Chromosomal studies in healthy blood donors with IgA deficiency

Chromosomal analysis was performed in 70 asymptomatic blood donors found over a 5-year period in a large screening programme to be IgA deficient. No abnormalities were found in any of these individuals in relation to their chromosomal constitution and, in particular, chromosome 18 was normal in all individuals. A further 10 symptomatic individuals with IgA deficiency also showed a normal chromosomal constitution with no abnormalities of chromosome no. 18.     

A unique structural abnormality of chromosome 16 resulting in a CBF beta-MYH11 fusion transcript in a patient with acute myeloid leukemia, FAB M4

A 43-year-old female with a peripheral white cell count of 118.0 x 10(9)/L and 96% blasts was diagnosed with acute myeloid leukemia (AML), FAB M4. Cytogenetics, performed on a bone marrow sample, revealed the following abnormal karyotype: 46,XX,ins(16)(q22p13.1p13. 3). Fluorescence in situ hybridization (FISH) confirmed the inter-arm insertion using a probe for 16p. The result of this structural rearrangement was the fusion of CBF beta to MYH11 seen commonly in inv(16)(p13q22). The patient commenced high-dose intensive combination chemotherapy (big ICE; Idarubicin, Cytarabine, and Etopiside). Five days post chemotherapy, she developed febrile neutropenia. Despite broad spectrum intravenous antibiotics and antifungal therapy, the patient died at day nine post chemotherapy. This case demonstrates a previously unreported structural abnormality of chromosome 16 in a patient with AML M4, which represents a third mechanism to inv(16)(p13q22) and t(16;16)(p13q22) in producing the CBF beta-MYH11 fusion. CBF beta-MYH11 fusions masked by cryptic translocations at the cytogenetic level have been detected by FISH and PCR techniques. Due to the improved prognosis associated with CBF beta-MYH11 fusions compared to the standard risk group for AML, its detection remains important.     

Treatment of chronic bacterial prostatitis with ciprofloxacin

Thirty two patients with proven chronic bacterial prostatitis were treated with ciprofloxacin 500 mg twice daily orally for four weeks. The causative organisms, cultured from prostatic fluid wereEnterobacteriaceae (19 patients), enterococci (9), staphylococci (4), streptococci (3), non-fermentative Gram-negative rods (2) and anaerobic bacteria (9). Nineteen patients had pure cultures, 13 mixed cultures. The susceptibility of all organisms to ciprofloxacin, sulfamethoxazole, trimethoprim and doxycyclin was determined by agar dilution. The effect of therapy was measured by clinical parameters and by repeated cultures of prostatic fluid during and after therapy upto six months. Clinical cure (at one month after therapy) was obtained in 22 patients, improvement in seven; two patients dit not respond, one patient had to stop during therapy because of severe nausea. No other side effects were noted. Ciprofloxacin may be a useful alternative drug in the treatment of prostatitis.     

Deletion of CBFB in a patient with acute myelomonocytic leukemia (AML M4Eo) and inversion 16

Acute myelomonocytic leukemia with bone marrow eosinophilia (AML M4Eo) is a subtype of AML with distinct morphological features. Inversion (16)(p13.1q22), t(16;16)(p13.1;q22), and del(16)(q22) are nonrandom abnormalities associated with AML M4Eo and a favorable prognosis, compared with the standard risk group for AML. Deletions of the proximal region of the MYH11 gene located at 16p13.1 have been detected in about 20% of patients with inv(16), with an undetermined effect on patient survival. We present the case of a patient with AML M4Eo and inversion 16 with a distal deletion of the CBFB gene at 16q22 detected with fluorescence in situ hybridization. To our knowledge, only one previous report of a similar deletion has appeared in the literature.