Identification of impurities in technical metalaxyl.

Impurities such as 2,6-dimethylaniline, N-methyl-2,6-dimethylaniline, N-(1-methoxycarbonyl-ethyl)-2,6-dimethylaniline, N-methyl-N-(1-methoxycarbonyl-ethyl)-2,6-dimethylaniline, N-methyl-N-(1-methoxyacetyl)-2,6-dimethylaniline, N-(1-methoxyacetyl)-2,6-dimethylaniline and N-ethyl-N-(methoxyacetyl)-2,6-dimethylaniline present in samples of technical metalaxyl were isolated by column chromatography and identified by nuclear magnetic resonance, mass spectroscopy and comparison with reference compounds.

Chronic inflammatory demyelinating polyradiculoneuropathy: a prevalence study in south east England.

Although there are now widely accepted diagnostic criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) there are few epidemiological data. A prevalence study was performed in the four Thames health regions, population 14 049 850. The prevalence date was 1 January 1995. Data were from a national consultant neurologist surveillance programme and the personal case series of two investigators. A diagnosis of CIDP was made according to definite, probable, possible, or suggestive diagnostic criteria. A wide difference in prevalence rates between the four health regions was noted, probably due to reporting bias. In the South East Thames Region, from which the data were most comprehensive the prevalence for definite and probable cases was 1.00/100 000; the highest total prevalence (if possible and suggestive cases were included) would have been 1.24/100 000. On the prevalence date 13% of patients required aid to walk and 54% were still receiving treatment.

Immunological investigation of chronic inflammatory demyelinating polyradiculoneuropathy.

In order to investigate the hypothesis that chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disease related to the acute inflammatory form of Guillain-Barre Syndrome (GBS), we studied 40 patients, 40 age and sex matched controls with other forms of peripheral neuropathy (ONP) and 37 controls from the same family or household (FC). We sought antibodies to gangliosides GM1 and LM1 by enzyme linked immunoassay (ELISA) confirmed by immuno-overlay. Only 6 (15%) CIDP patients had IgM antibodies to ganglioside GM1 (GM1) and none had IgG antibodies. We found IgM antibodies to ganglioside LM1 in 2 (5%) and IgG antibodies in 4 (10%) CIDP patients. Antibodies of IgG or IgM class were detected by ELISA to chondroitin sulphate C or sulfatide in up to 7.5% of CIDP patients. There were IgM antibodies in 3 (7.5%) and IgG in 4 (10%) patients against 25, 28 or 36 kD myelin proteins identified by immunoblot. Antibodies to any of these candidate myelin autoantigens were not significantly more frequent in CIDP than FC or ONP controls. Sera from 5 CIDP patients with active disease which subsequently responded to plasma exchange did not induce more demyelination upon intraneural injection into rat sciatic nerve than ONP sera. Serum tumor necrosis factor alpha (TNFalpha) concentrations were not increased in any of the CIDP patients. Serological evidence of Campylobacter jejuni (Cj) infection was present in 4 (10%) CIDP patients. IgM antibodies to cytomegalovirus (CMV) were not detected in any sera. CIDP is not commonly associated with either of these infections or with an antibody-mediated response to any of these glycolipid or myelin autoantigens.

Long-term treatment of chronic inflammatory demyelinating polyradiculoneuropathy with plasma exchange or intravenous immunoglobulin.

To assess long-term treatment of chronic idiopathic demyelinating polyradiculoneuropathy (CIDP) with plasma exchange (PE) and intravenous immunoglobulin (IVIg), we studied 105 patients retrospectively by case-notes and follow-up. Thirty-three were treated with PE; 23 responded well. Twenty-two were treated with IVIg; 14 responded well and one had a hypotensive reaction during the first infusion. For both treatments, responders were more likely to be female and younger, and to have a shorter duration of symptoms. Most patients required only one course of treatment. Seven patients received repeated courses of PE for 8.1-59.7 months; seven received repeated courses of IVIg for 6-51 months. Transient complications occurred with PE: hypotension in three, difficulty in gaining venous access in three, and haematoma, bleeding diathesis, hypocalcaemia, and septicaemia in one patient each. Four patients transferred from long-term PE to IVIg, but the fifth responded to PE only. Two patients who were transferred from PE to IVIg were eventually able to stop all treatments. Long-term use of IVIg was free of any significant complications. Both PE and IVIg are possible long-term treatments for CIDP, but both are expensive, and PE had more side-effects.