Subject(s)
Anemia, Hemolytic, Autoimmune/chemically induced , Anti-Bacterial Agents/adverse effects , Ceftazidime/adverse effects , Aged , Anemia, Hemolytic, Autoimmune/blood , Anemia, Hemolytic, Autoimmune/urine , Anti-Bacterial Agents/administration & dosage , Ceftazidime/administration & dosage , Hemoglobinuria/blood , Hemoglobinuria/drug therapy , Hemoglobinuria/urine , Humans , Severity of Illness IndexABSTRACT
There have been a few reported cases of immune hemolytic anemia induced by ceftriaxone. We encountered a patient with immune hemolytic anemia that seemed to be stimulated by a degradation product of ceftriaxone. The patient's direct antiglobulin test was positive only for C3d, and no ceftriaxone-dependent antibodies were detectable in the patient's serum. To demonstrate the presence of the ceftriaxone-induced antibodies, an ex-vivo antigen in urine was obtained from the patient. In addition, we prepared a 1 mg/mL suspension solution of ceftriaxone, and group AB serum as a complement source. Using several combinations of the above reactants, the indirect antiglobulin test was performed. Only the indirect antiglobulin test using the patient's serum with the ex-vivo urine antigen was found to be positive. Other combinations were not reactive. To our knowledge, this is the first reported case in Korea, in which the causative antibody appeared to be stimulated solely by a degradation product of ceftriaxone.
Subject(s)
Anemia, Hemolytic, Autoimmune/chemically induced , Anemia, Hemolytic, Autoimmune/diagnosis , Ceftriaxone/adverse effects , Cephalosporins/adverse effects , Anemia, Hemolytic, Autoimmune/immunology , Anemia, Hemolytic, Autoimmune/urine , Antigens/urine , Coombs Test , Humans , Male , Middle AgedABSTRACT
A 48-year-old man with idiopathic hypereosinophilic syndrome (IHS) developed blast crisis along with a fulminant autoimmune hemolytic anemia. Hemoglobinuria and anuric acute renal failure (ARF) ensued. Urinalysis revealed countless Charcot-Leyden crysals (CLC). This is the only known report of Charcot-Leyden crystalluria. The CLC protein (lysophospholipase) should normally undergo glomerular filtration and catabolism by the tubules during reabsorption. Its abundant presence in the urine of our patient may reflect impairment of tubular reabsorption, saturation of the tubular reabsorptive process by excessive CLC load through residual functioning glomeruli, or a combination thereof. The extreme degree of hypereosinophilia suggests a massive load of CLC protein and acute tubular necrosis implies impaired tubular function, so both mechanisms should have been operative. At the autopsy, no eosinophilic infiltrates were present in the kidneys, which points against a local spillage of CLC protein into the tubules.
