Adverse reactions develop in roughly one third of patients treated with gold, the proportion varying from 5",, to 80O, in several reported series.' Eosinophilia occurs in roughly 5O, of patients and has been directly correlated with the development of gold toxicity.2 Vasomotor reactions to gold are not uncommon, but whether they indicate the development of more serious gold toxicity is unknown. Neurological complications, including peripheral neuropathy, myokymia, and a syndrome like the Guillain-Barre syndrome,3 have received little attention even in major textbooks of rheumatology.4 Encephalopathy has been reported: McAuley et al described a patient who recovered fully one month after treatment with gold was stopped.0The severity of the illness in our patient, with residual neurological deficit nearly five months afterwards, shows the serious side effects that may occur during chrysotherapy. Nephrotic syndrome during treatment with interferonInterferon has activity against multiple myeloma. ' In a trial of lymphoblastoid interferon A (Wellferon) given by ambulatory intravenous infusion for myeloma a patient with renal damage developed a nephrotic syndrome. Case reportA 42 year old white woman presented with an IgGL myeloma in Februarv 1980. Serum urea and creatinine concentrations were normal, but her urine contained Bence Jones protein. She received oral melphalan, but the condition did not improve.She was referred to us in June 1983 suffering from back pain. She was kyphotic. Investigations showed extensive lytic bone disease and heavy infiltration of bone marrow with mveloma cells. Serum urea and creatinine concentrations were normal, and her creatinine clearance was 82 ml/min. The serum contained 45 g IgGI. paraprotein?/l. Urine contained 6 g protein f1 with a trace of Bence Jones protein and a prominent leak of paraprotein. There was severe immune suppression, with a serum IgA concentration of < 0-1 g/l. Intravenous cyclophosphamide produced transient benefit, but the disease progressed and in November she was admitted for a trial of interferon given by continuous intravenous infusion.The figure shows the interferon dosage and urinary protein excretion. The urine volume was consistently about two litres dailv. The maximum urinary protein concentration, 34 days after the start of interferon, was 37 g'l, with non-selective proteinuria including 14 g albumin 11, 11 g paraproteinll, and 2 g lambda light chain/l. The electrophoretic patterns of serum and urinarv protein were almost identical, indicating an almost complete leak. Her glomerular filtration rate was 44 ml/min. Her serum albuimin concentration fell to 17 g!l and she developed bilateral ankle oedema. TIhe serum creatinine concentration remained unchanged. Ultrasonography of the kidneys yielded normal results. There were no autoantibodies. Concentrations of C3 and (A were slightly reduced, possibly owing to loss of protein in the urine. Tests for immune complexes (Clq binding and the platelet aggregation test, yielded negative results.Interferon was...
Inhibitory effect of sodium saccharin in concentrations from 10––5 to 10––2M was tested on glycolytic enzymes involved in phosphate transfer in cell-free extracts of Streptococcus mutans NCTC 10449. In the presence of 10––2M sodium saccharin the enzymes hexokinase, glyceraldehyde-3-phosphate dehydrogenase, phosphoglycerate mutase, pyruvate kinase, 3-phosphoglycerate kinase and phosphofructokinase were inhibited 58, 45, ∼16, 12, 3 and 1.4%, respectively. 10––3–10––2M sodium chloride produced little if any inhibition of the glycolytic enzymes tested.
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