Bone marrow suppression is the dose limiting toxicity of Carboplatin. The nadir usually occurs about day 21 in patients receiving single agent therapy. Marrow suppression is usually more severe in patients with impaired kidney function. Patients with poor performance status have also experienced a higher incidence of severe leucopenia and thrombocytopenia. Anaemia with haemoglobin less than 11g/dl occurs in majority of the patients who start therapy with a baseline above the value. The incidence of anemia increases with increasing exposure to carboplatin.
Transfusions may be required in some patients treated with carboplatin. Bone marrow depression may be more severe when carboplatin is combined with other bone marrow suppressing drugs or with radiotherapy.
Vomiting occurs in about a quarter of patients receiving carboplatin vomiting has been reported in over half of the patients and about one-third of these suffer severe emesis. Nausea and vomiting are generally delayed until 6 to 12 hours after administration of carboplatin, usually disappear within 24 hours after treatment and are usually responsive to (and may be prevented by) anti-emetic medication. A quarter of patients experience no nausea or vomiting. Vomiting that could not be controlled by drugs was observed in only 1% of patients. Vomiting seems to occur more frequently in previously treated patients, particularly in patients pre-treated with cisplatin.
Peripheral neuropathies have been observed in small number of patients receiving carboplatin with mild paresthesias occurring most frequently. Patients older than 65 years have an increased risk for peripheral neuropathies. Clinical ototoxicity and other sensory abnormalities such as visual disturbances and change in taste occur rarely. Central nervous system symptoms have been reported in fewer patients and appear to be most often related to the use of antiemetics. Although the overall incidence of peripheral neurologic side effects induced by carboplatin is low, prolonged treatment may result in cumulative neurotoxicity.
Development of abnormal renal function test results is uncommon with carboplatin. Creatinine clearance has proven to be the most sensitive measure of kidney function in patients receiving carboplatin, and it appears to be measure of kidney function in patients receiving carboplatin, and it appears to be the most useful test for correlating drug clearance and bone marrow suppression. Nephrotoxicity may manifests as reduced creatinine clearance, elevated serum creatinine, blood urea nitrogen and uric acid levels.
Abnormal liver function tests in patients may be found with normal baseline value. These abnormalities (e.g.: SGOT, total bilirubin and alkaline phosphatase) have generally been mild and reversible in about one-half of the cases, although the role of metastatic tumor in the liver may complicate the assessment in many patients.
Hypocalcaemia, hypomagnesaemia, hypokalemia, hyponatremia, increased blood urea nitrogen, increased uric acid are some of the electrolyte abnormalities occurring with carboplatin Electrolyte supplementation is not routinely administered concomitantly with carboplatin, and these electrolyte abnormalities are rarely associated with symptoms.
Hypersensitivity to Carboplatin develops only in a small number of patients and consists of rash, urticaria, erythema, pruritus and rarely bronchospasm and hypotension. These reactions are successfully managed with standard epinephrine, corticosteroid and antihistamine therapy.
Ototoxicity may manifests as tinnitus and hearing loss in the higher frequency range. Hearing impairment may worsen with carboplatin therapy.
Pain and asthenia occur most frequently. Alopecia, cardiovascular, respiratory, genitourinary and mucosal side effects occur only in small number of patients. Pre-existing paraesthesia (especially those related to previous cisplatin therapy) may worsen during carboplatin therapy.