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Biomedical subjects

A K Lefvert

Publications and source records attributed to A K Lefvert.

At least 163 records · Page 9Linked to original sources
PubMed1982

Rapid improvement of myasthenia gravis after plasma exchange.

Neuromuscular transmission and the staircase phenomenon in the adductor pollicis muscle were studied in six patients with myasthenia gravis before and 24 hours after single plasma exchanges given in short series over one to four weeks. An improvement in neuromuscular transmission was observed in all patients but one within 24 hours, suggesting that an immunological block of receptor sites is reversible or that acetylcholine receptors are rapidly resynthesized. In addition to a neuromuscular transmission defect, two of the patients also showed evidence of impaired excitation-contraction coupling with a negative staircase phenomenon and reduced posttetanic twitch potentiation. This condition became normal after plasma exchange, which may indicate that a reversible immunological impairment of the sarcoplasmic reticulum was present. Improvement lasted up to several months. The anti-acetylcholine receptor antibody titers were lowered in response to single plasma exchanges, but actual titer levels showed poor correlation with clinical and electrophysiological changes.

Action Potentials↗
PubMed1982

Differences in the interaction of acetylcholine receptor antibodies with receptor from normal, denervated and myasthenic human muscle.

The interaction of acetylcholine receptor antibodies with different kinds of human skeletal muscle receptor was investigated. The reaction of most receptor antibodies was strongest with receptor from a patient with myasthenia gravis and with receptor from denervated muscle. Results obtained with these receptors were well correlated. The binding of most receptor antibodies to receptor from functionally normal muscle was much weaker and also qualitatively different. In a few patients with moderate and severe clinical symptoms the existence of acetylcholine receptor antibodies was revealed only by their reaction with receptor from myasthenic muscle. One patient had a clone of receptor antibodies reacting exclusively with receptor from her own muscle.

Aged↗
PubMed1981

Binding properties and subclass distribution of anti-acetylcholine receptor antibodies in myasthenia gravis.

Acetylcholine receptor antibodies were studied in the serum of 21 myasthenic patients. In 18 cases antibodies directed against sites other than the toxin binding were present whereas in 10 cases only there was a measurable inhibition of the ligand binding site. These 10 sera were from the 6 patients in stage IIB, III and IV and from 4 of the 12 patients in stage IIA. Antibodies against both non-toxin and ligand binding sites were measured in IgG subclasses. Most of the antibodies of the first type belonged to either subclass 1 or 3. They were, however, never absent from subclasses 2 and 4. Antibodies of the second type were not found in subclasses 2 and 4 except in one case. In 3 cases they were present exclusively in subclass 3. In 3 patients there was no correlation between the subclass distribution of the antibodies for the different binding sites.

Antibodies↗
PubMed1981

Thymoma-specific antibodies in sera from patients with myasthenia gravis demonstrated by indirect haemagglutination.

An indirect haemagglutination technique for the demonstration of antibodies to skeletal muscle is described. Eight out of 9 sera from unoperated myasthenia gravis (MG) patients with thymoma and 6 out of 22 sera taken from MG patients who had been operated upon for a thymoma, contained antibodies to this antigen. Twenty-five sera from MG patients with histologically verified thymus hyperplasia did not contain such antibodies. There was no relationship between these antibodies and antibodies to acetylcholine receptor.

Autoantibodies↗
PubMed1981

Anti-idiotypic antibodies against the receptor antibodies in myasthenia gravis.

Anti-idiotypic antibodies were prepared against purified acetylcholine receptor antibodies from two patients with myasthenia gravis. The purified idiotypes did not cross-react. Reaction with idiotypes from other patients were found in 8% and 37%, respectively, which suggests that shared idiotypic specificities occur. The anti-idiotypic IgG fractions had no receptor-like activity and did not bind cholinergic ligands. Receptor antibodies from two mothers and their newborn children with neonatal myasthenia gravis showed marked differences in the reactions with an anti-idiotypic antibody. This suggests that not passive transfer of maternal antibodies but a transient synthesis of a receptor antibody with a different specificity is an important factor in the pathogenesis of neonatal myasthenia gravis.

Atropine↗
PubMed1980

An automated turbidimetric immunoassay for plasma proteins.

The automated turbidimetric method presented allows a fast and accurate quantitation of plasma proteins. The analysis requires somewhat more antiserum than the radial immunodiffusion and the electroimmunoassay. However, this is compensated for by more rapid results and lower labour cost. The reference values for albumin, haptoglobin and IgG are the same as obtained by other immunological methods. The correlations with radial immunodiffusion and electroimmunoassay are good within the normal range. At high monoclonal IgG concentrations this method is better correlated to dye binding properties (scanning of electropherograms) than is the electroimmunoassay.

