Topic: What is Lupus exactly? Does anyone have it here or can you fill me in!?!?!?
June 16, 2019 / By Bonnie Question:
Please fill me in if you can. My best friend was just diagnosed today with Lupus. She is only 27. I looked up some stuff on the computer already but I want to hear back from real people...ya know. Not the text book stuff.
Thanks so much for the feed back & help =)
Alannis | 5 days ago
I have had systemic lupus eryethematosis, since the age of 22, I am 53 now, usually in women. a pregnancy will set off the Lupus, in other's no one really know's why it does. However, as you may have read its the body's own blood cells attacking the good cells and creating havoc in our bodies. It can affect the entire system, nerves, bones, joints, skin, heart, kidney's , liver, etc... Painful as ever, and chronic fatigue, most times, Fibromyalgia is also involved. There is no cure, and most doctor''s can only treat our symptoms. finding a good doctor is your friends best bet!! A good Rhuemotologist.. sorry spelled wrong I think.. however. we can look healthy, but feel awful, spend a lot of time seeing doctor's and listening to people who look down at us, thinking we are only looking for "attention", please continue to support your friend emotionally, she needs you now more than ever. Contact the National Lupus foundation and they will send you a ton of information that is very helpful, and join the lupus support group online, we are all very much supportive of all whom join. "[email protected]
My best to you and your friend. ((hugs)) midwestm/Gwendolene
Lupus is a chronic (it never goes away and there is no cure), autoimmune (the person's immune system attacks their own organs) and inflammatory disease.
I have it and have major organ involvement.
I facilitate a lupus support group and give lectures on the disorder.
Although there is no cure there are treatments that may control lupus. Some people do still die from lupus, but not as frequently as in the past
Read the link given for the Lupus Foundation of America. From that link, email your congressional rep asking them to sign on to the lupus REACH amendment.
Systemic lupus erythematosus (SLE) is an autoimmune disorder that affects many organ systems, including the central and peripheral nervous systems and muscles. SLE is in the differential diagnosis for many neurological conditions. A variety of neurologic complications may arise in patients with known SLE
The pathophysiology of SLE has not been defined fully, although many genes that affect immune function, particularly the human leukocyte antigen (HLA), may augment susceptibility to clinical disease. Most monozygotic (identical) twins are discordant for clinical SLE, strongly suggesting that additional factors, probably environmental, trigger the widespread development of autoimmunity in susceptible individuals.
Certain medications (eg, phenytoin, hydralazine, procainamide, and isoniazid) may produce drug-induced lupus, but this disorder differs from classic SLE in its autoantibody profile (eg, antihistone antibody positive) and in sparing the kidneys and central nervous system (CNS). Once triggered, SLE's autoimmune reaction affects many sites through multiple mechanisms such as deposition of immune complexes, effects of cytokines and other chemical neuromodulators, direct attack by autoantibodies or activated leukocytes, and others.
Non-neurologic sites of damage include the renal glomeruli, joints, pleural or pericardial serosa, integument, cardiac or vascular endothelium, cardiac valves, and the oral and conjunctival mucosa. Multiple sites may be involved within the nervous system.
Among the neurologic manifestations of SLE, the most common are the organic encephalopathies. These diffuse syndromes correlate poorly with the extent of vasculitis or frank thromboembolism. Functional studies such as positron emission tomography (PET), functional magnetic resonance imaging (MRI), or single photon emission computerized tomography (SPECT) demonstrate patchy areas of dysfunction in brain areas unaffected on conventional MRI, findings that suggest an uncoupling of metabolic processes independent of obstruction to cerebral blood flow. The mechanism of these apparent metabolic alterations is unknown.
In areas of apparent vasculitis, histology demonstrates degenerative changes in small vessel walls, often with minimal or no inflammatory infiltrates. Chronic effects of immune complex deposition offer one potential mechanism for SLE vasculopathy; cytokine-mediated effects on vascular endothelium or local brain parenchyma are another. Inflammatory and noninflammatory SLE vasculopathies may be clinically indistinguishable. The terms cerebritis and vasculitis are well embedded in the literature and will be used in this article, keeping in mind the evolving understanding of the underlying processes.
In addition to small vessel vasculopathy, inflammatory changes may occur in large- to medium-sized vessels, giving a more classic vasculitis, sometimes with clinical stroke syndromes resulting from local thrombosis or artery-to-artery emboli. Other potential stroke etiologies include local thrombosis from antiphospholipid antibodies, which may involve small or medium-sized arteries or veins, including the venous sinuses. Emboli can occur as a result of Libman-Sacks endocarditis (LSE), a sterile endocardial inflammation that produces vegetations on the heart valves, seen in greater frequency in the presence of antiphospholipid antibodies. LSE also may cause a diffuse microembolization pattern that is clinically hard to distinguish from vasculitis or cerebritis. In focal clinical syndromes, overt or covert cardiac emboli are more frequently responsible than focal vasculitic or thrombotic processes.
Antiphospholipid antibodies comprise one category of the multiple autoantibodies that may be associated with SLE. In addition to their association with LSE and local arterial or venous thrombosis, these antibodies also may be associated with a hemorrhagic diathesis, myelopathy, and non-neurologic manifestations such as spontaneous abortion.
Peripheral manifestations of SLE include peripheral nerve injury, myopathy, or disturbances of the neuromuscular junction, which may clinically duplicate myasthenia or myasthenic syndrome. Peripheral neuropathy may result from vasculitic insult to the vasa nervorum (clinically resulting in mononeuritis multiplex or a more confluent polyneuropathy) or from a demyelinating pathology (which clinically results in a chronic sensory or sensorimotor polyneuropathy or, more rarely, in an acute motor presentation resembling acute inflammatory demyelinating polyradiculoneuropathy).
Myopathy in SLE most commonly results from vasculitis of the small vessels feeding the muscle, with pathology reminiscent of dermatomyositis, although on rare occasions the pathophysiology more closely resembles polymyositis with inflammatory involvement of muscle fibers themselves. These findings may be distinguished pathologically from medication-associated myopathy resulting from steroids or hydroxychloroquine sulfate therapy.
In the US: Incidence is 14.6-50.8 cases per 100,000 people.
Internationally: Incidence is 12-39 cases per 100,000 people. Estimates of incidence and prevalence are hampered by inconsistencies in application of diagnostic criteria and selection bias.
With full access to medical care, overall survival for SLE is 85% at 5 years and 63% at 15 years.
Stroke, cerebral vasculitis, spinal cord injury, and infection all increase the risk of mortality.
SLE is found in all ethnic groups and races; referral bias complicates any assessment of relative prevalence.
Susceptibility genes, which may increase the risk of SLE, vary across ethnic populations.
Sex: As with most autoimmune disorders, SLE shows a strong female predominance (as high as 5:1 during childbearing years).
Age: All age groups are affected; however, peak incidence is in young adulthood. Clinical onset often coincides with menarche, pregnancy, postpartum, or menopause.
If you want or need more information, let me know.