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By a study of 87 oncologic hospitalized patients, affected by serious infectious complications and treated with high-dose antibiotic therapy including co-trimoxazole, the authors evaluate the allergic and immunologic reactions to the drug on clinical and serological basis and try to outline the pathogenic implicated mechanisms.

alpha-L-Fucosidase (EC 3.2.1.51; FUS) activity and isoenzyme characteristics were analyzed in normal lymphocytes, normal granulocytes (PMNs) and myeloid and lymphoid leukemic cells, (AML, AMMoL, ALL, CLL and CML). CLL lymphocytes had a lower mean specific activity than normal lymphocytes (2.5 v 4.0, p less than 0.05). ALL blasts had a higher mean specific activity compared to normal lymphocytes (9.7 v 4.0; p less than 0.001), CLL lymphocytes (9.7 v 2.5; p less than 0.001) and AML blasts (9.7 v 7.6 p = NS). Normal PMNs had a higher mean specific activity than normal lymphocytes (7.0 v 4.0 p less than 0.05) but similar activity when compared to CML cells or AML blasts. Blasts from AMMoL patients had higher activity than normal PMNs (9.0 v 7.0; p less than 0.05). The isoenzyme patterns of normal and leukemic granulocytes and lymphocytes were obtained by automated chromatofocusing on PBE-94 microcolumns with normal and leukemic lymphocyte lysates. With normal and leukemic lymphoid lysates two major isoenzyme components (B and A) were isolated. The isoenzyme pattern of PMN, AML, CML and AMMoL revealed 3 major peaks (B, A, I), totally different from that seen in lymphoid cells. The patterns of AML, CML and PMN appeared to be similar to each other; however, the isoenzyme pattern obtained from AMMoL cells could be distinguished from the others by a prominent I peak. Thus the FUS isoenzyme profile distinguishes the blasts of AMMoL from AML, and AMMoL and AML from ALL.

A new case of severe bone-marrow aplasia due to Ticlopidine therapy is described. On the basis also of immunologic findings, the drug seems to be the cause of the hematologic syndrome. The presence of an idiopathic hypothyroidism may have favored the immune mediated reaction to the drug.

In the present study, we examined 102 patients with chronic urticaria and angioedema. The incidence of immune complexes (CIC)-mediated chronic urticaria with complement activation (C3b+) was 11.7% (12/102 patients). The 12 patients with CIC and C3b was divided in three diagnostic groups: with drug adverse reactions; with systemic disorders; without apparent associated pathologies. On the basis of data obtained it is remarkable the necessity of a careful etiologic diagnosis in presence of CIC mediated-chronic urticaria particularly when it is associated with arthralgies and/or elevated erythrocyte sedimentation rate (ESR) because of a likely presence of a serious systemic pathology.

beta-Hexosaminidase (EC 3.2.1.20; Hex) activity and isoenzyme characteristics were analyzed in human normal and leukemic leukocytes. Unseparated CLL and CML cells had a specific activity that was lower, whereas ALL and AML blasts had a higher specific activity than normal lymphocytes and granulocytes. CLL B-cells had a lower specific activity compared with that in normal non-T-lymphocytes; CLL T-cells and normal T-cells had similar activity. Isoenzyme separation was performed by chromatofocusing on PBE-94 coupled with an automated enzyme assay. When using a single linear pH elution gradient, normal leukocytes and all leukemia cells contained two forms of isoenzyme (B and A). When a double pH elution gradient was performed, an extra distinct form of Hex (I) was recorded. Hex I was present in small amounts in normal granulocytes and PHA-stimulated normal lymphocytes; isoenzyme I was found in high amounts in all leukemias tested. The activity ratios I/B and I/A, as well as the I isoenzyme profile, may facilitate differentiation between normal and leukemic cells and between lymphoblastic and myeloblastic leukemias.

alpha-L-Fucosidase (EC 3.2.1.51; FUS) activity and isoenzyme characteristics were analyzed in normal lymphocytes, normal (polymorphonuclear leukocytes, PMNs), and myeloid and lymphoid leukemic cells. Chronic lymphocytic leukemia (CLL) lymphocytes had a lower mean specific activity than normal lymphocytes (2.5 vs. 4.0, p less than 0.05). Acute lymphoblastic leukemia (ALL) blasts had a higher mean specific activity compared to normal lymphocytes (9.7 vs. 4.0; p less than 0.001), CLL lymphocytes (9.7 vs. 2.5; p less than 0.001), and acute myeloid leukemic (AML) blasts (9.7 vs. 7.6; p = NS). Normal PMNs had a higher mean specific activity than normal lymphocytes (7.0 vs. 4.0; p less than 0.05) but similar activity when compared to CML cells or AML blasts. Blasts from acute myelomonocytic leukemia (AMMoL) patients had higher activity than normal PMNs (9.0 vs. 7.0; p greater than 0.05). The isoenzyme patterns of normal and leukemic granulocytes and lymphocytes were obtained by automated chromatofocusing on PBE-94 microcolumns with normal and leukemic lymphocyte lysates. With normal and leukemic lymphoid lysates two major isoenzyme components (B and A) were isolated. The isoenzyme patterns of PMN, AML, CML, and AMMoL revealed three major peaks (B, A, I), totally different from those seen in lymphoid cells. The patterns of AML, CML, and PMN appeared to be similar to each other; however, the isoenzyme pattern obtained from AMMoL cells could be distinguished from the others by a prominent I peak. Thus, the FUS isoenzyme profile distinguishes the blasts of AMMoL from AML; and AMMol and AML from ALL.

N-acetyl-beta-D-glucosaminidase (NAG) activity and isoenzyme profiles were studied in myeloid, histiocytic, B-lymphoid, T-lymphoid and lymphoblastoid continuous cell lines in order to determine if N-acetyl-beta-D-glucosaminidase isoenzyme expression may help to distinguish among various types of leukemic proliferation. Total NAG activity in myeloid, histiocytic, erythroleukemic cell lines were higher than Burkitt's lymphoma derived cell lines (B-lymphoid), T- or lymphoblastoid cell lines. On chromatofocusing by PBE 94 coupled with an automated enzyme assay an intermediate (I) beta-N-acetyl-glucosaminidase form, eluting between forms B and A, was found in all leukemic and in Epstein-Barr virus infected lymphoblastoid cell lines analysed. The different profiles recorded, the expression of the I form and the different I/B ratios may be useful as markers of tumour proliferation.