Journal articles: 'Relatives risks'

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Minkoff, Howard, and Mary Faith Marshall. "Fetal Risks, Relative Risks, and Relatives' Risks." American Journal of Bioethics 16, no. 2 (February 2016): 3–11. http://dx.doi.org/10.1080/15265161.2015.1120791.

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Minkoff, Howard, and Mary Faith Marshall. "Response to Open Peer Commentaries on “Fetal Risks, Relative Risks, and Relatives' Risks”." American Journal of Bioethics 16, no. 2 (February 2016): W13. http://dx.doi.org/10.1080/15265161.2016.1137168.

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Fenwick, Angela, Shiri Shkedi-Rafid, and Anneke Lucassen. "Relative Risk and Relatives' Risks in Genomic Medicine." American Journal of Bioethics 16, no. 2 (February 2016): 25–27. http://dx.doi.org/10.1080/15265161.2015.1120809.

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Knight, Ann, Sven Sandin, and Johan Askling. "Risks and relative risks of Wegener's granulomatosis among close relatives of patients with the disease." Arthritis & Rheumatism 58, no. 1 (2007): 302–7. http://dx.doi.org/10.1002/art.23157.

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Sadovnick, Adele D., Patricia A. Baird, Richard H. Ward, John M. Optiz, and James F. Reynolds. "Multiple sclerosis. Updated risks for relatives." American Journal of Medical Genetics 29, no. 3 (March 1988): 533–41. http://dx.doi.org/10.1002/ajmg.1320290310.

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Heath, John A., Elizabeth Smibert, Elizabeth M. Algar, Gillian S. Dite, and John L. Hopper. "Cancer Risks for Relatives of Children with Cancer." Journal of Cancer Epidemiology 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/806076.

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We determined the extent and distribution of cancers in relatives of 379 children newly diagnosed with cancer. Family history was collected from 1,337 first-degree and 3,399 second-degree relatives and incidence compared with national age- and gender-specific rates. Overall, 14 children (3.7%) had a relative with a history of childhood cancer and 26 children (6.9%) had a first-degree relative with a history of cancer, with only one of these having an identifiable familial cancer syndrome. There was a higher than expected incidence of childhood cancer among first-degree relatives (parents and siblings) (standardized incidence ratio (SIR) 1.43; 95% CI 0.54–5.08). There was also a higher than expected incidence of adult cancers among first-degree relatives (SIR 1.45; 95% CI 0.93–2.21), particularly in females (SIR 1.82; 95% CI 1.26–3.39). The increased family cancer history in first-degree females was largely attributable to an effect in mothers (SIR 1.78; 95% CI 1.27–3.33). The gender-specific association was reflected in higher than expected incidence rates of breast cancer in both mothers (SIR 1.92; 95% CI 0.72–6.83) and aunts (SIR 1.64; 95% CI 0.98–2.94). These findings support the hypothesis that previously undetected familial cancer syndromes contribute to childhood cancer.

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Lacroix, M., G. Nycum, B. Godard, and B. M. Knoppers. "Should physicians warn patients' relatives of genetic risks?" Canadian Medical Association Journal 178, no. 5 (February 26, 2008): 593–95. http://dx.doi.org/10.1503/cmaj.070956.

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Craddock, Nick, and Luis A. Giuffra. "Estimates of risks in relatives of psychotic probands." British Journal of Psychiatry 164, no. 5 (May 1994): 706–7. http://dx.doi.org/10.1192/bjp.164.5.706b.

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Vaupel, James W. "Relatives' risks: Frailty models of life history data." Theoretical Population Biology 37, no. 1 (February 1990): 220–34. http://dx.doi.org/10.1016/0040-5809(90)90037-v.

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Huang, Yu-Huei, Chang-Fu Kuo, Lu-Hsiang Huang, and Mei-Yun Hsieh. "Familial Aggregation of Psoriasis and Co-Aggregation of Autoimmune Diseases in Affected Families." Journal of Clinical Medicine 8, no. 1 (January 18, 2019): 115. http://dx.doi.org/10.3390/jcm8010115.

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Psoriasis is considered to result from the interaction of genetic factors and environmental exposure. The evidence for familial aggregation in psoriasis has been reported but population-based studies related to the magnitude of genetic contribution to psoriasis are rare. This study aimed to evaluate the relative risks of psoriasis in individuals with affected relatives and to calculate the proportion of genetic, shared, and non-shared environmental factors contributing to psoriasis. The study cohort included 69,828 patients diagnosed with psoriasis enrolled in National health Insurance in 2010. The adjusted relative risks (RR) for individuals with an affected first-degree relative and affected second-degree relative were 5.50 (95% CI (Confidence Interval), 5.19–5.82) and 2.54 (95% CI, 2.08–3.12) respectively. For those who have affected first-degree relatives, their RR was 1.45 (95% CI, 1.17–1.79) for Sjogren’s syndrome and 1.94 (95% CI, 1.15–3.27) for systemic sclerosis. This nationwide study ascertains that family history of psoriasis is a risk factor for psoriasis. Individuals with relatives affected by psoriasis have higher risks of developing some autoimmune diseases.

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Landgren, Ola, Lynn R. Goldin, Sigurdur Y. Kristinsson, Jan Samuelsson, and Magnus Bjorkholm. "Increased Risks of Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Myelofibrosis (MF) among 24577 First-Degree Relatives of 11039 Patients with Chronic Myeloproliferative Disorders (MPD) in Sweden." Blood 110, no. 11 (November 16, 2007): 680. http://dx.doi.org/10.1182/blood.v110.11.680.680.

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Abstract Background. Familial clustering of PV, ET, MF, and chronic myeloid leukemia (CML) has been reported through case reports and smaller case series. Recently, several studies reported that in families with multiple MPD patients, the JAK2 mutation is not an early germ line predisposing factor for MPD but rather a facilitator of proliferative advantages. However, the degree of familial clustering in the population has not been defined. We have conducted the first large population-based study to quantify risks of developing MPD and related malignancies in first-degree relatives of MPD patients. Methods. Using high-quality central population-based registries, we identified 6217 PV, 2838 ET, and 1984 MF patients diagnosed in Swedish hospitals 1958–2005 (Cancer and local hospital-based registries), with linkable relatives; 43550 frequency-matched controls (Population registry); and first-degree relatives of cases (n=24577) and controls (n=99542) (Multigenerational registry). Relatives of MPD patients and controls were linked with the Cancer and local hospital-based registries to define occurrence of MPD and other related neoplasms. We used a marginal survival model to calculate relative risks (RR) and 95% confidence intervals (CI) as measures of familial aggregation. Results. Compared with controls, relatives of MPD patients had significantly increased risks of PV (RR=5.70; 95% CI 3.55–9.14), ET (RR=7.37; 95% CI 3.67–14.81), and MF (RR=3.53; 95% CI 1.59–7.85). Risks were similar when we restricted the analyses to relatives of patients with the same MPD (PV-PV, ET-ET, and MF-MF) Also, risk-estimates were virtually the same for various types of first-degree relatives (parents, siblings, offspring); the same was true when we calculated risks by age at MPD of cases (above vs. below 65 yrs), and sex of relatives. Age at diagnosis of MPD was not different for case and control relatives. Furthermore, relatives of MPD patients (vs. controls) had a borderline increased risk of CML (RR=1.86; 95% CI 0.90–3.74; p=0.07). As expected, we found excess of subsequent acute myeloid leukemia (AML) (n=271; 2.5%) and myelodysplastic syndrome (MDS) (n=27; 0.2%) among MPD patients; however, there were no increased risks of AML or MDS among relatives of MPD patients. Conclusions. In this first large population-based study including more than 11000 MPD patients and their almost 25000 linkable first-degree relatives, we found 3- to 7-fold elevated risks of developing MPDs among first-degree relatives of MPD patients. Our results support the hypothesis that there are common, strong, shared susceptibility genes that predispose to PV, ET, MF, and possibly CML.

