Sodium Aurothiomalate Injection B.P.

10 mg/0.5 ml, 20 mg/0.5 ml, 
50 mg/0.5 ml, 50 mg/5ml, 


For the use of a Registered Medical Practitioner or a Hospital or a Institution only. 

Adult and juvenile rheumatoid arthritis
Psoriatic arthritis or Feltys syndrome

SODIUM AUROTHIOMALATE INJECTION B.P. (Sodium Aurothiomalate) is used in juvenile chronic arthritis and rheumatoid arthritis. Chemically, SODIUM AUROTHIOMALATE  INJECTION  B.P. is mixture of monosodium and disodium salts of (2RS)-2-(aurosulphanyl)
butanedioic acid. The molecular formula is C4H4AuNaO4S & C4H3AuNa2O4S and molecular weight is 368.09

Its structural formula is : 

Sodium Aurothiomalate Injection B.P.

SODIUM  AUROTHIOMALATE  INJECTION  B.P. is a clear pale yellow solution filled in an amber coloured glass ampoule of suitable size.

Each ml contains :
Sodium Aurothiomalate B.P.                       10 mg    
Benzyl Alcohol B.P.                                0.5 % v/v
(as preservative)
Water for Injections B.P.                                 q.s.

Each 0.5 ml contains :
Sodium Aurothiomalate B.P.                        10 mg    
Benzyl Alcohol B.P.                                 0.5 % v/v
(as preservative)
Water for Injections B.P.                                  q.s.

Each 0.5 ml contains :
Sodium Aurothiomalate B.P.                        20 mg    
Benzyl Alcohol B.P.                                 0.5 % v/v
(as preservative)
Water for Injections B.P.                                  q.s.

Each 0.5 ml contains :
Sodium Aurothiomalate B.P.                        50 mg    
Benzyl Alcohol B.P.                                 0.5 % v/v
(as preservative)
Water for Injections B.P.                                  q.s.

It exhibits anti-inflammatory, antiarthritic and immunomodulating effects. The predominant clinical effect of sodium aurothiomalate appears to be suppression of the synovitis in the active stage of the rheumatoid disease. The precise mechanism of action is unknown but it has been suggested that the drug may act by inhibiting cell-mediated and humoral immune mechanisms. Additional modes of action include alteration or inhibition of various enzyme systems, suppression of phagocytic activity of macrophage and polymorphonuclear leukocytes,and alteration of collagen biosynthesis. The metabolic fate of SODIUM  AUROTHIOMALATE  in humans is unknown but it is believed not to be broken down to elemental gold. It is very highly bound to plasma proteins. 60 % to 90 % is excreted very slowly by the renal route while 10 to 40 % is eliminated in the faeces mostly via biliary secretion. The biologic half-life of gold following a single 50 mg dose of parenteral gold has been reported to range from 6 to 25 days. It increases following successive weekly doses. The appearance of clinical effect is slow. It may take at least 8 weeks to become significant and the maximum benefits may not be achieved for at least 6 months.

SODIUM  AUROTHIOMALATE is absorbed readily after intramuscular injection and 85 to 95 % becomes bound to plasma proteins. With doses of 50 mg weekly a steady state serum concentration of gold of about 3 to 5 micrograms/ml is reached in 5 to 8 weeks. It is widely distributed to body tissues and fluids, including synovial fluid, and accumulates in the body. The serum half-life of gold is about 5 to 6 days but this increases after successive doses and after a course of treatment, gold may be found in the urine for up to 1 year or more owing to its presence in deep body compartments. SODIUM  AUROTHIOMALATE is mainly excreted in the urine, with smaller amounts in the faeces. Gold has been detected in the foetus when it was given to the mother. Gold is distributed into breast milk.

