Procile Gold

[Renita Lukins]

Contemporaryhandmade Irish jewellery designed and made in Dublin by goldsmith Eva Dorney using precious metals, diamonds and gemstones. Specialising in custom made engagement rings and handmade wedding bands that will last a lifetime.

Additionally Eva offers a remodelling service if you want to rework an existing piece and a remelting service, where she will recycle your old gold and make you something new from your own metal, sentiment intact.

Gold salts, including auranofin and gold sodium thiomalate, have been used for the therapy of rheumatoid arthritis for many decades, but have recently been replaced by more modern disease-modifying antirheumatic drugs. Parenteral gold therapy (chrysotherapy) can cause acute, clinically apparent hepatitis that is usually cholestatic and self-limited in nature, but can be severe and even fatal. In contrast, oral gold preparations (such as auranofin) are associated with a low rate of serum enzyme elevations during treatment, but have not been convincingly linked to clinically apparent liver injury.

Gold given as a conjugate with thioglucose, thiosulphate or thiomalate salt has disease modifying activity in rheumatoid arthritis and can induce remission in up to 50% of patients. The mechanism of action is not well defined, but gold has clear antiinflammatory activity and lowers serum immunoglobulin levels. The use of gold as an antiinflammatory agent arose out of observations by Robert Koch who reported that gold salts had in vitro activity against mycobacterium tuberculosis. Trials of gold therapy in tuberculosis were unsuccessful, but clinically apparent antiinflammatory activity was found during treatment of patients with discoid lupus erythematosus, which at that time was believed to be due to tuberculosis. Chrysotherapy was introduced in the treatment of rheumatoid arthritis in the 1930s and it became a common approach to management of severe rheumatoid arthritis until the 1960s, when it was gradually replaced by more modern forms of disease modifying antirheumatic drugs (DMARDs) such as methotrexate, leflunomide, d-penicillamine, hydroxychloroquine, sulfasalazine, enteracept and imfliximab. Previous formulations of gold salts included a parenteral form as gold sodium thiomalate which was available as 50 mg/mL under brand names including Aurolate and Myochrysine (now no longer generally available in the United States). The recommended dose was 10 mg intramuscularly once weekly, gradually increasing to a maintenance dose of 25 to 50 mg weekly or every other week. An oral form of gold, audafolin (aw ran' o fin), continues to be available as capsules of 3 mg under the brand name of Ridaura, the recommended dose of which is 3 to 9 mg daily. Therapy with gold salts is often limited by toxicity, some of which is cumulative. The effect may take weeks to months to occur, but therapy should be discontinued after an accumulative dose of 1 gram if beneficial results are not achieved. Common side effects include abdominal discomfort, nausea, pruritus, skin rash, urticaria and proteinuria. Fatal instances of hypersensitivity reactions, renal dysfunction and bone marrow suppression have been reported.

Therapy with parenterally administered gold salts was linked with instances of acute liver injury shortly after being introduced into therapy in the 1930s. The nature of the liver injury was not well defined. The more modern formulations of gold appear to have a lower overall incidence of toxicity, including hepatotoxicity. Mild elevations in serum aminotransferase levels are not infrequent during therapy with gold, but clinically apparent liver injury is rare and appears to be idiosyncratic in nature and has been reported only with parenteral gold therapy. The onset of injury is within 1 to 8 weeks of starting therapy and presents with fever and rash, followed by malaise, nausea, right upper quadrant pain, dark urine and jaundice. Pruritus can be prominent and the typical pattern of serum enzyme elevations is cholestatic or mixed. Recovery may be delayed but is usually complete within 6 to 8 weeks. Transient thrombocytopenia and anemia can occur, particularly in children. Autoantibody formation is not typical, although patients with rheumatoid arthritis are prone to have preexisting autoantibodies. A less frequent pattern of injury from gold therapy is marked by acute hepatic necrosis, usually arising within 1 to 4 weeks of starting therapy with marked elevations in serum aminotransferase levels (20 to 100 fold) and minimal increases in alkaline phosphatase. These cases of acute hepatocellular injury may be associated with high doses of parenteral gold salts and can be severe and have resulted in fatalities. A striking phenomenon is that symptoms of arthritis frequently improve during acute hepatic injury whether due to gold therapy or viral hepatitis. The improvements, however, are transient and of no lasting benefit.