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Goldin, Lynn R., Ruth M. Pfeiffer, Xinjun Li, and Kari Hemminki. "Familial risk of lymphoproliferative tumors in families of patients with chronic lymphocytic leukemia: results from the Swedish Family-Cancer Database." Blood 104, no. 6 (September 15, 2004): 1850–54. http://dx.doi.org/10.1182/blood-2004-01-0341.

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Abstract The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.

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Coppens, Michiel, Marlène van de Poel, Saskia Middeldorp, Karly Hamulyák, Ivan Bank, Nic Veeger, Martin Prins, Harry Büller, Jan van der Meer, and Willem Lijfering. "The risk of venous and arterial thrombosis in hyperhomocysteinaemia is low and mainly depends on concomitant thrombophilic defects." Thrombosis and Haemostasis 98, no. 08 (2007): 457–63. http://dx.doi.org/10.1160/th07-02-0138.

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SummaryAs homocysteine-lowering treatment has not reduced the risk of recurrent thrombosis in recent clinical trials, we hypothesized that mild hyperhomocysteinaemia is an epiphenomenon or associated with a low absolute risk of thrombosis. In this retrospective study, we enrolled 478 evaluable first-degree relatives of consecutive patients with venous thrombosis or premature atherosclerosis, and hyperhomocysteinemia. Absolute risks of thrombosis and effects of concomitant thrombophilic defects were compared. Relative risks were adjusted for clustering in families, age, sex, and atherosclerotic risk factors, where appropriate. Annual incidence of venous thrombosis was 0.16% (95% confidence interval [CI], 0.08–0.30) in hyperhomocysteinemic relatives versus 0.11% (CI, 0.05–0.20) in normohomocysteinemic relatives; adjusted relative risk 1.6 (CI, 0.6–4.5). Annual incidences of arterial thrombosis were 0.34% (CI, 0.21–0.52) and 0.24% (CI, 0.15–0.37) in hyperhomocysteinemic and normohomocysteinemic relatives, respectively; adjusted relative risk 1.5 (CI, 0.6–3.5). Concomitance of multiple thrombophilic risk factors increased the risk of venous thrombosis in hyperhomocysteinemic relatives 20 fold, but a comparable effect was demonstrated in normohomocysteinemic relatives. We conclude that hyperhomocysteinaemia is associated with a low absolute risk of venous and arterial thrombosis. Concomitant thrombophilic defects are probably main determinants on the risk of venous thrombosis, rather than hyperhomocysteinaemia itself.

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Win, Aung Ko, Rhiannon J. Walters, Daniel D. Buchanan, Mark A. Jenkins, Kevin Sweet, Wendy L. Frankel, Albert de la Chapelle, et al. "Cancer Risks for Relatives of Patients With Serrated Polyposis." American Journal of Gastroenterology 107, no. 5 (May 2012): 770–78. http://dx.doi.org/10.1038/ajg.2012.52.

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Kano, Yukiko, James F. Leckman, and David L. Pauls. "CLINICAL CHARACTERISTICS OF TOURETTE SYNDROME PROBANDS AND RELATIVES’ RISKS." Journal of the American Academy of Child & Adolescent Psychiatry 41, no. 10 (October 2002): 1148–49. http://dx.doi.org/10.1097/00004583-200210000-00005.

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Landgren, Ola, Lynn R. Goldin, Sigurdur Y. Kristinsson, Elin A. Helgadottir, Jan Samuelsson, and Magnus Björkholm. "Increased risks of polycythemia vera, essential thrombocythemia, and myelofibrosis among 24 577 first-degree relatives of 11 039 patients with myeloproliferative neoplasms in Sweden." Blood 112, no. 6 (September 15, 2008): 2199–204. http://dx.doi.org/10.1182/blood-2008-03-143602.

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Abstract Previous small studies have reported familial clustering of myeloproliferative neoplasms (MPNs), including polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF). We identified 6217 PV, 2838 ET, 1172 MF, and 812 MPN unclassifiable (NOS) patients diagnosed in Sweden, 43 550 controls, and first-degree relatives of cases (n = 24 577) and controls (n = 99 542). Using a marginal survival model, we calculated relative risks (RRs) and 95% confidence intervals as measures of familial aggregation. Relatives of MPN patients had significantly increased risks of PV (RR = 5.7; 3.5-9.1), ET (RR = 7.4; 3.7-14.8), and MPN NOS (RR = 7.5; 2.7-20.8). Analyses stratified by type of first-degree relative revealed consistently higher risks for siblings, compatible with a model of recessive genetic inheritance, which can be confirmed only by identifying the susceptibility gene(s). Mean age at MPN diagnosis was not different (P = .20) for affected relatives of cases (57.5 years) versus controls (60.6 years), and risk of MPN by age was not different for parents versus offspring of MPN cases (P = .10), providing no support for anticipation. Relatives of MPN patients had a borderline increased risk of chronic myeloid leukemia (CML; RR = 1.9; 0.9-3.8; P = .09). Our findings of 5- to 7-fold elevated risk of MPNs among first-degree relatives of MPN patients support the hypothesis that common, strong, shared susceptibility genes predispose to PV, ET, MF, and possibly CML.

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Isomura, K., M. Boman, C. Rück, E. Serlachius, H. Larsson, P. Lichtenstein, and D. Mataix-Cols. "Population-based, multi-generational family clustering study of social anxiety disorder and avoidant personality disorder." Psychological Medicine 45, no. 8 (September 12, 2014): 1581–89. http://dx.doi.org/10.1017/s0033291714002116.