SODIUM  AUROTHIOMALATE  INJECTION  B.P. is indicated in the treatment of both adult and juvenile rheumatoid arthritis. SODIUM  AUROTHIOMALATE  INJECTION  B.P. may also be of benefit in the treatment of patients with psoriatic arthritis or Felty’s syndrome. It is usually used for treating patients who show evidence of continued or additional disease activity despite conservative drug therapy,e.g.,with salicylates or other anti-inflammatory agents. SODIUM  AUROTHIOMALATE  INJECTION  B.P . may induce partial or complete remission of rheumatoid arthritis. In chronic advanced rheumatoid arthritis, it may prevent further damage to affected joints ; however, it does not reverse existing damage.


Administration :
SODIUM  AUROTHIOMALATE  INJECTION  B.P. should be administered by the intramuscular route only, preferably in the gluteal muscle.

Warning : 
It is advisable to inject SODIUM AUROTHIOMALATE  INJECTION  B.P. immediately after transfer into syringe because exposure to daylight will produce a rapid discoloration of the solution. DO NOT ADMINISTER THE SOLUTION IF DARKER THAN PALE YELLOW.
Because of the possibility of an anaphylactic reaction, it is recommended that patients be kept under medical observation for a period of 30 minutes after administration of the drug.

The ampoule used in this product is equipped with O.P.C (One Point Cut) opening system. No ampoule file is needed to open the ampoule. The neck of the ampoule is prescored at the point of constriction. A coloured dot on the ampoule head helps to orientate the ampoule. Take the ampoule and face the coloured dot. Let the solution at the head of the ampoule to flow down by shaking or a gentle stroke. The ampoule opens easily by placing the thumb on the coloured dot and gently pressing downwards as shown.

Dosage :
SODIUM  AUROTHIOMALATE  INJECTION  B.P. must be given by deep intramuscular injection and the area gently massaged. A test dose of 10 mg must be given followed by doses of 50 mg at weekly intervals until there is definite evidence of remission. Benefit is not to be expected until about 300–500 mg has been given ; it should be discontinued if there is no remission after 1 g has been given. In patients who do respond, the interval between injections is then gradually increased to 4 weeks and treatment is continued for up to 5 years after complete remission. If relapse occurs the dosage frequency may be immediately increased to 50 mg weekly and only once control has been obtained again should the dosage frequency be decreased ; if no response is seen within 2 months, alternative
treatment should be sought. It is important to avoid complete relapse since second courses of gold are not usually effective. 

In children :
For children with progressive juvenile idiopathic arthritis the suggested initial weekly dose of SODIUM  AUROTHIOMALATE  INJECTION  B.P. is 1 mg/kg by deep intramuscular injection to a maximum of 50 mg weekly (one-tenth to one-fifth of the calculated initial weekly dose may be given for 2 to 3 weeks to test the patient’s tolerance). Weekly doses should continue until signs of remission occur, at which point the dosage interval may be increased to fortnightly. With full remission, the dosage interval may again be increased gradually to every 4 weeks. If no improvement has occurred after 20 weeks, the dose could be raised slightly or another antirheumatic drug tried.

Sodium aurothiomalate is contraindicated in patients with known hypersensitivity to gold. It is also contraindicated in patients who have experienced the following serious adverse effects with previous gold therapy : bone marrow aplasia or other haematological disorders, exfoliative dermatitis, necrotizing enterocolitis or pulmonary fibrosis.

The following conditions may aggravate or precipitate adverse reactions to SODIUM  AUROTHIOMALATE  INJECTION  B.P. , or their symptoms may mask the forwarning signs of gold toxicity :

  • Blood dyscrasias or a history of agranulocytosis, haemorrhagic diathesis or drug induced granulocytopaenia or anaemia ;
  • Renal disease ;
  • Hepatic dysfunction ;
  • Systemic lupus erythematosus ;
  • Significant dermatitis including urticaria or eczema.

Any of the above conditions should be considered as a relative contraindication to the use of SODIUMAUROTHIOMALATE  INJECTION  B.P.  In such cases, treatment should be initiated with extreme caution and only after careful assessment of expected benefits versus the potential risks. Rarely, anaphylactic shock, syncope, bradycardia, thickening of the tongue, difficulty in swallowing and breathing, and angiooedema may occur in the minutes that follow the injection of SODIUM  AUROTHIOMALATE  INJECTION  B.P.. If an anaphylactic reaction occurs, treatment should be discontinued. A vasomotor (nitritoid) reaction may occur within several minutes of a SODIUM  AUROTHIOMALATE  INJECTION  B.P. injection. The nitritoid reaction is characterized by flushing, tachycardia and faintness. When it occurs, caution should be exercised before resuming therapy in patients with compromised cardiovascular status.

