Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neither pneumothorax or mediastinal emphysema are well recognized pulmonary manifestations of systemic lupus erythematosus (SLE). We describe a 41-year-old woman with severe lupus pneumonitis complicated by recurrent pneumothoraces and mediastinal emphysema. Other features of SLE were minimal. She died of progressive respiratory failure. Autopsy revealed innumerable blebs in both lungs responsible for the pneumothoraces and mediastinal emphysema. Both pneumothoraces and mediastinal emphysema occurred during a course of corticosteroid therapy. The course of her illness was unaffected by treatments that included high dose corticosteroids, immunosuppressives and plasmapheresis. Better medical treatment for these lupus complications should be sought in addition to surgery.
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PMID:Recurrent pneumothoraces and mediastinal emphysema in systemic lupus erythematosus. 234 34

Alpha1 antitrypsin (AAT) deficiency is an autosomic codominant inherited disorder characterized by inefficient or non-functional serum AAT. The principal clinical manifestations are panlobular emphysema and cirrhoses. Among cutaneous aspects, about 30 cases of panniculitis have been reported in the literature, likewise rare clinical cases: pemphigus herpetiformis, Muir Torre syndrome, urticaria and angioedema, cutis laxa and Marshall syndrome, lupus erythematosus, psoriasis, vasculitis. Probably because of it's high frequency, numerous others diseases have been reported described in association. Acting on several factors of inflammation, AAT deficiency seems product or modify the expression of some, notably cutaneous diseases.
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PMID:[Alpha-1-antitrypsin deficiency. Role in skin disorders]. 1266 63

What's new in medicine in 2007? Find out what has changed in medicine in 2007 in the field of inflammatory and autoimmune diseases. The year has been productive with many fundamental advances. 2007 was the year of genetics in autoimmune diseases (rheumatoid arthritis, lupus, scleroderma, vascularities, etc.), coming notably from work by the WTCCC. The comprehension of inflammatory diseases is based on increasingly detailed knowledge of epigenetic regulation and posttranscriptional mechanisms. The small RNA play a fundamental role and potentially offer many therapeutic applications.Sex and stress play a role in the appearance of inflammatory diseases. The mechanisms are progressively being better understood.More and more illnesses have autoimmune mechanisms, such as emphysema in the ex-smoker or pustulosis palmaris et plantaris. The revolution in biological therapies is continuing to grow. Medications that modulate innate immunity are being evaluated in inflammatory, allergic, and neoplastic diseases. Other, sometimes surprising options such as arsenic are now possible.
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PMID:[What's new in medicine in 2007?]. 1867 38

The role of autoimmune pathology in development and progression of chronic obstructive pulmonary disease (COPD) is becoming increasingly appreciated. In this study, we identified serum autoantibody reactivities associated with chronic bronchitis or emphysema, as well as systemic autoimmunity and associated lung disease. Using autoantigen array analysis, we demonstrated that COPD patients produce autoantibodies reactive to a broad spectrum of self-antigens. Further, the level and reactivities of these antibodies, or autoantibody profile, correlated with disease phenotype. Patients with emphysema produced autoantibodies of higher titer and reactive to an increased number of array antigens. Strikingly, the autoantibody reactivities observed in emphysema were increased over those detected in rheumatoid arthritis patients, and included similar reactivities to those associated with lupus. These findings raise the possibility that autoantibody profiles may be used to determine COPD risk, as well as provide a diagnostic and prognostic tool. They shed light on the heterogeneity of autoantibody reactivities associated with COPD phenotype and could be of use in the personalization of medical treatment, including determining and monitoring therapeutic interventions.
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PMID:COPD is associated with production of autoantibodies to a broad spectrum of self-antigens, correlative with disease phenotype. 2294 90

The cell danger response (CDR) is the evolutionarily conserved metabolic response that protects cells and hosts from harm. It is triggered by encounters with chemical, physical, or biological threats that exceed the cellular capacity for homeostasis. The resulting metabolic mismatch between available resources and functional capacity produces a cascade of changes in cellular electron flow, oxygen consumption, redox, membrane fluidity, lipid dynamics, bioenergetics, carbon and sulfur resource allocation, protein folding and aggregation, vitamin availability, metal homeostasis, indole, pterin, 1-carbon and polyamine metabolism, and polymer formation. The first wave of danger signals consists of the release of metabolic intermediates like ATP and ADP, Krebs cycle intermediates, oxygen, and reactive oxygen species (ROS), and is sustained by purinergic signaling. After the danger has been eliminated or neutralized, a choreographed sequence of anti-inflammatory and regenerative pathways is activated to reverse the CDR and to heal. When the CDR persists abnormally, whole body metabolism and the gut microbiome are disturbed, the collective performance of multiple organ systems is impaired, behavior is changed, and chronic disease results. Metabolic memory of past stress encounters is stored in the form of altered mitochondrial and cellular macromolecule content, resulting in an increase in functional reserve capacity through a process known as mitocellular hormesis. The systemic form of the CDR, and its magnified form, the purinergic life-threat response (PLTR), are under direct control by ancient pathways in the brain that are ultimately coordinated by centers in the brainstem. Chemosensory integration of whole body metabolism occurs in the brainstem and is a prerequisite for normal brain, motor, vestibular, sensory, social, and speech development. An understanding of the CDR permits us to reframe old concepts of pathogenesis for a broad array of chronic, developmental, autoimmune, and degenerative disorders. These disorders include autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), asthma, atopy, gluten and many other food and chemical sensitivity syndromes, emphysema, Tourette's syndrome, bipolar disorder, schizophrenia, post-traumatic stress disorder (PTSD), chronic traumatic encephalopathy (CTE), traumatic brain injury (TBI), epilepsy, suicidal ideation, organ transplant biology, diabetes, kidney, liver, and heart disease, cancer, Alzheimer and Parkinson disease, and autoimmune disorders like lupus, rheumatoid arthritis, multiple sclerosis, and primary sclerosing cholangitis.
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PMID:Metabolic features of the cell danger response. 2398 37