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BackgroundWe aimed to provide unbiased estimates of familial risk and heritability of social anxiety disorder (SAD) and avoidant personality disorder (AVPD).MethodWe identified 18 399 individuals diagnosed with SAD and 2673 with AVPD in the Swedish National Patient Register between 1997 and 2009. Risks (odds ratios; OR) for SAD in all biological and non-biological relatives of probands, compared to relatives of unaffected individuals were calculated. We also estimated the risks for AVPD in relatives of probands with SAD.ResultsThe risk for SAD among relatives of SAD probands increased proportionally to the degree of genetic relatedness. The risks for first-degree relatives [OR 4.74, 95% confidence interval (CI) 4.28–5.25] were significantly higher than for second-degree and third-degree relatives. Second-degree relatives (OR 2.30, 95% CI 2.01–2.63) had significantly higher risk than third-degree relatives (OR 1.72, 95% CI 1.52–1.94). Relatives at similar genetic distances had similar risks for SAD, despite different degrees of shared environment. Heritability was estimated to be approximately 56%. There were no significant sex differences in the familial patterns. The risk of AVPD in relatives of SAD probands was significantly elevated, even after excluding individuals with both diagnoses (first-degree OR 3.54, second-degree OR 2.20, third-degree OR 1.62). Non-biological relatives (spouses/partners) also had elevated risks for both SAD (OR 4.01) and AVPD (OR 3.85).ConclusionsSAD clusters in families primarily due to genetic factors. SAD and AVPD are aetiologically related and may represent different expressions of the same vulnerability. The strong marital concordance observed in SAD/AVPD may indicate assortative mating but the exact mechanisms and implications require further investigation.

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Landgren, Ola, Sigurdur Y. Kristinsson, Lynn R. Goldin, Neil E. Caporaso, Cecilie Blimark, Ulf-Henrik Mellqvist, Anders Wahlin, Magnus Bjorkholm, and Ingemar Turesson. "Risk of plasma cell and lymphoproliferative disorders among 14621 first-degree relatives of 4458 patients with monoclonal gammopathy of undetermined significance in Sweden." Blood 114, no. 4 (July 23, 2009): 791–95. http://dx.doi.org/10.1182/blood-2008-12-191676.

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Abstract Familial clustering of the precursor condition, monoclonal gammopathy of undetermined significance (MGUS) has been observed in case reports and in smaller studies. Using population-based data from Sweden, we identified 4458 MGUS patients, 17505 population-based controls, and first-degree relatives of patients (n = 14621) and controls (n = 58387) with the aim to assess risk of MGUS and lymphoproliferative malignancies among first-degree relatives of MGUS patients. Compared with relatives of controls, relatives of MGUS patients had increased risk of MGUS (relative risk [RR] = 2.8; 1.4-5.6), multiple myeloma (MM; RR = 2.9; 1.9-4.3), lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM; RR = 4.0; 1.5-11), and chronic lymphocytic leukemia (CLL; RR = 2.0; 1.2-2.3). Relatives of patients with IgG/IgA MGUS had a 4.0-fold (1.7-9.2), 2.9-fold (1.7-4.9), and 20-fold (2.3-170) elevated risk of developing MGUS, MM, and LPL/WM, respectively. Relatives of IgM MGUS patients had 5.0-fold (1.1-23) increased CLL risk and nonsignificant excess MM and LPL/WM risks. The results were very similar when we assessed risk by type of first-degree relative, age at MGUS (above/below 65 years), or sex. Risk of non-Hodgkin lymphoma or Hodgkin lymphoma was not increased among MGUS relatives. Among first-degree relatives of a nationwide MGUS cohort, we found elevated risks of MGUS, MM, LPL/WM, and CLL, supporting a role for germline susceptibility genes, shared environmental influences, or an interaction between both.

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Lijfering, Willem M., Nic J. G. M. Veeger, Jan-Leendert P. Brouwer, Marlene H. W. van de Poel, and Jan van der Meer. "Methionine-Loading and Random Homocysteine Tests Have No Added Value in Risk Assessment for Venous and Arterial Thrombosis." Blood 108, no. 11 (November 16, 2006): 1486. http://dx.doi.org/10.1182/blood.v108.11.1486.1486.

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Abstract Hyperhomocysteinemia is a risk factor for venous and arterial thrombosis. Different diagnostic strategies are used to identify subjects at risk of thrombosis, related to hyperhomocysteinemia. Measurements of fasting and methionine-loading levels are usually recommended. Alternatively, random homocysteine measurements may simplify the procedure. Random levels < 10 and > 20 μmol/l are considered to indicate normohomocysteinemia and hyperhomocysteinemia, respectively, while consecutive fasting and methionine-loading tests are required at levels 10–20 μmol/l. We performed a study to assess the most suitable strategy in a large cohort of families with hereditary (index) deficiencies of protein S, protein C or antithrombin. Random, fasting and methionine-loading homocysteine samples were measured in 713 relatives. According to predefined cut-off levels hyperhomocysteinemic and normohomocysteinemic relatives were identified and their absolute risks of thrombosis were compared. Relatives with random homocysteine levels > 20 μmol/l were not at risk of venous or arterial thrombosis compared to relatives with levels < 10 μmol/l (relative risks 0.9 [95% CI, 0.4–2.3] and 1.7 [0.5–5.7], respectively). Fasting hyperhomocysteinemia (homocysteine levels > 18.5 μmol/l) was associated with an increased risk of venous and arterial thrombosis (relative risks 2.6 [1.3–4.8] and 3.7 [1.5–8.4)], respectively) (Table). Relatives with normal fasting homocysteine levels, but methionine-loading hyperhomocysteinemia (homocysteine levels > 58.8 μmol/l) were not at risk; relative risk 0.8 (0.2–1.9) for venous thrombosis and 1.1 (0.2–3.9) for arterial thrombosis. Exclusion of relatives with an index deficiency did not alter the risk estimates, while annual incidences of normohomocysteinemic relatives decreased to 0.19% per year (0.12–0.29), which is comparable with the annual incidence in the normal population. As only fasting homocysteine identified subjects at risk of thrombosis, random homocysteine and methionine-loading tests can be omitted in clinical practice. Venous Thrombosis Observation Relatives Incidence/year (%) Relative Risk years with event (95% CI) (95% CI) * Methionine-loading performed in relatives with no fasting hyperhomocysteinemia Fasting Homocysteine No hyperhomocysteinemia 10408 55 0.53 (0.40–0.69) Reference Hyperhomocysteinemia 804 11 1.37 (0.68–2.45) 2.6(1.3–4.8) Methionine-loading test* No hyperhomocysteinemia 9341 50 0.54 (0.40–0.71) Reference Hyperhomocysteinemia 986 4 0.41 (0.11–1.04) 0.8(0.2–1.9) Arterial Thrombosis Fasting Homocysteine No hyperhomocysteinemia 11096 21 0.19 (0.12–0.29) Reference Hyperhomocysteinemia 1004 7 0.70 (0.28–1.44) 3.7(1.5–8.4) Methionine-loading test* No hyperhomocysteinemia10008 10008 19 0.19 (0.11–0.30) Reference Hyperhomocysteinemia 1000 2 0.20 (0.02–0.72) 1.1(0.2–3.9)

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Bombard, Yvonne, Kenneth Offit, and Mark E. Robson. "Risks to Relatives in Genomic Research: A Duty to Warn?" American Journal of Bioethics 12, no. 10 (October 2012): 12–14. http://dx.doi.org/10.1080/15265161.2012.699157.

