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Rheumatology and immunology
Published in Michael McGhee, A Guide to Laboratory Investigations, 2019
Sodium aurothiomalateFBC (including Hb, WCC, MCV and platelets) should be performed at week 1, week 3 and then monthly after initiation of treatment and after any increase in dose.Check urine for protein and blood each time.Creatinine (or eGFR) alkaline phosphatase and ALT should also be monitored at week 1, week 3 and then monthly after initiation of treatment and after any increase in dose.
Orthopaedic Pharmacology
Published in Manoj Ramachandran, Tom Nunn, Basic Orthopaedic Sciences, 2018
Manoj Ramachandran, Daud Chou, Natasha Rahman
Sodium aurothiomalate is administered by deep intramuscular injection and the maximum effect is seen after 3 months. The exact mechanism of action is unknown; however, it is proposed that it is able to inhibit macrophage activation.
Statistics in medical research
Published in Douglas G. Altman, Practical Statistics for Medical Research, 1990
10.5 A study was made of 65 patients who had received or were receiving sodium aurothiomalate as a treatment for rheumatoid arthritis (Ayeshet al., 1987). The aim was to examine the possibility that toxicity to sodium aurothiomalate (SA) might be linked to sulphoxidation capacity, as assessed by the sulphoxidation index (SI). The data were given in Exercise 3.1. Values of SI > 6.0 were taken as indicating impaired sulphoxidation. They obtained the following table: Major adverse reaction(toxicity)YesNoTotalImpairedYes30939sulphoxidationNo71926Total372865
GOLD: human exposure and update on toxic risks
Published in Critical Reviews in Toxicology, 2018
Gold exhibits oxidation states ranging from −1 to +5 and theoretically has the capacity to form a large number of inorganic and organic compounds, but compounds of Au(I) and Au(III) are predominant (Henderson and Raynor 1962; Mohr et al. 2006). Gold chloride (AuCl3) is hygroscopic and highly soluble in water; it decomposes at 160° to form AuCl. Chloroauric acid (HAuCl4.xH20) formed when gold dissolves in aqua regia is also highly soluble, but corrosive and very toxic. The principle compounds listed in formularies for treatment of rheumatoid arthritis include auranofin (Ridaura®) (Figure 1), sodium aurothiomalate (Mycrisin™) sodium aurothiosulphate, aurothiopropanol sulfate (Allocristin™) and aurothioglucose (Solganal™) (Best and Sadler 1996). Auranofin contains 29% gold and is administered orally, whereas the gold thiolates are injectable. Following administration of gold salts, plasma gold is associated with red blood cells and plasma proteins. The exact metabolic fate of sodium aurothiomalate and aurothioglucose is not understood. Pharmacokinetics have shown that with aurothioglucose administration, approximately 85% of plasma gold is metabolized to lymph nodes, bone marrow, liver, skin and bone. Auranofin is metabolized rapidly such that the intact molecule is not detectable in blood (Blocka 1983).
Critical review of renal tubule karyomegaly in non-clinical safety evaluation studies and its significance for human risk assessment
Published in Critical Reviews in Toxicology, 2018
Another example of a therapeutic used in humans that was a consistent inducer of renal tubule karyomegaly in rats is auranofin. This drug has been marketed since 1985 when it was approved for treatment of rheumatoid arthritis. It is now being considered for repurposing with new therapeutic potential for many serious human diseases (Roder and Thompson 2015). The primary adverse effects of auranofin in humans concern gastrointestinal tract symptoms and skin irritations, but not commonly, renal conditions, a profile that contrasts directly with the karyomegalic kidney effects of auranofin in the rat. In the early development of auranofin, rheumatoid arthritis patients receiving either auranofin or sodium aurothiomalate did not show any clinical chemistry indications of nephrotoxicity after 6 months of treatment (Crisp et al. 1983). From the long history of clinical use, it can be inferred that renal tubule karyomegaly is not a human response to this compound. These examples suggest that the induction of renal tubule karyomegaly in laboratory animals is not generally predictive of similar kidney changes in humans.
Association of rheumatoid arthritis disease activity and antibodies to periodontal bacteria with serum lipoprotein profile in drug naive patients
Published in Annals of Medicine, 2020
Aulikki Kononoff, Pia Elfving, Pirkko Pussinen, Sohvi Hörkkö, Hannu Kautiainen, Leena Arstila, Leena Laasonen, Elina Savolainen, Helena Niinisalo, Jarno Rutanen, Olga Marjoniemi, Mari Hämäläinen, Katriina Vuolteenaho, Eeva Moilanen, Oili Kaipiainen-Seppänen
All patients were on anti-rheumatic therapy with disease-modifying antirheumatic drugs, two-thirds mainly with a combination of two or three of the following drugs: methotrexate, hydroxychloroquine and sulphasalazine and half were also on low-dose prednisolone. One-year follow-up data were available for 54 persons. At one year, the therapy was continued mainly with the combinations of the aforementioned disease-modifying antirheumatic drugs and a third of the patients were still on low-dose prednisolone. Two patients were on azathioprine and one on sodium aurothiomalate. One patient was also on anakinra due to systemic features of the disease and one was treated with rituximab during the first year. The benefit of therapy was shown, as the mean DAS28(ESR) (SD) decreased from 4.3 (1.3) to 2.0 (1.2) with a mean difference of 2.3 (95% CI; 1.89–2.69, p<.001), between the baseline and follow-up visits. DAS28(ESR) at baseline showed a weak association with an increase in LDL concentration between baseline and one-year follow-up, whereas the increase was more significant in HDL concentration and in anti-MAA-IgM level as shown in Table 3. The mean diameter of LDL particles decreased significantly. Decrease in anti-MAA-LDL-IgM level showed a moderate positive association with a combination therapy of disease-modifying antirheumatic drugs (n = 29, r = 0.40, 95% CI; 0.15–0.60, p=.003) and a weak positive association with the use of prednisolone (n = 19, r = 0.30, 95% CI; 0.03–0.53, p=.024) or sulphasalazine (n = 28, r = 0.33, 95% CI; 0.06–0.55, p=.011) as a part of medication, but not with the use of hydroxychloroquine (n = 31) or methotrexate (n = 31).