PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MYASTHENIA GRAVIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1991

Myasthenia gravis patients with thymus hyperplasia and myasthenia gravis patients with thymoma display different HLA associations.

Thirty myasthenia gravis (MG) patients (9 with thymoma, 12 with thymus hyperplasia and 9 with thymic atrophy) and 181 Norwegian healthy controls were serologically typed for HLA-A, -B and -DR antigens and genomically typed for HLA-DQA1 and HLA-DQB1 alleles by probing in vitro amplified DNA with sequence-specific oligonucleotides. In patients with thymus hyperplasia the frequency of the DQB1*0201 allele was increased compared to controls (RR = 3.5, p less than 0.05), whereas among the patients with thymoma this allele was not observed (RR = 0.06, p less than 0.01). The frequencies of HLA-B8, -DR3 and -DQA1*0501, which are in strong linkage disequilibrium with DQB1*0201, were increased in patients with hyperplasia and reduced in patients with thymoma. The data suggest that different HLA genes predispose to two different forms of MG.

Alleles↗
PubMed1991

Anti-skeletal muscle and anti-acetylcholine receptor antibodies in patients with thymoma without myasthenia gravis: relation to the onset of myasthenia gravis.

We measured the anti-skeletal muscle (SM) antibody titers in sera from 46 patients with thymoma but without Myasthenia gravis (MG) in order to determine whether the presence of anti-SM antibody is linked to the combination of thymoma-MG, or to thymoma alone. We detected anti-SM antibodies in 18 of these sera, of which 15 had concomitantly elevated titers of anti-AChR antibodies. Moreover, 9 of whom had experienced the onset of MG after surgery. In contrast, no patient without elevations in both antibodies developed MG during the followup. We conclude that the presence of anti-SM antibodies is linked strongly with thymoma associated with MG, but not with thymoma alone.

Adolescent↗
PubMed2002

Outcome of thymectomy in patients with Myasthenia Gravis.

OBJECTIVE: Myasthenia Gravis is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscles. Thymectomy is now beneficial even for non-thymomatous patients. The aim of this paper is to evaluate the role of thymectomy as on the treatment options for myasthenia gravis. METHODS: Thirty patients underwent thymectomy in the period from April 1999 through to July 2000. They were collected from different teaching hospitals in Baghdad, Iraq. All these cases were studied conventionally including history, physical and neurological examination in addition to investigations with particular emphasis on connective tissue screen and thyroid function test. RESULTS: The age in this study ranged between 17-55 years. The preoperative duration ranged between 2-20 months and the postoperative follow up period ranged between 6 months-14 years. The most favorable results were obtained in patients without thymoma with short duration. CONCLUSION: Early thymectomy carries the best results in Myasthenia Gravis and every effort should be made to shorten the preoperative duration for both thymomatous and nonthymomatous patients. Patients with symptoms can be better controlled with anticholinesterase drugs than patients using steroid and cytotoxic drugs. Thymectomy is beneficial for most patients with Myasthenia Gravis and especially in those with benign folicular hyperplasia.

Adolescent↗
PubMed1984

Myasthenia gravis with thymoma: analysis of and postoperative prognosis for 65 patients with thymomatous myasthenia gravis.

Sixty-five patients with thymomatous myasthenia gravis were investigated. Thymomas were present in 44% of the male patients and 19% of the female patients with myasthenia gravis. The incidence of thymomatous disease in male patients was higher than in female patients in all age groups. Eighty percent of men more than 50 years old and women more than 60 years old had myasthenia gravis with thymoma. Germinal center formation in the thymus of patients with thymomatous myasthenia gravis was positive in 91% and was high grade. The prognosis for patients undergoing extended thymectomy of thymomatous myasthenia gravis was significantly better than in those having transsternal simple thymectomy, but it was worse than the prognosis for patients with nonthymomatous myasthenia gravis. No increase in the rate of remission or palliation was seen one year after thymectomy. It is concluded that early thymectomy is effective in control of myasthenia gravis in thymomatous myasthenia gravis.

Adult↗
PubMed1981

Desensitization to acetylcholine at motor end plates in normal humans, patients with myasthenia gravis, and experimental models of myasthenia gravis.