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Anderson, D. E., and M. D. Badzioch. "Breast Cancer Risks in Relatives of Male Breast Cancer Patients." JNCI Journal of the National Cancer Institute 84, no. 14 (July 15, 1992): 1114–17. http://dx.doi.org/10.1093/jnci/84.14.1114.

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Simon, Michael S., Jeannette F. Korczak, Cecilia L. Yee, Kathleen E. Malone, Giske Ursin, Leslie Bernstein, Jill A. McDonald, et al. "Breast Cancer Risk Estimates for Relatives of White and African American Women With Breast Cancer in the Women's Contraceptive and Reproductive Experiences Study." Journal of Clinical Oncology 24, no. 16 (June 1, 2006): 2498–504. http://dx.doi.org/10.1200/jco.2005.04.1087.

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Purpose Family history is a well-recognized risk factor for breast cancer. Familial aggregation and segregation analyses have estimated breast cancer risk based on family history primarily for white women; such information is limited for African American (AA) women. The purpose of this report is to update breast cancer risk estimates associated with a family history of breast cancer for white and AA women. Methods We used family cancer history from 2,676 white and 1,525 AA women with breast cancer (probands) in the population-based National Institute of Child Health and Human Development's Women's Contraceptive and Reproductive Experiences (CARE) Study to estimate age-specific breast cancer risks in their first degree adult female relatives. Cumulative hazard curves were calculated for relatives of all probands using Cox proportional hazards models, and were stratified by the proband's race and age at diagnosis and number of relatives affected. Results Breast cancer risks for white and AA women with a family history of the disease are similar through age 49 years, but diverge afterwards, with higher risks by age 79 in white women than in AA women (17.5% [SE, 0.9%] v 12.2% [SE, 1.1%]; P < .001). These risks increase as the number of affected first degree relatives increases, reaching 25.2% (SE, 3.4%) and 16.9% (SE, 4.0%) in white and AA women with more than one affected relative, respectively (P = .3). Conclusion We found age-related racial differences in breast cancer risk in women with a family history of breast cancer and have updated risk estimates for white and AA women for clinical use.

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Zeegers, Maurice P., Leo J. Schouten, R. Alexandra Goldbohm, and Piet A. van den Brandt. "A compendium of familial relative risks of cancer among first degree relatives: A population-based study." International Journal of Cancer 123, no. 7 (October 1, 2008): 1664–73. http://dx.doi.org/10.1002/ijc.23615.

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Landgren, Ola, Sigurdur Y. Kristinsson, Lynn R. Goldin, Neil E. Caporaso, Cecilie Blimark, Ulf-Henrik Mellqvist, Anders Wahlin, Magnus Bjorkholm, and Ingemar Turesson. "Increased Risk of Monoclonal Gammopathy of Undetermined Significance (MGUS) and Lymphoproliferative Tumors among 14689 First-Degree Relatives of 4488 MGUS Patients in Sweden." Blood 110, no. 11 (November 16, 2007): 660. http://dx.doi.org/10.1182/blood.v110.11.660.660.

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Abstract Background. Evidence from multiply affected families, case-control and population-based registry studies implicate a role for genetic factors in multiple myeloma (MM). Previous studies based on small numbers have suggested excess risk of MGUS in relatives of MM patients. Aims of this large nationwide MGUS study were to quantify risks of developing MGUS and lymphoproliferative malignancies in first-degree relatives and to define characteristics of familial aggregation. Methods. We identified 4488 MGUS patients diagnosed in all major hematology/oncology outpatient units in Sweden (1967–2005), with linkable relatives. Using the population-based central Multigenerational Registry, we obtained 17628 frequency-matched controls and first-degree relatives of cases (n=14689) and controls (n=58698). Relatives of MGUS cases and controls were linked with hospital-based outpatient registries and the central Swedish Cancer Registry to define occurrence of MGUS and lymphoproliferative tumors. Measures of familial aggregation were calculated by a marginal survival model using relatives as the cohort. Results. Compared with controls, relative risk (RR) of MGUS was significantly increased (RR=2.84; 95% CI 1.45–5.57) in relatives of MGUS cases. Relatives of MGUS cases (vs. controls) also had excess risk of MM (RR=2.87; 95% CI 1.92–4.27), Waldenstrom’s macroglobulinemia (WM) (RR=4.94; 95% CI 1.32–18.46), and chronic lymphocytic leukemia (CLL) (RR=2.05; 95% CI 1.22–3.43). Risk-estimates were similar for various types of first-degree relatives (parents, siblings, offspring); the same was true when we estimated risks by age at MGUS of cases (above vs. below 65 yrs), and sex of relatives. Age at onset of MGUS and lymphoproliferative tumors was virtually the same for case and control relatives. There was no increased risk (RR∼1) of NHL or HL among relatives of MGUS cases. Conclusions. Among first-degree relatives of a large nationwide MGUS cohort in Sweden, we found 2- to 3-fold elevated risks of developing MGUS, MM, WM, and CLL. These results suggest the operation of shared common germ line susceptibility genes in the pathway to MGUS and certain lymphoproliferative tumors. Better characterization of early genetic lesions mediating monoclonal plasma-cell proliferation, survival, and migration in the bone marrow microenvironment will ultimately enhance our understanding of MGUS, MM, WM, and CLL pathophysiology, provide clues to etiology, and allow identification of novel molecular targets.

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Clift, Louise. "Relatives in the resuscitation room: a review of benefits and risks." Paediatric Nursing 18, no. 5 (June 2006): 14–18. http://dx.doi.org/10.7748/paed.18.5.14.s23.

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Ma, Tara, Anita Heywood, and C. Raina MacIntyre. "Chinese travellers visiting friends and relatives – A review of infectious risks." Travel Medicine and Infectious Disease 13, no. 4 (July 2015): 285–94. http://dx.doi.org/10.1016/j.tmaid.2015.05.004.

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Robertson, N. P., M. Fraser, J. Deans, D. Clayton, N. Walker, and D. A. S. Compston. "Age–adjusted recurrence risks for relatives of patients with multiple sclerosis." Brain 119, no. 2 (1996): 449–55. http://dx.doi.org/10.1093/brain/119.2.449.

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Carton, H., R. Vlietinck, J. Debruyne, J. De Keyser, M. B. D'Hooghe, R. Loos, R. Medaer, L. Truyen, I. M. Yee, and A. D. Sadovnick. "Risks of multiple sclerosis in relatives of patients in Flanders, Belgium." Journal of Neurology, Neurosurgery & Psychiatry 62, no. 4 (April 1, 1997): 329–33. http://dx.doi.org/10.1136/jnnp.62.4.329.

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Fulford, Martha, and Jay S. Keystone. "Health risks associated with visiting friends and relatives in developing countries." Current Infectious Disease Reports 7, no. 1 (February 2005): 48–53. http://dx.doi.org/10.1007/s11908-005-0023-z.