Blood Proteins↗
PubMed1979

Myasthenia gravis and monoclonal IgG gammopathy.

Monoclonal IgG gammopathy of the lambda light-chain type was detected in a 51-year-old woman who had unexplained fever, muscle fatigue, and myalgia. One year later, myasthenia gravis was diagnosed. There was no evidence of myelomatosis or other malignancy. On the assumption that her M-component (gammopathic paraprotein) was related to myasthenia, she was treated with melphalan and cyclophosphamide, but her clinical condition was not improved. Despite therapeutic trials of other agents and a time course of 6 years, the quantity of the M-component remained unchanged. Serum AChR antibody activity was not located in the paraprotein peak. The findings do not support a relationship between the M-component and myasthenia gravis.

Acetylcholine↗
PubMed1978

Acetylcholine receptor antibody in myasthenia gravis: purification and characterization.

Acetylcholine receptor antibody was measured in serum and IgG fractions from patients with myasthenia gravis using different analyses for antibody interfering with the toxin binding site and for antibody directed against other sites. No correlation was found between the concentration of receptor antibody as measured with the two assays. The different antibody activities also showed different isoelectric spectra. Receptor antibody was purified about 1000 times from IgG by affinity chromatography on a partially purified human skeletal muscle receptor preparation. The purified antibody was homogeneous in SDS-gel electrophroesis and showed a polyclonal pattern in agarose gel electrophoresis and isoelectric focusing. Both kinds of light chains were demonstrated. The results imply that the acetylcholine receptor antibody found in myasthenia gravis is heterogeneous and of multiclonal origin.

Acetylcholine↗
PubMed1978

No significant correlation of HLA-B8 and amount of antibodies directed to acetylcholine receptor protein in patients with myasthenia gravis.

Forty patients with myasthenia gravis were HLA tissue typed and the amount of anti-acetylcholine receptor protein antibody determined. Sera from seven patients were tested for antibody titer by repeated determinations and the serum concentration was found to be stable. Patients with thymoma had higher titers than patients with normal thymus histology or hyperplasia. Individuals with thymoma lacking HLA-B8 were found to have a higher concentration of antibodies than HLA-B8 negative individuals with hyperplasia. No statistically significant differences were obtained when comparing the amount of antibody in HLA-B8 positive and negative individuals. Titers in patients subjected to thymectomy more than 8 years before sampling did not deviate from those in non-thymectomized myasthenics.

Acetylcholine↗
PubMed1978

Determination of acetylcholine receptor antibody in myasthenia gravis: clinical usefulness and pathogenetic implications.

Antibodies to cholinergic receptor structures were found in 75% of 76 Finnish and 93% of 175 Swedish patients with myasthenia gravis. The amount of antibodies showed a positive correlation to the severity of the disease, and was reduced during immunosuppressive treatment, and by thymectomy. Thymoma patients had high values. The antibody was also found in the cerebrospinal fluid. Two healthy newborn babies of myasthenic mothers had antibodies during the first weeks of life, in spite of no clinical symptoms. The occurrence of IgM antibodies before IgM antibodies in two patients during the early stages of myasthenia gravis suggests that the antibody is not a primary cause of the disease.

Adrenocorticotropic Hormone↗
PubMed1978

Immunoglobulins in myasthenia gravis. Kinetic properties of the acetylcholine-receptor antibody studied during lymph drainage.

A specific immunoglobulin, the receptor antibody, can be found in most patients with myasthenia gravis. In order to study the kinetic properties of this antibody, serial determinations of receptor antibody, total IgG and IgG 3 were made during drainage of thoracic duct lymph in three patients. The values obtained were used in a mathematical model to calculate some kinetic parameters. Values for T 1/2 and fractional rates of synthesis and catabolism obtained for total IgG and IgG 3 by this method were shown to agree with those found with other techniques. Most of the receptor antibody activity was found in the IgG 3 fraction but the receptor antibody had a shorter T 1/2 and higher fractional rates of synthesis and catabolism than IgG 3. These kinetic characteristics are consistent with rapid variations in plasma concentration of the receptor antibody. The cause of this rapid turnover could be strong antigenic stimuli and rapid elimination by the antigen, the cholinergic receptor protein.

Acetylcholine↗