Survivors of Hodgkin’s lymphoma are at increased risk for treatment-related subsequent malignant neoplasms. The effect of less toxic treatments, introduced in the late 1980s, on the long-term risk of a second cancer remains unknown.

Research from JAMA Internal Medicine — Cardiovascular Disease After Hodgkin Lymphoma Treatment — 40-Year Disease Risk

Purpose: Cardiovascular diseases are increasingly recognized as late effects of Hodgkin lymphoma (HL) treatment. The purpose of this study was to identify the risk factors for coronary heart disease (CHD) and to quantify the effects of radiation dose to the heart, chemotherapy, and other cardiovascular risk factors. Patients and Methods: We conducted a nested case-control study in a cohort of 2,617 5-year HL survivors, treated between 1965 and 1995. Cases were patients diagnosed with CHD as their first cardiovascular event after HL. Detailed treatment information was collected from medical records of 325 cases and 1,204 matched controls. Radiation charts and simulation radiographs were used to estimate in-field heart volume and mean heart dose (MHD). A risk factor questionnaire was sent to patients still alive. Results: The median interval between HL and CHD was 19.0 years. Risk of CHD increased linearly with increasing MHD (excess relative risk [ERR]) per Gray, 7.4%; 95% CI, 3.3% to 14.8%). This results in a 2.5-fold increased risk of CHD for patients receiving a MHD of 20 Gy from mediastinal radiotherapy, compared with patients not treated with mediastinal radiotherapy. ERRs seemed to decrease with each tertile of age at treatment (ERR/Gy_<27.5years, 20.0%; ERR/Gy_{27.5-36.4years}, 8.8%; ERR/Gy_{36.5-50.9years}, 4.2%; P_interaction = .149). Having ≥ 1 classic CHD risk factor (diabetes mellitus, hypertension, or hypercholesterolemia) independently increased CHD risk (rate ratio, 1.5; 95% CI, 1.1 to 2.1). A high level of physical activity was associated with decreased CHD risk (rate ratio, 0.5; 95% CI, 0.3 to 0.8). Conclusion: The linear radiation dose-response relationship identified can be used to predict CHD risk for future HL patients and survivors. Appropriate early management of CHD risk factors and stimulation of physical activity may reduce CHD risk in HL survivors.

PURPOSE: To quantify the long-term risk of second primary cancers (SCs) in patients diagnosed with Hodgkin’s disease (HD) during adolescence or young adulthood. PATIENTS AND METHODS: The risk of SCs was assessed in 1,253 patients diagnosed with HD before the age of 40 years and treated in two Dutch cancer centers between 1966 and 1986. The median follow-up duration was 14.1 years. RESULTS: In all, 137 patients developed SCs, compared with 19.4 cases expected on the basis of incidence rates in the general population (relative risk [RR] = 7.0; 95% confidence interval, 5.9 to 8.3). The 25-year actuarial risk of SC overall was 27.7%. The RR of solid tumors increased greatly with younger age at the first treatment of HD, not only for breast cancer but also for all other solid tumors, with RRs of 4.9, 6.9, and 12.7 for patients first treated at ages 31 to 39 years, 21 to 30 years, and ≤ 20 years, respectively. Among patients first treated at the age of 20 years or younger, the RR of developing a solid tumor before the age of 40 years was significantly greater than the RR of solid tumor development at ages 40 to 49 years (RR = 27.9 v RR = 4.2; P = .0001). Patients who received salvage chemotherapy had significantly greater risk of solid cancers other than breast cancer than did patients whose treatment was restricted to initial radiotherapy or initial combined-modality treatment (RR = 9.4 and 4.7, respectively; P = .004). CONCLUSION: After more than 20 years of follow-up, the risk of solid tumors is still much greater in survivors of HD than in the population at large. Reassuringly, the greatly increased risk of solid tumors in patients who were young (≤ 20 years of age) at the first treatment seems to decrease as these patients grow older. Our data suggest that chemotherapy may increase the risk of solid tumors from radiotherapy.

Background: Inadvertent enterotomy is a feared complication of adhesiotomy during abdominal reoperation. The nature and extent of this adhesion-associated problem are unknown. Methods: The records of all patients who underwent reoperation between July 1995 and September 1997 were reviewed retrospectively for inadvertent enterotomy, risk factors were analysed using univariate and multivariate parameters, and postoperative morbidity and mortality rates were assessed. Results: Inadvertent enterotomy occurred in 52 (19 per cent) of 270 reoperations. Dividing adhesions in the lower abdomen and pelvis, in particular, caused bowel injury. In univariate analysis body mass index was significantly higher in patients with inadvertent enterotomy (mean(s.d.) 25·5(4·6) kg/m2) than in those without enterotomy (21·9(4·3) kg/m2) (P < 0·03). Patient age and three or more previous laparotomies appeared to be independent parameters predicting inadvertent enterotomy (odds ratio (95 per cent confidence interval) 1·9 (1·3–2·7) and 10·4 (5·0–21·6) respectively; P < 0·001). Patients with inadvertent enterotomy had significantly more postoperative complications (P < 0·01) and urgent relaparotomies (P < 0·001), a higher rate of admission to the intensive care unit (P < 0·001) and parenteral nutrition usage (P < 0·001), and a longer postoperative hospital stay (P < 0·001). Conclusion: The incidence of inadvertent enterotomy during reoperation is high. This adhesion-related complication has an impact on postoperative morbidity.