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Boardman, Lisa A., Bruce W. Morlan, Kari G. Rabe, Gloria M. Petersen, Noralane M. Lindor, Sandra K. Nigon, Julia Goldberg, and Steven Gallinger. "Colorectal Cancer Risks in Relatives of Young-Onset Cases: Is Risk the Same Across All First-Degree Relatives?" Clinical Gastroenterology and Hepatology 5, no. 10 (October 2007): 1195–98. http://dx.doi.org/10.1016/j.cgh.2007.06.001.

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Cannon-Albright, Lisa A., Norman L. Foster, Karen Schliep, James M. Farnham, Craig C. Teerlink, Heydon Kaddas, Joann Tschanz, Chris Corcoran, and John S. K. Kauwe. "Relative risk for Alzheimer disease based on complete family history." Neurology 92, no. 15 (March 13, 2019): e1745-e1753. http://dx.doi.org/10.1212/wnl.0000000000007231.

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ObjectiveThe inherited component for Alzheimer disease (AD) risk has focused on close relatives; consideration of the full family history may improve accuracy and utility of risk estimates.MethodsA population resource including a genealogy of Utah pioneers from the 1800s linked to Utah death certificates was used to estimate relative risk for AD based on specific family history constellations, including from first- to third-degree relatives.ResultsAny affected first-degree relatives (FDR) significantly increased risk of AD (≥1 FDRs: relative risk [RR] 1.73, 95% confidence interval [CI] [1.59–1.87]; ≥2 FDRs: RR 3.98 [3.26–4.82]; ≥3 FDRs: RR 2.48 [1.07–4.89]; ≥4 FDRs: RR 14.77 [5.42–32.15]). Affected second-degree relatives (SDR) increased risk even in the presence of affected FDRs (FDR = 1 with SDR = 2: RR 21.29 [5.80–54.52]). AD only in third-degree relatives (TDR) also increased risk (FDR = 0, SDR = 0, TDR ≥3: RR 1.43 [1.21–1.68]). Mixed evidence was observed for differences in risk based on maternal compared to paternal inheritance; higher risks for men than women with equivalent family history, and higher risk for individuals with at least one affected FDR regardless of the relative's age at death, were observed.ConclusionsThis population-based estimation of RRs for AD based on family history ascertained from extended genealogy data indicates that inherited genetic factors have a broad influence, extending beyond immediate relatives. Providers should consider the full constellation of family history when counseling patients and families about their risk of AD.

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Dove, Edward S., Vicky Chico, Michael Fay, Graeme Laurie, Anneke M. Lucassen, and Emily Postan. "Familial genetic risks: how can we better navigate patient confidentiality and appropriate risk disclosure to relatives?" Journal of Medical Ethics 45, no. 8 (May 23, 2019): 504–7. http://dx.doi.org/10.1136/medethics-2018-105229.

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This article investigates a high-profile and ongoing dilemma for healthcare professionals (HCPs), namely whether the existence of a (legal) duty of care to genetic relatives of a patient is a help or a hindrance in deciding what to do in cases where a patient’s genetic information may have relevance to the health of the patient’s family members. The English case ABC v St George’s Healthcare NHS Trust and others considered if a duty of confidentiality owed to the patient and a putative duty of care to the patient’s close relatives could coexist in this context. This article examines whether embracing the concept of coexisting duties could enable HCPs to respect duties in line with their clinical judgement, thereby providing legal support and clarity to professionals to allow them to provide the best possible genetics service to both the patient and their family. We argue that these dual duties, framed as a novel, composite duty to consider the interests of genetic relatives, could allow HCPs to exercise and act on their professional judgements about the relative value of information to family members, without fears of liability for negligence or breach of confidence.

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Wang, Chun-Li, Chang-Fu Kuo, Yung-Hsin Yeh, Mei-Yun Hsieh, Chi-Tai Kuo, and Shang-Hung Chang. "Familial aggregation of myocardial infarction and coaggregation of myocardial infarction and autoimmune disease: a nationwide population-based cross-sectional study in Taiwan." BMJ Open 9, no. 3 (March 2019): e023614. http://dx.doi.org/10.1136/bmjopen-2018-023614.

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ObjectiveThis study examined how a history of myocardial infarction (MI) in a person’s first-degree relatives affects that person’s risk of developing MI and autoimmune diseases.DesignNationwide population-based cross-sectional studySettingAll healthcare facilities in Taiwan.ParticipantsA total of 24 361 345 individuals were enrolled.MethodsUsing data from the National Health Insurance Research Database in Taiwan, we conducted a nationwide cross-sectional study of data collected from all beneficiaries in the Taiwan National Health Insurance system in 2015, of whom 259 360 subjects had at least one first-degree relative affected by MI in 2015. We estimated the absolute risks and relative risks (RRs) of MI and autoimmune disease in those subjects, and the relative contribution of genetic and environmental factors to their MI susceptibility.ResultsThe absolute risks of MI for subjects with at least one affected first-degree relative and the general population were 0.87% and 0.56%, respectively, in 2015. Patients with affected first-degree relatives were significantly associated with a higher RR of MI (1.76, 95% CI: 1.68 to 1.85) compared with the general population. There was no association with a higher RR of autoimmune disease. The sibling, offspring and parental MI history conferred RRs (95% CI) for MI of 2.35 (1.96 to 2.83), 2.21 (2.05 to 2.39) and 1.60 (1.52 to 1.68), respectively. The contributions of heritability, shared environmental factors and non-shared environmental factors to MI susceptibility were 19.6%, 3.4% and 77.0%, respectively.ConclusionsIndividuals who have first-degree relatives with a history of MI have a higher risk of developing MI than the general population. Non-shared environmental factors contributed more significantly to MI susceptibility than did heritability and shared environmental factors. A family history of MI was not associated with an increased risk of autoimmune disease.

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Kristinsson, Sigurdur Y., Magnus Björkholm, Lynn R. Goldin, Mary L. McMaster, Ingemar Turesson, and Ola Landgren. "Risk of lymphoproliferative disorders among first-degree relatives of lymphoplasmacytic lymphoma/Waldenström macroglobulinemia patients: a population-based study in Sweden." Blood 112, no. 8 (October 15, 2008): 3052–56. http://dx.doi.org/10.1182/blood-2008-06-162768.

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Abstract A role for genetic factors in the etiology of lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM) is implicated based on prior findings from multiply affected families and small case-control and cohort studies. We identified 2144 LPL/WM patients (1539 WM [72%] and 605 LPL [28%]) diagnosed in Sweden, 8279 population-based matched controls, and linkable first-degree relatives of patients (n = 6177) and controls (n = 24 609). Using a marginal survival model, we calculated relative risks and 95% confidence intervals as measures of familial aggregation. We found first-degree relatives of LPL/WM patients to have 20-fold (4.1-98.4), 3.0-fold (2.0-4.4), 3.4-fold (1.7-6.6), and 5.0-fold (1.3-18.9) increased risks of developing LPL/WM, non-Hodgkin lymphoma (NHL), chronic lymphocytic leukemia (CLL), and monoclonal gammopathy of undetermined significance (MGUS), respectively. However, there was no evidence of an increased risk of developing multiple myeloma or Hodgkin lymphoma. In analyses stratified by type of first-degree relative (parent, sibling, offspring), age at diagnosis of the probands (greater or less than 70 years), and sex of the first-degree relative, we did not observe the risk estimates to be significantly different compared with the overall analyses. Our findings of highly increased risks of developing LPL/WM, NHL, CLL, and MGUS support the operation of shared susceptibility genes that predispose to LPL/WM and other lymphoproliferative disorders.

