Myasthenia gravis associated with etanercept therapy

Etanercept is an antagonist of tumor necrosis factor alpha that was developed to treat rheumatoid arthritis. In this report we present a patient who developed myasthenia gravis while taking etanercept and had resolution of symptoms after stopping it. This is the first report of this potential side effect and is of additional interest, because etanercept has been proposed as a treatment for myasthenia gravis. Muscle Nerve, 2009     

Myasthenia gravis: clinical and surgical treatment]

The indication for thymectomy in myasthenia gravis still is controversial, and it is uncommon to find in the present days studies comparing conservative treatments, due to the widespread surgical treatment adopted in most centers. We studied 65 cases divided into three groups of patients: (1) 15 thymectomized patients and 50 with conservative treatment; (2) 15 thymectomized patients paired with 15 on conservative treatment; (3) 49 patients treated with corticosteroids against 16 without corticosteroids. These three groups where compared regarding age, age when the symptoms began, disease duration, clinical severity and functional scale, studying remission, stability or worsening of the symptoms and death rate after several years of treatment. It was found a reduction of the symptoms (p < 0.05) in the thymectomized patients of group 1; the remaining parameters of all three groups did not show any statistical significance. These results suggest that the type of treatment did not interfere with evolution of myasthenia gravis in this group of patients.     

Myasthenia gravis and pregnancy

Treatment considerations for women who have MG and are of childbearing age are complicated. When possible, before pregnancy, establishing a plan for therapy is ideal, recognizing the potential concerns for the patient and the fetus. Decisions about treatment during pregnancy must balance the potential complications for the fetus, the patient, and even the integrity of the pregnancy. Most women who have MG are able to complete pregnancy successfully and deliver a healthy baby; however, there always is some risk that NMG may occur. Pregnant patients who have MG are served best at centers capable of providing coordinated expert care from neurologic, obstetric, and pediatric providers.     

Myasthenia gravis and pregnancy

Myasthenia gravis (MG) is an autoimmune disorder with bimodal age of presentation, occurring in young women of reproductive age and at an older age in men. Occasionally, MG is diagnosed during pregnancy. Management of MG includes symptomatic treatment with cholinesterase inhibitors and immunosuppressive therapy for controlling the disease activity. Treatment of MG in women of reproductive age, who may be contemplating pregnancy, requires discussion regarding the choice of medication as well as the understanding of risks/adverse effects involved with various treatments. During the peripartum period, it is essential to ensure careful monitoring of the disease state along with the well-being of the mother and fetus and to coordinate neonatal monitoring overseen by a multidisciplinary team comprising a high-risk maternal fetal medicine specialist, a neurologist familiar with these complex issues, and a neonatologist.     

Myasthenia gravis and pregnancy

Myasthenia gravis is an autoimmune disease characterised by fluctuating muscle weakness, which worsens during activity. It affects particularly scapular and pelvic girdles, axial and bulbar muscles. Myasthenia gravis is twice more frequent in women and symptoms often appear in the second and third decade of life. Thus, a growing number of women affected by this condition become pregnant. To minimise the effects of myasthenia gravis on pregnancy and the newborn, and to avoid myasthenia crisis in the post-partum, the pregnancy must be planned as far as possible. During pregnancy, treatment must be reviewed due to the threat of teratogenic effects (mycophenolate mofetil, rituximab), and the follow-up must be multidisciplinary.     

Myasthenia gravis: diagnosis

The clinical history and neurological examination provide the most important data on which the diagnosis of autoimmune myasthenia gravis (MG) is based. MG produces symptomatic weakness that predominates in certain muscle groups and typically fluctuates in response to effort and rest. The diagnosis of MG therefore depends on the recognition of this distinctive pattern of fatigable weakness. Laboratory confirmation of the clinical diagnosis may be obtained using pharmacological, electrophysiological, and serological (immunological) tests. This article reviews the tests used to confirm the diagnosis of MG.     

Myasthenia gravis during pregnancy

Myasthenia gravis (MG) affects women in the second and third decades of life, overlapping with the childbearing years. During pregnancy, the course of this disease is unpredictable; worsening of symptoms occurs more likely during the first half of pregnancy and postpartum. MG can be well managed during pregnancy with relatively safe and effective therapies. Cesarean section is recommended only for obstetric reasons; epidural anesthesia is advised to reduce physical and emotional stress. Anticholinesterase drugs are the mainstay of treatment, when MG symptoms are not satisfactorily controlled, corticosteroids, azathioprine and in some cases cyclosporin A may be used. Life-threatening conditions (e.g., respiratory insufficiency) may occur during pregnancy; therefore, intensive check-ups by a gynecologist and a neurologist are necessary.     

Myasthenia gravis and psoriasis vulgaris

Myasthenia gravis is a rare autoimmune disorder in which antibodies form against acetylcholine nicotinic postsynaptic receptors at the myoneural junction. Psoriasis vulgaris is a chronic, recurring, and an inflammatory skin disease. Myasthenia gravis and psoriasis are both autoimmune diseases and correlated with specific human histocompatibility antigens. In this report, a 53-year-old woman who has myasthenia gravis accompanied with psoriasis vulgaris is presented. To conclude, this association is extremely rare and the pathogenetic etiology was thought to depend on a generalized immunological disturbance.     

Myasthenia gravis and myasthenic syndromes

More than a decade ago myasthenic symptoms were observed in rabbits immunized with acetylcholine receptor (AChR) [119] and AChR deficiency was found at the neuromuscular junction in human myasthenia gravis (MG) [36]. By 1977 the autoimmune character of MG and the pathogenic role of AChR antibodies had been established by several measures. These included the demonstration of circulating AChR antibodies in nearly 90% of patients with MG [87], passive transfer with IgG of several features of the disease from human to mouse [149], localization of immune complexes (IgG and complement) on the postsynaptic membrane [30], and the beneficial effects of plasmapheresis [20, 123]. Substantial subsequent progress has occurred in understanding the structure and function of AChR and its interaction with AChR antibodies. The relationships of the concentration, specificities, and functional properties of the antibodies to the clinical state in MG have been carefully analyzed, and the mechanisms by which AChR antibodies impair neuromuscular transmission have been further investigated. The clinical classification of MG has been refined, the role of the thymus gland in the disease has been further clarified, and new information has become available on transient neonatal MG. The prognosis for generalized MG is improving, but there is still no consensus on its optimal management. Novel therapeutic approaches to MG are now being explored in animal models. Recognition of the autoimmune origin of acquired MG also implied that myasthenic disorders occurring in a genetic or congenital setting had a different cause. As a result, a number of congenital myasthenic syndromes have come to be recognized and investigated. Finally, an acquired disorder of neuromuscular transmission different from MG, the Lambert-Eaton myasthenic syndrome, has also been shown to have an autoimmune basis. In this syndrome, active zone particles of the presynaptic membrane are direct or indirect targets of the pathogenic autoantibodies.