Desensitization to ionophoretically applied ACh at the motor end plates of normal humans and patients with MG was studied. The pattern of desensitization at the normal human motor end plate was completely consistent with that observed in muscles of various animals. At motor end plates of MG patients there was greater desensitization and slower recovery from desensitization than in normals. A similar pattern of desensitization was observed at normal end plates when they were exposed to serum globulins of MG patients, and at end plates of muscles from mice than were repeatedly injected with serum globulins of MG patients. Despite the reported reduction in the number of ACh receptors, our calculations show that there is a large pool of spare receptors forming a sizeable margin of safety at the end plates of MG patients. The number of receptors may not show additional progressive reduction in number during repetitive motor activity. Our results indicate that desensitization could play a significant role in the development of neuromuscular block following repetitive motor activity in MG patients. The mechanism by which desensitization is augmented in MG patients in not yet clear.

Acetylcholine↗
PubMed2002

Thymectomy by partial sternotomy for the treatment of myasthenia gravis.

BACKGROUND: Myasthenia gravis is an autoimmune disease characterized by weakness and fatigue of voluntary muscles. Surgical treatment of choice for myasthenia gravis has been thymectomy. However, thymectomy indications and surgical approach are still controversial. The purpose of this study is to evaluate the efficacy of partial median sternotomy approach to the thymus. METHODS: From 1973 to 1999, 478 patients with myasthenia gravis underwent thymectomy through a partial median sternotomy. RESULTS: Sixty-one patients (12.7%) had complete remission of symptoms, 299 (62.5%) had a significant improvement, and 83 (17.4%), a mild improvement; whereas 35 patients (7.4%) had no improvement of clinical symptoms. CONCLUSIONS: Partial median sternotomy has shown to be a useful surgical approach to the thymus, as demonstrated by the good functional and aesthetic results, associated with low morbidity and no mortality.

Adult↗
PubMed1997

Altered intrathymic T-cell repertoire in human myasthenia gravis.

In myasthenia gravis, the thymus is thought to be the primary site of autosensitization. We investigated the V beta T-cell repertoire at different intrathymic differentiation stages in 17 patients with myasthenia gravis and 8 age-matched control subjects by tricolor immunofluorescence, using a panel of six anti-V beta antibodies. We observed an increased expression of V beta 5.1 and V beta 8 subfamilies in the patients compared to the control subjects. These increases were observed not only in mature cells but also in the latest thymic precursors of mature cells (double-positive CD3 high), while there was no change in intermediate precursors (double-positive CD3 low), pointing to biased selection during intrathymic differentiation. In addition, there was a strong correlation between the percentage of V beta 5.1+ and V beta 8+ cells among both the CD4 and CD8 subsets in the patients, but not in control subjects, suggesting that thymic events relevant to the disease lead to these selected populations. Finally, location studies of V beta 5.1+ cells on thymic sections indicated that these cells were overrepresented both in the core of germinal centers and in perifollicular areas of hyperplastic thymuses, suggesting a role in the autoimmune response. Taken together, these findings are compatible with the hypothesis of a biased intrathymic selection in myasthenia gravis.

Adolescent↗
PubMed1993

A randomised clinical trial comparing prednisone and azathioprine in myasthenia gravis. Results of the second interim analysis. Myasthenia Gravis Clinical Study Group.

From January 1983 to October 1990, 41 patients with generalised myasthenia gravis were randomly given either prednisone or azathioprine. The main goal was to record the time to the occurrence of the first episode of deterioration. During a mean follow-up of 30 months, 21 patients showed deterioration, 12 in the prednisone group and nine in the azathioprine group (p = 0.40). No difference was observed between the two groups in muscular score and functional grade, assessed at the end of each treatment year, or in tolerance. Treatment failure occurred in 17 patients, 12 in the prednisone group and five in the azathioprine group (p = 0.02); even after adjustment for imbalances in prognostic features, the failure rate remained 2.8 times higher in the prednisone group than in the azathioprine group (p = 0.5). In the patients in whom treatment failed, symptoms were initially more severe than in the others, but the combination of prednisone and azathioprine resulted in clinical improvement, consisting of remission or only minor deficits in half of the patients after two years of treatment. These findings indicate that azathioprine increases treatment response compared with prednisone, although no difference in the duration of improvement was demonstrated. Nevertheless, it appears that the most severe forms of the disease, often resistant to prednisone or azathioprine alone, could benefit from the combination of both drugs.

Adult↗
PubMed1976

Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies.

