Studies with Radioactive Gold

Six patients with chronic knee effusions were given single intravenous tracer doses of 195Au-aurothiomalate; tracer and stable gold content of serum and synovial fluid were studied. The average concentration of tracer gold in synovial fluid was 56% of that in corresponding serum specimens. The rate at which gold disappeared from serum and synovial fluid conformed to first-order kinetics, while observed from Day 1 through Day 7 after injection. Half-time for tracer disappearance was 5.2 days for serum and 6.2 days for synovial fluid.T h e principle site of the action of gold is unknown. Although previous studies have suggested that it is concentrated in the joint (1, 2) and has an affinity for inflamed tissue (3), little information is available on the distribution of gold between plasma and synovial spaces. Accordingly, we have studied the kinetics of 1 9 5 A~-aurothiomalate in serum and synovial fluid in a group of patients with inflammatory synovitis.

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Kinetics of aurothiomalate in serum and synovial fluid

Gerber¹,

Paulus²,

Bluestone³

et al. 1972

“…T' issue distribution of gold, on the other hand, has been adequately studied only in animals (7,8) Submitted for publication Apr 6, 1971; accepted June 21, 1971. tissues has never been systematically measured. There are scanty reports of gold levels in human skin, synovium, synovial fluid, etc, but methods of gold analysis were relatively insensitive and some of the patients studied had received only one injection of a radioactive gold-labeled compound rather than a course of gold therapy (2,3,9,10). No information is available regarding gold concentrations in internal organs or in the musculoskeletal system of a patient with rheumatoid arthritis on longterm chrysotherapy.…”

mentioning

confidence: 99%

Tissue gold concentration in a rheumatoid arthritic receiving chrysotherapy

Gottlieb

Smith

1972

133

Postmortem specimens from a patient with rheumatoid arthritis who had received 5 g of aurothioglucose were examined histologically, and their gold content was determined by activation analysis. The highest concentration of gold was found in the lymph nodes followed by the adrenal gland, renal cortex and other organs of the reticuloendothelial system. Comparatively low concentrations were found in tissues comprising the joint structure. Organs in which the greatest quantities of gold were stored include the bone marrow, liver, skin and bone. These findings demonstrate the body's capacity to store relatively large quantities of gold without adverse reaction, support the concept of a systemic rather than local mechanism of action (at the joint level) and demonstrate in vivo gold concentrations in the range expected to produce local cellular biologic effects.The metabolic and excretory pathways of gold compounds have been of interest to investigators since their benefit in the treatment of rheumatoid arthritis was first reported more than 40 years ago (1). Abundant data are available regarding gold concentrations in blood and its components and in the urine and feces of human and experimental animal models (2-6). T' issue distribution of gold, on the other hand, has been adequately studied only in animals (7,8) Submitted for publication Apr 6, 1971; accepted June 21, 1971. tissues has never been systematically measured. There are scanty reports of gold levels in human skin, synovium, synovial fluid, etc, but methods of gold analysis were relatively insensitive and some of the patients studied had received only one injection of a radioactive gold-labeled compound rather than a course of gold therapy (2,3,9,10). No information is available regarding gold concentrations in internal organs or in the musculoskeletal system of a patient with rheumatoid arthritis on longterm chrysotherapy. The sudden death of such a patient afforded us the opportunity to analyze tissues for their gold content. CASE REPORTMV was a 68-year-old white female with classic rheumatoid arthritis, by the ARA criteria. of 16 years duration who died in November 1969, of an overdose of barbiturate. When first seen in the Arthritis Clinic at Jackson Memorial Hospital in June 1958, she related a 5-year history of progressive polyarthritis with morning stiffness. Physical examination showed active synovitis of metacarpal phalangeal and proximal interphalangeal joints, 16Arthritis and Rheumatism, Vol. 15, No. 1 (Januafy-FebrurIy 1 9 n )

“…In 1 of these cases, proteinuria cleared with steroids, while in the other it persisted after steroids and after a combination of steroids and Iniuran. Three other patients (Cases 7,8 and 12), showed moderate-to-marked basement membrane thickening. I n none, did proteinuria clear with steroids alone.…”

Section: Clinical-pathologic Cbirelotionmentioning

confidence: 93%

Gold nephropathy a clinical and pathologic study

Silverberg

Kidd

Shnitka

et al. 1970

127

Proteinuria developed in 5 of 75 rheumatoid arthritis patients treated with gold salts. In 2 of these 5 patients criteria for the nephrotic syndrome were fulfilled. Two other cases of gold‐induced nephrotic syndrome are also reported. Blood and urine gold levels were measured on 27 of the 75 patients and no difference was found between the 2 patients who eventually developed the nephrotic syndrome and the 25 who did not. Light, electronmicroscopic and histochemical studies revealed no difference in the site or degree of gold deposition in the 4 cases with nephrotic syndrome, as compared with 1 patient who did not have proteinuria. Eventual clearing of the proteinuria was fairly closely related to the degree of glomerular basement membrane thickening, as judged by light microscopy.