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Win, AK, RJ Walters, DD Buchanan, MA Jenkins, K. Sweet, DM McKeone, MD Walsh, et al. "A study of cancer risks in relatives of patients with serrated polyposis." Hereditary Cancer in Clinical Practice 10, Suppl 2 (2012): A21. http://dx.doi.org/10.1186/1897-4287-10-s2-a21.

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Li, Philip Kam-Tao, Jack Kit-Chung Ng, Yuk Lun Cheng, Tze Hoi Kwan, Chi Bon Leung, Miu Fong Lau, Koon Shing Choi, et al. "Relatives in silent kidney disease screening (RISKS) study: A Chinese cohort study." Nephrology 22 (November 20, 2017): 35–42. http://dx.doi.org/10.1111/nep.13148.

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Pang, Dong, Robert D. Alston, Tim O. B. Eden, and Jillian M. Birch. "Cancer risks among relatives of children with Hodgkin and non‐Hodgkin lymphoma." International Journal of Cancer 123, no. 6 (September 15, 2008): 1407–10. http://dx.doi.org/10.1002/ijc.23651.

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Hammoud, A. O., H. Nezam, C. M. Peterson, D. Carrell, and M. Gibson. "Risks of urogenital anomalies in male relatives of females with mullerian anomalies." Fertility and Sterility 94, no. 4 (September 2010): S74. http://dx.doi.org/10.1016/j.fertnstert.2010.07.286.

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Yang, Xin, Honglin Song, Goska Leslie, Christoph Engel, Eric Hahnen, Bernd Auber, Judit Horváth, et al. "Ovarian and Breast Cancer Risks Associated With Pathogenic Variants in RAD51C and RAD51D." JNCI: Journal of the National Cancer Institute 112, no. 12 (February 28, 2020): 1242–50. http://dx.doi.org/10.1093/jnci/djaa030.

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Abstract Background The purpose of this study was to estimate precise age-specific tubo-ovarian carcinoma (TOC) and breast cancer (BC) risks for carriers of pathogenic variants in RAD51C and RAD51D. Methods We analyzed data from 6178 families, 125 with pathogenic variants in RAD51C, and 6690 families, 60 with pathogenic variants in RAD51D. TOC and BC relative and cumulative risks were estimated using complex segregation analysis to model the cancer inheritance patterns in families while adjusting for the mode of ascertainment of each family. All statistical tests were two-sided. Results Pathogenic variants in both RAD51C and RAD51D were associated with TOC (RAD51C: relative risk [RR] = 7.55, 95% confidence interval [CI] = 5.60 to 10.19; P = 5 × 10-40; RAD51D: RR = 7.60, 95% CI = 5.61 to 10.30; P = 5 × 10-39) and BC (RAD51C: RR = 1.99, 95% CI = 1.39 to 2.85; P = 1.55 × 10-4; RAD51D: RR = 1.83, 95% CI = 1.24 to 2.72; P = .002). For both RAD51C and RAD51D, there was a suggestion that the TOC relative risks increased with age until around age 60 years and decreased thereafter. The estimated cumulative risks of developing TOC to age 80 years were 11% (95% CI = 6% to 21%) for RAD51C and 13% (95% CI = 7% to 23%) for RAD51D pathogenic variant carriers. The estimated cumulative risks of developing BC to 80 years were 21% (95% CI = 15% to 29%) for RAD51C and 20% (95% CI = 14% to 28%) for RAD51D pathogenic variant carriers. Both TOC and BC risks for RAD51C and RAD51D pathogenic variant carriers varied by cancer family history and could be as high as 32–36% for TOC, for carriers with two first-degree relatives diagnosed with TOC, or 44–46% for BC, for carriers with two first-degree relatives diagnosed with BC. Conclusions These estimates will facilitate the genetic counseling of RAD51C and RAD51D pathogenic variant carriers and justify the incorporation of RAD51C and RAD51D into cancer risk prediction models.

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Couldwell, William T., and Lisa A. Cannon-Albright. "Co-prevalence of other tumors in patients harboring pituitary tumors." Journal of Neurosurgery 121, no. 6 (December 2014): 1474–77. http://dx.doi.org/10.3171/2014.8.jns132139.

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Object The cause of most pituitary tumors remains unknown, although a genetic contribution is recognized for some. The prevalence of pituitary tumors in the general population is high. Analyzing the Utah Population Database (UPDB), the authors investigated the co-prevalence of other independent primary tumors in patients with known pituitary tumors, both benign and malignant, and in the relatives of these patients. Methods The authors identified individuals in the Utah Cancer Registry diagnosed with pituitary tumors who also had genealogy data in the UPDB and then calculated relative risks (RRs) of other tumors in these patients and their relatives. Results Among the 591 individuals with pituitary tumors, 16 (2.7%) had a malignant pituitary tumor and 77 (13%) had independent primary tumors of other origin. Overall, this is significantly higher than expected (70.6 expected, p = 0.009) within the general population (RR = 1.32, 95% CI 1.06–1.61). A significant excess for several different cancer sites was observed among the first-, second-, and third-degree relatives of the cases, including prostate and other cancers. Independent primary tumors at other sites have markedly elevated co-prevalence in patients harboring pituitary tumors and among their close and distant relatives. Conclusions This information will prove useful for counseling patients in whom pituitary tumors have been diagnosed and suggests strong genetic or environmental co-risks for the development of other tumors.

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Cederlöf, Martin, Sarah E. Bergen, Henrik Larsson, Mikael Landén, and Paul Lichtenstein. "Acute intermittent porphyria: Comorbidity and shared familial risks with schizophrenia and bipolar disorder in Sweden." British Journal of Psychiatry 207, no. 6 (December 2015): 556–57. http://dx.doi.org/10.1192/bjp.bp.114.157073.

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SummaryAcute intermittent porphyria (AIP) has been associated with schizophrenia in some studies, but prior research is limited by the absence of comparison populations. Here, we linked Swedish registers to examine the risk of schizophrenia and bipolar disorder in 717 individuals diagnosed with AIP and their first-degree relatives, compared with matched individuals without AIP and their first-degree relatives. Individuals with AIP had a fourfold increased risk of schizophrenia or bipolar disorder. Similarly, relatives of individuals with AIP had double the risk of schizophrenia or bipolar disorder, suggesting that these associations may be as a result of common genetic influences.