Carcinogenicity/Tumorigenicity : 
Renal adenoma and adenocarcinoma have been reported in rats after prolonged administration of frequent, high doses of parenteral gold compounds (2 mg/kg/week for 45 weeks followed by  6 mg/kg/day for 47 weeks in one study ; 3 mg/kg/day or 6 mg/kg/day for up to 2 years in a second study). The adenomas were similar to those produced in rats by chronic administration of other heavy metals such as lead or nickel. The relevance of these findings to man is unknown. Renal adenomas have not been reported in humans receiving therapeutic doses of sodium aurothiomalate.SODIUM  AUROTHIOMALATE  INJECTION  B.P. contains benzyl alcohol as preservative. Benzyl alcohol has been reported to be associated with a fatal “Gasping Syndrome” in premature infants. Symptoms include a striking onset of gasping syndrome, hypotension, bradycardia and cardiovascular collapse. 

SODIUM  AUROTHIOMALATE  INJECTION  B.P. should be administered only to selected patients who are under the supervision of a physician experienced with chrysotherapy and thoroughly familiar with the toxicity and benefits of the drug. Patient monitoring : Toxic reactions to SODIUM  AUROTHIOMALATE  INJECTION  B.P. are relatively frequent and, in certain cases, may be quite severe. Thus emphasis should be placed on careful clinical and laboratory monitoring and early detection of adverse reactions. Baseline evaluation should include a biochemical profile to identify any preexisting conditions. Before receiving gold, patients should also have a complete blood cell count with differential, platelet count, haemoglobin determination and urinalysis for protein, white cells, red cells and casts ; these tests should be repeated before each injection and patients should have an examination of the skin and buccal mucosa for skin rash, bruising or mouth ulcers. They should be questioned for the presence of pruritus, rash, stomatitis or metallic taste.

Dermatitis and lesions of the mucous membranes are common and may be serious ; pruritus may precede the early development of a skin reaction. Renal toxicity ranges from mild proteinuria to the nephrotic syndrome ; prognosis is usually good. Haematologic reactions have been observed rarely but fatalities have ensued. Other severe toxic manifestations include cholestatic jaundice, enterocolitis and interstitial lung disease. If toxicity develops, SODIUM  AUROTHIOMALATE  INJECTION  B.P. should be discontinued immediately and symptomatic treatment be given as required. If the reaction to gold therapy is not of a serious type, injections may be cautiously resumed 2 or 3 weeks after the toxic reaction has subsided. In these circumstances, from 5 to 10 mg of gold is administered ; if the challenge dose is tolerated, SODIUM  AUROTHIOMALATE  INJECTION  B.P. may be administered cautiously in larger doses on subsequent injections. Severe reactions are a contraindication to further gold therapy.


Pregnancy : Category C 
While reassuring, the information concerning the administration of gold during pregnancy is sparse and largely anecdotal ; there have been no controlled prospective studies of the effect of sodium aurothiomalate on human foetal development. Gold is known to cross the placenta and it can reach significant concentrations in the foetus. Gold therapy is seldom needed during pregnancy. If its use is nevertheless contemplated, the risk/benefit ratio should be considered keeping in mind the potential of sodium aurothiomalate for teratogenicity.

Nursing mothers : 
Parenterally administered gold is excreted in human breast milk and has been detected in the blood of a nursing infant. Although problems in humans have not been documented, the use of SODIUM  AUROTHIOMALATE  INJECTION  B.P. in nursing mothers is not usually recommended because of the potential for serious adverse effects in the infant.

Paediatric Use : 
Although appropriate studies have not been done in the paediatric population, it is being used in the treatment of juvenile arthritis. For aurothioglucose and gold sodium thiomalate—Studies performed to date have not demonstrated paediatrics-specific problems that would limit the usefulness of these medications in children.

