The most serious side effects of NSAIDs are
hypersensitivity reactions like hematologic (aplastic
anemia, trombocytopenia, agranulocytosis, hemolytic
anemia), erythema multiforme and hepatitis
2-5.
Multisystem toxicities including Coombs positive
hemolytic anemia, acute liver failure and acute renal
failure with acute tubular necrosis cases are also
reported in the literature
1. Analgesics or sometimes
contaminants of pharmacologic composition are reported
to be the cause of acute hemolytic reactions generally by immunologic pathway
6. The mechanism of acute liver
injury associated with NSAIDs is poorly understood,
however a possible mechanism may be the interaction of
NSAIDs' metabolites with some hepatocellular proteins.
This interaction causes immunologic reactions and may
produce hepatotoxicity in susceptible patients
7,8. The
renal effects of NSAIDs especially in patients with
varying degrees of kidney disfunction are generally due
to altered hemodynamics because of the inhibition of
renal prostoglandin production. This process can emerge
as fluid and electrolyte imbalance, acute renal
disfunction, nephrotic syndrome, interstitial nephritis or
renal papillary necrosis
9.
In our patient, systemic toxicities including hemolytic
anemia, elevation of liver enzymes and acute renal
failure were all emerged after the administation of
diclofenac. After cessation of this molecule and following
supportive and therapeutic interventions, her general
status and biochemical parameters recovered.
In conclusion, it should be remembered by the
clinicians that NSAIDs can cause multisystemic toxicities
such as hemolytic anemia, liver disfunction and kidney
failure. Immediate treatment attempts after the early
diagnosis can be life-saving.