Paraneoplastic Hypereosinophilia in Locally Advanced Clear Cell Renal Carcinoma.

Renal cell carcinoma (RCC) can cause various paraneoplastic syndromes, including metabolic and hematologic disturbances. Paraneoplastic hypereosinophilia has been reported in a variety of hematologic and solid tumors. Hypereosinophilia due to RCC is very rare and is only available as case reports in the literature. A 66-year-old male patient's thoracoabdominal computed tomography (CT) performed showed an increase in size in the right kidney and a heterogeneous contrasting solid mass of approximately 12 cm × 9 cm, which formed lobulations in its contours. The patient was diagnosed with clear-cell renal carcinoma as a result of a kidney biopsy. In the patient with stage cT4NxM0, the leukocyte count was 40.000/µl and the eosinophil count was 20% in biochemical tests. With these results, the patient was evaluated as having severe paraneoplastic hypereosinophilia due to RCC. The patient was started on sunitinib 50 mg for two weeks on/one week off. No symptoms were observed due to hypereosinophilia. In the evaluation made two weeks after the start of the treatment, it was observed that eosinophil levels decreased to normal rates. Paraneoplastic hypereosinophilia due to renal cell carcinoma may indicate poor prognosis and rapid disease progression. Myelosuppressive therapy is required for symptomatic patients.

In vitro inhibition of salicylic acid derivatives on human cytosolic carbonic anhydrase isozymes I and II.

The inhibition of two human cytosolic carbonic anhydrase (hCA, EC 4.2.1.1) isozymes, hCA I and II, with a series of salicylic acid derivatives was investigated by using the esterase method with 4-nitrophenyl acetate as substrate. IC(50) values for sulfasalazine, diflunisal, 5-chlorosalicylic acid, dinitrosalicylic acid, 4-aminosalicylic acid, 4-sulfosalicylic acid, 5-sulfosalicylic acid, salicylic acid, acetylsalicylic acid (aspirin) and 3-metylsalicylic acid were of 3.04 microM, 3.38 microM, 4.07 microM, 7.64 microM, 0.13 mM, 0.29 mM, 0.42 mM, 0.56 mM, 2.71 mM and 3.07 mM for hCA I and of 4.49 microM, 2.70 microM, 0.72 microM, 2.80 microM, 0.75 mM, 0.72 mM, 0.29 mM, 0.68 mM, 1.16 mM and 4.70 mM for hCA II, respectively. Lineweaver-Burk plots were also used for the determination of the inhibition mechanism of these substituted phenols, most of which were noncompetitive inhibitors with this substrate. Some salicylic acid derivatives investigated here showed effective hCA I and II inhibitory activity, and might be used as leads for generating enzyme inhibitors eventually targeting other isoforms which have not been assayed yet for their interactions with such agents.