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Pujol, Pascal, Nathalie Alegre, Pierre vande Perre, Yves-Jean Bignon, Jean Chiesa, Marie Christine Picot, Virginie Galibert, Helena Bertet, and Carole Corsini. "Psychosocial and clinical factors of probands impacting intrafamilial disclosure and uptake of genetic testing in families with BRCA1/2 or MMR gene mutations." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e13151-e13151. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e13151.

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e13151 Background: Intrafamilial disclosure of hereditary cancer predisposition in BRCA1/2 and mismatch repair gene (MMR) syndromes allows appropriate prevention strategies in at-risk relatives. We previously showed in a nationwide study that the uptake of genetic targeted testing (GTT) in these families by relatives was only 30%. We aimed to identify the medical and psychosocial factors affecting the proband’s intrafamilial disclosure and relatives’ uptake of GTT in BRCA1/2 or MMR syndromes. Methods: We assessed clinical variables, family history and several psychological variables of probands (depression, anxiety, alexithymia, optimism, coping, family relationship, perception of cancer risks and of hereditary transmission risks), together with disclosure and verified uptake of GTT in BRCA1/2 or MMR families. Results: Among relatives eligible for GTT, 68% were informed of the predisposition and 37% underwent GTT, according to proband reports. Intrafamilial disclosure was inversely associated with the degree of kinship (P < 0.01). In multivariable analysis, disclosure increased with time since proband’s genetic diagnosis (P < 0.01) and proband’s feeling of family cohesion (P = 0.01). GTT uptake increased with proband’s depression score (P = 0.02) and decreased with proband’s perception of cancer risks (P = 0.03). BRCA1/2 and MMR groups did not differ in findings concerning family information and GTT uptake. Conclusions: This study identified factors affecting disclosure to relatives and GTT uptake in BRCA1/2 and MMR syndromes and gives new insights to improve probands’ follow-up and intrafamilial sharing of genetic information.

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KNIGHT, ANN, SVEN SANDIN, and JOHAN ASKLING. "Increased Risk of Autoimmune Disease in Families with Wegener’s Granulomatosis." Journal of Rheumatology 37, no. 12 (October 1, 2010): 2553–58. http://dx.doi.org/10.3899/jrheum.091280.

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Objective.The etiology of Wegener’s granulomatosis (WG) is unknown. Susceptibility genes for WG that also affect the risks of other autoimmune/inflammatory diseases have been identified, indicating the existence of shared interdisease genetic susceptibilities. To determine the effect, on a population level, of shared susceptibility on disease risk, we assessed the occurrence of autoimmune/inflammatory disease in first-degree relatives of patients with WG.Methods.In the Swedish Hospital Discharge Register we identified 2288 individuals discharged with the diagnosis of WG between 1970 and 2003. Through linkage to the Swedish Multi-generation Register we identified 787 parents, 1212 siblings, and 3650 children of these patients. From the Register of Total Population we identified 10 controls for each patient with WG, and 65,000 of their first-degree relatives. Through linkage to the nationwide Outpatients Register, we identified autoimmune/inflammatory disease among all relatives. Relative risks were estimated as hazard ratio (HR) using Cox regression. The study period was 2001–2006.Results.Biological first-degree relatives of patients with WG were at a moderately increased risk of any autoimmune/inflammatory disease (HR 1.32, 95% CI 1.18–1.49), including specific associations with, for example, multiple sclerosis (HR 1.92, 95% CI 1.16–3.16), Sjögren’s syndrome (HR 2.00, 95% CI 1.07–3.73), and seropositive rheumatoid arthritis (HR 1.54, 95% CI 1.09–2.19).Conclusion.Relatives of patients with WG are at increased risk of being diagnosed with other autoimmune/inflammatory diseases, indicating shared susceptibility between WG and other auto-immune/inflammatory disease.

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Goldstein, Jill M., Stephen V. Faraone, Wei J. Chen, and Ming T. Tsuang. "The Role of Gender in Understanding the Familial Transmission of Schizoaffective Disorder." British Journal of Psychiatry 163, no. 6 (December 1993): 763–68. http://dx.doi.org/10.1192/bjp.163.6.763.

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The purpose of this study was to test the effect of gender on the familial risk for schizophrenia and affective disorders in probands with schizoaffective disorder. The sample consisted of 42 DSM–III schizoaffective probands and 149 first-degree relatives from the retrospective cohort family studies, the Iowa 500 and non-500. Survival analysis estimated differences in morbidity risks, analysed by sex of proband and of relative. Findings showed that, among probands, relatives of females had significantly higher rates of schizophrenia and unipolar disorder than relatives of males. Further, among relatives, males were at significantly higher risk for schizophrenia spectrum disorders than females. Results were similar when probands were subdivided into their primary symptom patterns, that is ‘mainly schizophrenic’ or ‘mainly affective’, as well as by ‘schizoaffective, depressed’ or ‘schizoaffective, manic’. Implications for the taxonomy of schizoaffective disorder suggest a stronger relationship with schizophrenia, although the relationship with affective disorder remains unclear.

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Li, Xinjun, Jan Sundquist, Kristina Sundquist, and Bengt Zöller. "Determination of age-specific and sex-specific familial risks for the different manifestations of venous thromboembolism: A nationwide family study in Sweden." Thrombosis and Haemostasis 106, no. 07 (2011): 102–12. http://dx.doi.org/10.1160/th10-10-0655.

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SummaryThis nationwide study aimed to determine whether differences exist in age-specific and sex-specific familial risks for pulmonary embolism (PE), venous thrombosis of the lower limbs (VT) and other forms of venous thromboembolism (OVTE) among offspring, siblings and spouses of affected individuals. The Swedish Multi-Generation Register was linked to the Hospital Discharge Register data for the period 1987–2007. Standardised incidence ratios (SIRs) were calculated for individuals whose relatives were hospitalised for venous thromboembolism (VTE), as determined by the International Classification of Diseases (ICD), and those whose relatives were unaffected by VTE. The total number of hospitalised VTE patients was 45,362. All VTE patients were categorised as PE, VT or OVTE according to ICD at first hospitalisation. For example, the parental SIRs for PE, VT and OVTE in offspring at age 10–19 years were 2.89 (95% CI 1.48–5.06), 4.99 (95% CI 3.22–6.10) and 3.89 (95% CI 2.51–5.75), respectively. The low spousal risks of PE (1.08; 95% CI 1.02–1.13), VT (1.06; 95% CI 1.011.12) and OVTE (1.07; 95% CI 1.00–1.15) suggest the familial risks to be largely genetic. In both men and women, familial relative risks were increased for all the different manifestations of VTE with the exception of those older than 70 years. Familial history is a risk indicator in both sexes, and is potentially useful for clinical risk assessment for the different manifestations of VTE.

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Larsson, Henrik, Eleonore Rydén, Marcus Boman, Niklas Långström, Paul Lichtenstein, and Mikael Landén. "Risk of bipolar disorder and schizophrenia in relatives of people with attention-deficit hyperactivity disorder." British Journal of Psychiatry 203, no. 2 (August 2013): 103–6. http://dx.doi.org/10.1192/bjp.bp.112.120808.