There is an increased risk of toxicity when gold compounds are given with other nephrotoxic, hepatotoxic, or myelosuppressive drugs. Use of gold compounds with penicillamine may increase the risk of haematologic or renal adverse reactions. 
The following medicines may interact with SODIUM  AUROTHIOMALATE  INJECTION  B.P. :

  • Aspirin
  • Oxyphenbutazone
  • Phenylbutazone
  • ACE inhibitors

Patients taking ACE inhibitors may be at increased  risk of nitritoid reactions It is recommended that a patient never be started on   ACE inhibitor if considering to start or currently on gold therapy. If a patient is already on an ACE inhibitor, an alternative hypertensive should be considered. 

Interference with drugs : 
The concurrent use of D-penicillamine or other drugs with potential bone marrow toxicity may increase the potential for serious haematologic and/or renal adverse reactions.

The most frequent adverse reactions with SODIUM  AUROTHIOMALATE  INJECTION  B.P. involve the skin (ranging from simple rash to severe exfoliative dermatitis) and mucous membranes (ulcers) and may affect 30 % of patients. Renal effects are next in frequency with proteinuria being observed in 10 to 15 % of patients. The severe adverse reactions are those affecting the bone marrow (agranulocytosis, thrombocytopaenia and aplastic anaemia), exfoliative dermatitis, enterocolitis, liver failure, anaphylactoid reactions and nephropathy ;these are rare but may be fatal. It has been proposed that serious reactions may be the result of failure to discontinue therapy when earlier less serious symptoms occur. Close patient monitoring will not eliminate untoward effects but may help reduce their severity. 

The following side effects have been reported :
Skin and Mucous Membranes : Pruritus and rash (30  %) ranging from simple erythema to exfoliative dermatitis, and mucous membrane lesions (20 %) including stomatitis. Haematological : Leukopaenia (2 %), thrombocytopaenia (1 - 3 %) eosinophilia, agranulocytosis and aplastic anaemia.
Renal : Proteinuria (10 – 15 %), nephrotic syndrome, acute renal failure.
Allergic : Anaphylactoid and vasomotor (nitritoid) reactions.
Digestive : Metallic taste, diarrhoea, enterocolitis, cholestatic jaundice.
Miscellaneous : Other very rare reactions include encephalitis, peripheral neuropathy and pulmonary infiltrates.
Chrysiasis (affecting the skin and mucous membranes) and corneal gold deposits have been noted in some patients.
A transient flare of articular inflammation appearing within 24 hours of injection and lasting 2 or 3 days has also been reported.

Symptoms are those of heavy metal toxicity ; they include pruritus, dermatitis, stomatitis, vague gastrointestinal discomfort, albuminuria with or without a nephrotic syndrome, haematuria, agranulocytosis, thrombocytopaenic purpura, and aplastic anaemia.

Gold therapy should be discontinued promptly and supportive treatments should be given as required for specific complications. Patients with severe dermatitis may benefit from oral antihistamines, topical corticosteroids or emollients. For the management of severe renal, haematologic, pulmonary enterocolic or generalized pruritic reactions, moderate to high dose corticosteroid therapy (e.g. prednisone 20 - 100 mg daily in divided doses) reportedly is beneficial. When high-dose corticosteroid therapy is ineffective or substantial adverse reactions to steroidsoccur, a chelating agent (e.g. dimercaprol) or a drug such as N-acetylcysteine may be used to enhance the elimination of gold.

Parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.

Store below 25°C (77°F), protected from light. 
Do not refrigerate.

24 months from the date of manufacture.

SODIUM  AUROTHIOMALATE  INJECTION  B.P. is supplied as per below table :

Sodium Aurothiomalate Injection B.P.



Disclaimer : For the use of a Registered Medical Practitioner or a Hospital or a Institution only. Also it is not intended to be used by healthcare professionals or patients for the purpose of prescribing or administering these products. Questions regarding the complete and current content of product labeling / specification / presentation should be directed to SGPharma.

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