Oral gold therapy has been associated with transient, mild elevations in serum aminotransferase levels, but there have been no convincing cases of clinically significant liver injury linked to oral preparations. Thus, idiosyncratic acute liver injury due to auranofin must be very rare, if it occurs at all.

The typical acute liver injury from parenteral gold therapy appears to be related to hypersensitivity and is often accompanied by other allergic manifestations such as fever, rash, lymphadenopathy and eosinophilia. Cases of short latency onset, acute hepatic necrosis due to injections of gold more closely resemble direct, acute toxicity and have been reported after acute intentional or unintentional overdose of gold salts.

Most cases of jaundice from parenteral gold therapy are self-limited, although recovery may be prolonged. There is little evidence that chelation improves outcome or speeds recovery, although it is often used with acute overdose of a gold containing compound. Rare instances of acute hepatic necrosis soon after initiation of gold therapy have been reported, some of which have been fatal. Rechallenge after clinically apparent hepatotoxicity can lead to severe recurrence and should be avoided. In situations of mild serum aminotransferase elevations during gold therapy, reinstitution of treatment without recurrent elevations is typical.

A 10 year old boy with suspected juvenile idiopathic (rheumatoid) arthritis was started on parenteral gold therapy in a dose of 40 mg daily for eight days (in error, as it was meant to be given twice weekly) and developed fever, rash and headaches by day nine, followed by severe nausea and vomiting leading to electrolyte imbalance and dehydration. Three days after stopping the gold injections, he was found to be jaundiced with pruritus, dark urine and light stools. The serum bilirubin was 14.6 mg/dL, alkaline phosphatase 630 U/L and ALT 130 U/L (Table). His fever and rash persisted for a week, but then improved rapidly with prednisone therapy. He remained jaundiced for a month with symptoms of pruritus and prominent elevations in serum alkaline phosphatase. A liver biopsy showed intrahepatic cholestasis. Electron microscopy demonstrated scattered gold particles in lysosomes of Kupffer cells and hepatocytes. Over the following 4 weeks the jaundice cleared and, by 6 weeks, laboratory abnormalities had returned to normal. His arthritis was managed with indomethacin.

A cholestatic hepatitis in a child arising within a few days of stopping an 8 day course of gold therapy. The dose of gold was excessive and was meant to be given twice weekly rather than daily. Nevertheless, the pattern of injury was typical of a hypersensitivity reaction with fever and rash (DRESS syndrome, although no mention made of eosinophil counts). While the rash and fever appeared to respond to prednisone therapy, the jaundice was more persistent. Chelation therapy was not used.

There are two types of gold traded in India, i.e, 24K and 22K. The first one is considered the purest form of gold with a purity of 99.99 per cent. It is too soft to be moulded into jewellery. On the other hand, 22k gold is basically 22 parts of gold and two other metals like copper and zinc. It is used to make jewellery.

The price of gold depends on several factors including currency, global developments, interest rates etc. If the rupee weakens against US dollar, the price of gold will go up. Gold price is also dependent on international factors like global economic growth, volatile policies and interest rates.

In Indian cities, gold prices depend on various factors like demand, state taxes, octroi, interest levied etc. Gold can be bought in the form of bars, coins and jewellery. The investment options include physical gold, exchange trade funds and sovereign bonds.

In India, gold is officially marked by the Bureau of Indian Standards. It is called hallmarking and acts as a guarantee of the precious metal's purity. It protects the buyer from adulteration of gold.

Gold prices in India are determined on several factors including currency, global demand, interest rates and government policies. If the rupee slides against the US dollar in India, gold will become expensive.

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