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BackgroundAttention-deficit hyperactivity disorder (ADHD) is associated with bipolar disorder and schizophrenia, and it has been suggested that combined bipolar disorder and ADHD is aetiologically distinct from the pure disorders.AimsTo clarify whether ADHD shares genetic and environmental factors with bipolar disorder and schizophrenia.MethodBy linking longitudinal Swedish national registers, we identified 61 187 persons with ADHD (the proband group) and their first- and second-degree relatives, and matched them with a control group of people without ADHD and their corresponding relatives. Conditional logistic regression was used to determine the risks of bipolar disorder and schizophrenia in the relatives of the two groups.ResultsFirst-degree relatives of the ADHD proband group were at increased risk of both bipolar disorder (odds ratio (OR) = 1.84−2.54 for parents, offspring and full siblings) and schizophrenia (OR = 1.71−2.22 for parents, offspring and full siblings). The risks of bipolar disorder and schizophrenia among second-degree relatives were substantially lower than among full siblings.ConclusionsThese findings suggest that the co-occurrence of ADHD and bipolar disorder as well as ADHD and schizophrenia is due to shared genetic factors, rather than representing completely aetiologically distinct subsyndromes.

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Middleton, Anna, Richard Milne, Lauren Robarts, Jonathan Roberts, and Christine Patch. "Should doctors have a legal duty to warn relatives of their genetic risks?" Lancet 394, no. 10215 (December 2019): 2133–35. http://dx.doi.org/10.1016/s0140-6736(19)32941-1.

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Cannon-Albright, Lisa Anne, Sue Dintelman, Tim Maness, Johni Cerny, Alun Thomas, Steven Backus, James Michael Farnham, et al. "Population genealogy resource shows evidence of familial clustering for Alzheimer disease." Neurology Genetics 4, no. 4 (August 2018): e249. http://dx.doi.org/10.1212/nxg.0000000000000249.

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ObjectiveTo show the potential of a resource consisting of a genealogy of the US record linked to National Veterans Health Administration (VHA) patient data for investigation of the genetic contribution to health-related phenotypes, we present an analysis of familial clustering of VHA patients diagnosed with Alzheimer disease (AD).MethodsPatients with AD were identified by the International Classification of Diseases code. The Genealogical Index of Familiality method was used to compare the average relatedness of VHA patients with AD with expected relatedness. Relative risks for AD were estimated in first- to fifth- degree relatives of patients with AD using population rates for AD.ResultsEvidence for significant excess relatedness and significantly elevated risks for AD in relatives was observed; multiple pedigrees with a significant excess of VHA patients with AD were identified.ConclusionsThis analysis of AD shows the nascent power of the US Veterans Genealogy Resource, in early stages, to provide evidence for familial clustering of multiple phenotypes, and shows the utility of this VHA genealogic resource for future genetic studies.

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Lin, Huan-Tang, Fu-Chao Liu, Shu-Fu Lin, Chang-Fu Kuo, Yu-Ying Chen, and Huang-Ping Yu. "Familial Aggregation and Heritability of Nonmedullary Thyroid Cancer in an Asian Population: A Nationwide Cohort Study." Journal of Clinical Endocrinology & Metabolism 105, no. 7 (April 25, 2020): e2521-e2530. http://dx.doi.org/10.1210/clinem/dgaa191.

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Abstract Purpose The purpose of this work is to assess the extent of familial aggregation of nonmedullary thyroid cancer (NMTC) and the relative risks (RRs) of chronic thyroid diseases and common malignancies in first-degree relatives of NMTC patients. Methods In the National Health Insurance Research database of Taiwan, all eligible individuals in 2016 were analyzed (n = 23 696 659) and the family structures of 38 686 patients diagnosed with NMTC between 1997 and 2016 were identified. The prevalence and RRs of NMTC, chronic thyroid diseases, and common malignancies in individuals with first-degree relatives with NMTC were examined. The accountability of heritability and environmental factors to NMTC susceptibility was estimated using the polygenic liability model. Results The prevalence of NMTC was 0.16% in the general population and 0.64% in individuals with first-degree relatives with NMTC. Regarding affected relatives, the RR (95% CI) for NMTC was 20.12 (4.86-83.29) for twins, 6.43 (4.80-8.62) for siblings, 5.24 (4.55-6.03) for offspring, 5.07 (4.41-5.81) for parents, and 2.07 (1.53-2.81) for spouses. The estimated genetic, common environmental, and nonshared environmental contributions to NMTC were 28.0%, 14.3%, and 57.7%, respectively. A family history of NMTC was associated with higher risks of thyroid nodules (RR, 2.26; 95% CI, 2.18-2.35), Hashimoto thyroiditis (2.11; 1.89-2.36), Graves disease (1.49; 1.42-1.57), lung cancer (1.56; 1.32-1.85), and leukemia and lymphoma (1.24; 1.03-1.50). Conclusion Our findings demonstrate the importance of genetic and environmental contributions to NMTC susceptibility and highlight the coaggregation of chronic thyroid diseases and multiple malignancies with NMTC.

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Razzak, A. Rab, Lauren Bailey, Brandon Yu, Mohammed Abusamaan, In Guk Kang, Brittany Ma, Bunmi Emidio, Oluwafemi Owodunni, Thomas J. Smith, and Joann Bodurtha. "Hereditary cancer prevalence and communication about family history risks in palliative care." Journal of Clinical Oncology 35, no. 31_suppl (November 1, 2017): 56. http://dx.doi.org/10.1200/jco.2017.35.31_suppl.56.

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56 Background: Hereditary cancer (CA) assessment & communication about family history (FH) risks in palliative care are underexplored & could be critical for surviving relatives. FH may not be adequately reviewed & appropriate information conveyed in the palliative care (PC) setting, even though family health is a legacy concern of patients. Cancer patients seeking PC never wish for their relatives to have CA & may be an important resource for communication about their relative’s CA risk & appropriate referrals. Methods: This prospective observational study among cancer patients receiving PC consultations was conducted at a 977-bed academic urban hospital between June 2016 & March 2017. Data were collected through structured interviews and chart review during hospitalizations. Results: 75 adult cancer patients were enrolled. Patients’ average age at diagnosis was 55.3 ± 15.7 years. 41(55%) self-identified as male; 34(45%) as female; 20(27%) as black, 49 (65%) white, and 6(8%) other. 24 patients (32%) were considered to have pedigrees that merited referral as high-risk. 32 patients (43%) thought that their CA had a likely genetic or inherited component. 48(64%) thought the palliative care setting was an appropriate place to discuss the implications. The mean comfort level in addressing these questions was 8.7 on a 10 point scale with 10 indicating extremely comfortable. Conclusions: Review of FH may be an intervention that PC providers & families can discuss & incorporate in legacy activities. This could enhance CA prevention, especially among high-risk families. There is room for enhancement in how FH & patient and family concern are integrated in the palliative & cancer care continuum.

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Journal articles on the topic 'Relatives risks'

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