0,0006). CONCLUSIONS: The increased levels of the soluble forms of the two IL-1 receptors IL-1R1 and IL-1R2 suggest the need to dampen IL-1-mediated inflammation at the tissue level. Elevated circulating ST2/sIL-1R4 levels may represent the marker of an ongoing protective mechanism, but their contribution to organ damage cannot be excluded. On the whole, the data suggest a tight control of IL-1 family cytokines signalling in IgG4-RD

Skull-Base Inflammatory Pseudotumor Involving the Trigeminal and Facial Nerves: A Singular Presentation of a Rare Disease

Inflammatory pseudotumor (IPT) is a rare disease that is often misinterpreted as a lymphoma or carcinoma. It may involve different body regions but most commonly the lungs and the orbital cavity. We report the case of a patient affected by an IPT of the trigeminal and facial nerves. A 69-year-old male presented to our hospital with a right facial palsy arisen suddenly 2 days before. A magnetic resonance imaging (MRI) of the head showed an abnormal mass with homogeneous enhancement involving the deep lobe of the parotid gland, the parapharyngeal space, and the infratemporal fossa, extending along the trigeminal nerve and the facial nerve. The patient was planned for multiple transnasal biopsies in the nasopharynx, the region of the foramen ovale, and the deep lobe of the parotid gland, but the results were inconclusive, with no evidence of a malignant process. We considered the possibility that the lesion could be an IPT, and the patient was treated with prednisone and cyclophosphamide. Three months after the conclusion of the treatment, an MRI showed a complete radiological response

Application of the ICHD - II diagnostic criteria for paediatric headache using a computerized structured record. A multicentre study

Rome 27-30 sept. The Journal of Headache and Pain 7(4) p. 25

Participation of the liver gluconeogenesis in the glibenclamide-induced hypoglycaemia in rats

We previously demonstrated an increased liver gluconeogenesis (LG) during insulin-induced hypoglycaemia. Thus, an expected effect of sulphonylureas induced hypoglycaemia (SIH) could be the activation of LG. However, sulphonylureas infused directly in to the liver inhibits LG. Considering these opposite effects we investigated herein LG in rats submitted to SIH. For this purpose, 24 h fasted rats that received glibenclamide (10 mg kg(-1)) were used (SIH group). Control group received oral saline. Glycaemia at 30, 60, 90, 120 and 150 min after oral administration of glibenclamide were evaluated. Since the lowest glycaemia was obtained 120 min after glibenclamide administration, this time was chosen to investigate LG in situ perfused livers. The gluconeogenesis from precursors that enters in this metabolic pathway before the mitochondrial step, i.e. L-alanine (5 mM), L-lactate (2 mM), pyruvate (5 mM) and L-glutamine were decreased (p < 0.05). However, the gluconeogenic activity using glycerol (2 mM), which enters in the gluconeogenesis after the mitochondrial step was maintained. Taken together, the results suggest that the inhibition of LG promoted by SIH overcome the activation of this metabolic pathway promoted by IIH and could be attributed, at least in part, to its effect on mitochondrial function. Copyright (C) 2011 John Wiley & Sons, Ltd.Brazilian Council of Scientific and Technological Development (CNPq)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação AraucáriaAraucaria FoundationNational Institute of Obesity and Diabetes (INCT)National Institute of Obesity and Diabetes (INCT