Ku70 (Lupus Ku autoantigen p70) is essential in nonhomologous end joining DNA double-strand break repair, and ku70(-/-) mice age prematurely because of increased genomic instability and DNA damage responses. Previously, we found that Ku70 also inhibits Bax, a key mediator of apoptosis. We hypothesized that Bax-mediated apoptosis would be enhanced in the absence of Ku70 and contribute to premature death observed in ku70(-/-) mice. Here, we show that ku70(-/-) bax(+/-) and ku70(-/-) bax(-/-) mice have better survival, especially in females, than ku70(-/-) mice, even though Bax deficiency did not decrease the incidence of lymphoma observed in a Ku70-null background. Moreover, we found that ku70(-/-) mice develop lung diseases, like emphysema and pulmonary arterial (PA) occlusion, by 3 months of age. These lung abnormalities can trigger secondary health problems such as heart failure that may account for the poor survival of ku70(-/-) mice. Importantly, Bax deficiency appeared to delay the development of emphysema. This study suggests that enhanced Bax activity exacerbates the negative impact of Ku70 deletion. Furthermore, the underlying mechanisms of emphysema and pulmonary hypertension due to PA occlusion are not well understood, and therefore ku70(-/-) and Bax-deficient ku70(-/-) mice may be useful models to study these diseases.
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PMID:Bax deficiency extends the survival of Ku70 knockout mice that develop lung and heart diseases. 2581 3

An 83-year-old man, who was a former smoker, with anti-ribonucleoprotein (RNP) antibody-positive combined pulmonary fibrosis and emphysema presented with a cough and dyspnea. A chest radiograph showed bilateral pleural effusions. His laboratory data showed proteinuria and elevated levels of anti-nuclear antibodies, anti-double strand DNA antibodies, and CA125, with decreased serum complement levels. Thoracentesis showed an exudative pleural effusion with an increased lymphocyte count and elevated CA125 levels. A thoracoscopic biopsy specimen showed proliferation of CA125-positive mesothelial cells. Systemic lupus erythematosus was diagnosed. His symptoms and pleural effusion resolved after the initiation of systemic corticosteroid therapy. The detection of anti-RNP antibody and CA125 levels are helpful in the diagnosis of lupus pleuritis.
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PMID:Combined Pulmonary Fibrosis and Emphysema Preceding Lupus Pleuritis. 2704 Nov 65

The obesity epidemic in the United States has been well documented and serves as the basis for a number of health interventions across the nation. However, those who have served in the U.S. military (Veteran population) suffer from obesity in higher numbers and have an overall disproportionate poorer health status when compared to the health of the older non-Veteran population in the U.S. which may further compound their overall health risk. This study examined both the commonalities and the differences in obesity rates and the associated co-morbidities among the U.S. Veteran population, utilizing data from the 2018 Behavioral Risk Factor Surveillance System (BRFSS). These data are considered by the Centers for Disease Control and Prevention (CDC) to be the nation's best source for health-related survey data, and the 2018 version includes 437,467 observations. Study findings show not only a significantly higher risk of obesity in the U.S. Veteran population, but also a significantly higher level (higher odds ratio) of the associated co-morbidities when compared to non-Veterans, including coronary heart disease (CHD) or angina (odds ratio (OR) = 2.63); stroke (OR = 1.86); skin cancer (OR = 2.18); other cancers (OR = 1.73); chronic obstructive pulmonary disease (COPD) (OR = 1.52), emphysema, or chronic bronchitis; arthritis (OR = 1.52), rheumatoid arthritis, gout, lupus, or fibromyalgia; depressive disorders (OR = 0.84), and diabetes (OR = 1.61) at the 0.95 confidence interval level.
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PMID:Obesity and Morbidity Risk in the U.S. Veteran. 3261 Jun 37