The effect of intensity-modulated radiotherapy on radiation-induced second malignancies.

PURPOSE: To compare intensity-modulated radiotherapy (IMRT) with three-dimensional conformal radiotherapy (3D-CRT) in terms of carcinogenic risk for actual clinical scenarios. METHOD AND MATERIALS: Clinically equivalent IMRT plans were generated for prostate, breast, and head-and-neck cases treated with 3D-CRT. Two possible dose-response models for radiocarcinogenesis were generated based on A-bomb survivor data corrected for fractionation. Dose-volume histogram analysis was used to determine dose and its distribution to nontargeted tissues within the planning CT scan volume and thermoluminescent dosimetry for the rest of the body. Carcinogenic estimates were calculated with and without a correction factor accounting for cancer patients' advanced age and reduced longevity. RESULTS: For the model assuming a plateau in risk above 2-Gy single-fraction-equivalent (SFE), IMRT and 3D-CRT produced risks of 1.7% and 2.1%, respectively, for prostate; 1.9% and 1.8%, respectively, for nasopharynx; 1% each for tonsil; and 1.4-2.2% and 1.5-1.6%, respectively, depending on technique, for breast. Assuming a reduction in risk above 2-Gy SFE, risks for IMRT and 3D-CRT were 1.1% and 1.5%, respectively, for prostate; 1.4% and 1.2%, respectively, for nasopharynx; 1% each for tonsil; and 1.3-1.8% vs. 1.3-1.6%, respectively, for breast. Applying a correction factor of 0.5 for cancer patients halved these risks and their relative differences. CONCLUSIONS: Carcinogenic risks were comparable in absolute terms between modalities. Risks are dependant on technique used. Risks with IMRT are influenced by monitor unit demand and are therefore software/hardware dependant. The dose-response model accounting for cell killing at higher doses fitted best with actual observed risks.

Investigation of transfusion transmission of a WA1-type babesial parasite to a premature infant in California.

BACKGROUND: A premature infant in California developed respiratory distress associated with infection with a protozoal parasite, Babesia. The infant had received two blood transfusions, one from the father and one from an anonymous donor (Donor A). This study describes the follow-up required to identify the source and species of Babesia that infected the infant. STUDY DESIGN AND METHODS: At the time of the infant's illness, whole blood from the infant, father, and mother was evaluated for Babesia infection. Similar evaluation of whole blood from Donor A was performed 2 months after the suspected donation to the infant. Samples were tested using blood smear examination, serology, PCR, and hamster inoculation. Identity of the recovered Babesia parasites was confirmed by DNA amplification by PCR, genetic sequencing of the 18S gene, and phylogenetic analysis. RESULTS: WA1-type Babesia was recovered from the infant. Neither parent was the source of infection. Serology and hamster inoculation confirmed WA1-type Babesia infection in Donor A. DNA sequences of the 18S gene from the infant and donor isolates were 100% identical. CONCLUSION: WA1-type Babesia infections may be difficult to detect among blood donors because such infections can be subclinical. This is the second WA1-type Babesia transmission via blood transfusion and the first in an infant. Physicians in the western United States should consider Babesia as a possible cause of nonspecific febrile illness after a blood transfusion.