Sjögren's syndrome (SS) is a complex autoimmune exocrinopathy with multifactorial pathogenesis and multisystem manifestation. It is called primary Sjögren's syndrome (PSS) when the manifestations are seen without any other co-existent rheumatic diseases. The incidence of respiratory system involvement varies widely in the reported medical literature, partly due to lack of a universal agreement over the diagnostic criteria of the disease and the type of study methods employed. Respiratory system manifestations are protean; upper airway symptoms are very common and so is the complaint of dry cough. The PSS patients may develop interstitial lung diseases (ILDs) such as usual interstitial pneumonia (UIP), non-specific interstitial pneumonia (NSIP), lymphocytic interstitial pneumonia (LIP), bronchiolitis obliterans and organising pneumonia (BOOP), etc. They may also develop the whole spectrum of lymphoproliferative disorders of the lung ranging from LIP to follicular bronchiolitis, nodular lymphoid hyperplasia and low-grade lymphomas. Therapeutic options include symptomatic and supportive measures and corticosteroids as the mainstay of the treatment for ILDs occurring in these patients. In recent years, rituximab (anti-CD20) has emerged as a promising treatment for this disease, though data from controlled trials are still lacking. Pulmonary involvement may be a source of significant morbidity in these patients, though only rarely, it is the cause of death.
Download full-text PDF |
Source |
---|
JAMA Psychiatry
January 2025
Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania.
Importance: Mania/hypomania is the pathognomonic feature of bipolar disorder (BD). As BD is often misdiagnosed as major depressive disorder (MDD), replicable neural markers of mania/hypomania risk are needed for earlier BD diagnosis and pathophysiological treatment development.
Objective: To replicate the previously reported positive association between left ventrolateral prefrontal cortex (vlPFC) activity during reward expectancy (RE) and mania/hypomania risk, to explore the effect of MDD history on this association, and to compare RE-related left vlPFC activity in individuals with and at risk of BD.
Int J Cardiovasc Imaging
January 2025
Department of Cardiovascular Surgery, JCHO Kyushu Hospital, Kitakyushu City, Japan.
World J Pediatr
January 2025
The First Hospital of Peking University, Beijing, China.
Background: Glucose transporter 1 deficiency syndrome (Glut1DS) was initially reported by De Vivo and colleagues in 1991. This disease arises from mutations in the SLC2A1 and presents with a broad clinical spectrum. It is a treatable neuro-metabolic condition, where prompt diagnosis and initiation of ketogenic dietary therapy can markedly enhance the prognosis.
View Article and Find Full Text PDFIndian J Pediatr
January 2025
Pediatric Neurology Unit, Department of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Neurol Sci
January 2025
Division of Pediatric Neurology, Ankara University Faculty of Medicine, Ankara, Turkey.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!