Ionizing radiation exposure as a result of diagnostic imaging in patients with lymphoma.

PURPOSE: Survival rates among patients with lymphoma continue to improve. Strategies aimed at reducing potential treatment-related toxicity are increasingly prioritized. While radiological procedures play an important role, ionizing radiation exposure has been linked to an increased risk of malignancy, particularly among individuals whose cumulative radiation exposure exceeds a specific threshold (75 millisieverts). METHODS: Within this retrospective study, the cumulative radiation exposure dose was quantified for 486 consecutive patients with lymphoma. RESULTS: The median estimated total cumulative effective dose (CED) of ionizing radiation per subject was 69 mSv (42-118). However, younger patients (under 40 years) had a median CED of 89 mSv (55-124). CONCLUSION: This study highlights the considerable radiation exposure occurring among patients with lymphoma as a result of diagnostic imaging. To limit the risk of secondary carcinogenesis, consideration should be given to monitoring cumulative radiation exposure in individual patients as well as considering imaging modalities, which do not impart an ionizing radiation dose.

Age-related decline in cell-mediated immunity in the C58 leukemic mouse strain.

The leukemia-prone C58 strain of mouse was examined for age-related changes in cellular immune function. Proliferative responses of lymphocytes to autologous and allogeneic stimulator cells [autologous mixed lymphocyte response (AMLR) and mixed lymphocyte response (MLR), respectively] and to mitogens were tested both prior to and around the usual age of disease onset which occurs at 7-8 months. Leukemia in these animals was defined by elevated peripheral blood and splenic white blood cell counts. The AMLR declined greater than 30% by 6-7 months of age and was virtually absent by 8 months of age even in animals that were not overtly leukemic. The MLR declined precipitously (greater than 95%) at 9 months of age. Both declines occurred at a younger age in C58 mice than in nonleukemic strains. Mixing experiments with cells from young and old animals indicate a defect in the Ly 1+23-, L3T4+ responding T cells. No evidence indicating a role for suppressor cell activity in this decline of cell-mediated immunity could be found. Deficiencies in cytokine (IL-2 and IL-1) production were not observed except in the oldest mice tested. Around the usual time of disease onset, splenic natural killer (NK) cell activity declines sharply even in nonleukemic mice. Cell-mixing experiments showed no evidence of suppressor cell activity by spleen cells from older mice, leukemic or nonleukemic, on the NK cell activity of young adult animals. Interferon alpha, beta treatment enhanced the NK activity of cells from old mice but did not restore the level of activity seen in young mice. Evidence has therefore been found for a premature decline in cellular immune function in two responses with proposed immunoregulatory roles, the AMLR and NK cell activity. It is possible that their decline could play a predisposing role in the onset of this retroviral leukemia or that these cell populations may be the target of the retrovirus.

Administration of bovine superoxide dismutase fails to prevent chronic pulmonary sequelae of neonatal oxygen exposure in the rat.

Using a rat model, we assessed the efficacy of varying doses of superoxide dismutase of (SOD) to affect plasma and tissue SOD concentrations and to attenuate dysplastic changes of lung and pulmonary vascular growth, which are chronic sequelae of neonatal oxygen exposure. One hundred forty-three 1-day-old Sprague-Dawley rats were divided into two groups and exposed to hyperoxia (0.96 to 1.0 Fio2) or room air for 8 postnatal days. Each group was subdivided into five treatment groups, which received 6, 20, 100, or 200 mg/kg/d SOD or a placebo, intramuscularly every 12 hours. All rats were then placed in room air; 52 were killed, and lung tissue and blood samples were obtained for measurement of bovine SOD concentration. The remaining rats received routine care until 58 to 60 days of age, when functional and morphologic cardiopulmonary changes were assessed. Bovine SOD concentration of pooled plasma samples increased 26-fold, from 2 to 50 micrograms/mL, between the 6 and 200 mg/kg/d SOD groups, but mean tissue concentration increased only six-fold, from 0.34 to 2.1 micrograms/lung. Cardiovascular and pulmonary changes found in each oxygen group, regardless of SOD dosage, included elevated right ventricular pressure, increased right ventricular weight, decreased number of small pulmonary arteries/mm2, decreased number of alveoli/mm2, and increased volume proportion of lung parenchyma. Thus, high plasma concentrations of bovine SOD failed to prevent the chronic cardiovascular and pulmonary sequelae of neonatal oxygen exposure in the rat, possibly because SOD did not reach the intracellular sites of action.

Neonatal pulmonary hypoplasia with premature rupture of fetal membranes and oligohydramnios.

We assessed pulmonary function and compression deformities in 76 preterm infants less than or equal to 34 weeks gestation who had premature rupture of membranes (PROM) for longer than 5 days (mean +/- SD 18.8 +/- 15.4 days, range 6 to 90 days). Twenty-one of the 76 infants had oligohydramnios and positional deformities at birth; however, only two infants met all the criteria for the oligohydramnios tetrad. All 21 required assisted ventilation from the moment of birth. Twenty infants had clinical evidence of pulmonary hypoplasia; 18 of these died. Pulmonary hypoplasia was confirmed by significantly low wet lung weights, low lung DNA content, or low radial alveolar counts in the 13 infants with postmortem examinations. Fifty-five infants with PROM for longer than 5 days did not have positional deformities. Twenty-one required assisted ventilation, of whom 10 had severe oligohydramnios. Eleven of the 21 died; autopsies were performed. All had normal wet lung weights, but seven had significantly decreased radial alveolar counts, implying a less severe but still fatal form of pulmonary hypoplasia. None of the remaining 34 infants had lung disease, and only three had oligohydramnios. We conclude that pulmonary hypoplasia can result from PROM associated with severe oligohydramnios of as short as 6 days duration. Furthermore, fatal pulmonary hypoplasia can occur with little or no external deformation.