Passive transfer of experimental autoimmune myasthenia gravis (EAMG) was achieved using the gamma globulin fraction and purified IgG from sera of rats immunized with Electrophus electricus (eel) acetylcholine receptor (AChR). This demonstrates the critical role of anti-AChR antibodies in impairing neuromuscular transmission in EAMG. Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells. Clinical, eletrophysiological, histological, and biochemical signs of acute EAMG were observed by 24 h after antibody transfer. Recipient rats developed profound weakness and fatigability, and the posture characteristic of EAMG. Striking weight loss was attributable to dehydration. Recipient rats showed large decreases in amplitude of muscle responses to motor nerve stimulation, and repetitive nerve stimulation induced characteristic decrementing responses. End-plate potentials were not detectable in many muscle fibers, and the amplitudes of miniature end-plate potentials were reduced in the others. Passively transferred EAMG more severely affected the forearm muscles than diaphragm muscles, though neuromuscular transmission was impaired and curare sensitivity was increased in both muscles. Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased. The quantitative decrease in AChR approximately paralleled in time the course of clinical and electrophysiological signs. The amount of AChR increased to normal levels and beyond at the time neuromuscular transmission was improving. The excess of AChR extractable from muscle as the serum antibody level decreased probably represented extrajunctional receptors formed in response to functional denervation caused by phagocytosis of the postsynaptic membrane by macrophages. The amount of antibody required to passively transfer EAMG was less than required to bind all AChR molecules in a rat's musculature. The effectiveness of samll amounts of antibody was probably amplified by the activation of complement and by the destruction of large areas of postsynaptic membrane by phagocytic cells. A self-sustaining autoimmune response to AChR was not provoked in animals with passively transferred EAMG.

Animals↗
PubMed1981

Myasthenia gravis: antibodies to acetylcholine receptor in ocular myasthenia gravis.

To improve the sensitivity of the radioimmunoassay method for anti-AChR-antibody, large amounts of sera from patients with myasthenia gravis, and higher concentrations of antigens and rabbit anti-human-IgG-antiserum, were used. These procedures enabled measurement of the titre value of over 0.04 pmol/ml serum and this value revealed a sensitivity about 10 times higher than that predicted using the previous model. Antibodies against AChR were found in 13 out of 17 ocular myasthenia patients (70%) and 35 of 37 with generalized myasthenia (90%). However, the average titre value of sera in those with ocular myasthenia was significantly lower than the value obtained in the generalized cases. Even in the patients with ptosis or ophthalmoparesis, in the early stage (less than one year) of ocular myasthenia, anti-AChR-antibodies were not detectable using this more sensitive assay method.

Adult↗
PubMed1987

Disorders affecting the acetylcholine receptor: myasthenia gravis and congenital myasthenia.

Myasthenia gravis (MG) is an autoimmune disease in which anti-acetylcholine receptor antibodies (anti-AChR) cause loss of functional endplate AChR by increasing AChR degradation, and by complement-mediated destruction. MG anti-AChR binds to regions on the human AChR which can be defined by monoclonal antibodies (mabs). Several congenital forms of myasthenia have been described, three of which may directly involve abnormalities of the AChR, including one in which the open-time of the ion channel is prolonged.

Antibodies, Monoclonal↗
PubMed1998

Determinant spreading and immune responses to acetylcholine receptors in myasthenia gravis.

In myasthenia gravis (MG), antibodies to the muscle acetylcholine receptor (AChR) cause muscle weakness. Experimental autoimmune myasthenia gravis (EAMG) can be induced by immunisation against purified AChR; the main immunogenic region (MIR) is a conformation-dependent site that includes alpha 67-76. EAMG can also occur after immunisation against extracellular AChR sequences, but this probably involves intramolecular determinant spreading. In MG patients, thymic hyperplasia and germinal centres are found in about 50%, and thymoma in 10-15%. The heterogeneous, high affinity, IgG anti-AChR antibodies appear to be end-products of germinal centre responses, and react mainly with the MIR or a site on fetal AChR; the latter contains a gamma subunit and is mainly expressed on myoid cells in the thymic medulla. T cells cloned against recombinant AChR subunits recognise principally two naturally processed epitopes: epsilon 201-219 derived from adult AChR which is expressed in muscle, and sometimes in thymic epithelium, and alpha 146-160, common to fetal and adult AChR. Since AChR is not normally co-expressed with class II, it is unclear how CD4+ responses to AChR alpha and epsilon subunits are initiated, and how and where these spread to induce antibodies against fetal AChR. Various possibilities, including upregulation of class II on muscle/myoid cells and involvement of CD8+ responses to AChR and other muscle antigens, are discussed.

Animals↗