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The condition known as cryptorchidism – undescended testis – is one of the most common congenital abnormalities found among males, and is one of the few known risk factors for testicular cancer (TC). Like testicular cancer, the key exposures in the occurrence of cryptorchidism remain elusive. Testicular descent is thought to occur during two hormonally-controlled phases – between 8–15 weeks and 25–35 weeks gestation – and while it is clear that a failure of testes to descend permanently is likely due to disruptions to one or both of these phases, the cause(s) and mechanism(s) of such disruption are still unclear. In this manuscript, we review the broad range of putative risk factors that have been evaluated in relation to the development of cryptorchidism to date, discuss their plausibility, and make suggestions regarding further approaches to understand aetiology. There are few exposures for which there is consistent evidence of an association with cryptorchidism; and in those cases where evidence appears unequivocal – for example, the relationship between cryptorchidism and gestational measures such as low birth weight – the measured exposure is likely to be a surrogate for the true causal exposure. The relative importance of each risk factor may vary considerably between mother/son pairs depending on an array of genetic, maternal, placental and foetal factors – all of which could vary between regions.

Using a large, well-defined, national prevalent cohort of people with diabetes, we found that being male, indigenous Māori, living in deprivation, having a high comorbidity burden and/or having a previous amputation were strongly associated with subsequent risk of lower limb amputation. The use of this prevalent cohort strengthens the value of our estimates in terms of applicability to the general population, and highlights the subgroups at greatest risk of lower limb amputation.

Background:It is known that cancer stage is affected by comorbidity, but the evidence regarding the magnitude and even direction of this effect is highly inconsistent and poorly understood. The aims of this study were to establish the impact of comorbidity on cancer stage at diagnosis, using both specific individual comorbid conditions and a global measure of comorbidity; and to assess whether this impact varied by cancer site, level of comorbidity burden and individual comorbidity type.Methods:We examined comorbidity among 14 096 patients with breast, colon, rectal, liver, stomach, ovarian, uterine, bladder or kidney cancer. Patients were identified from cancer registry data, and then linked to hospitalisation data to determine the presence of comorbidity in the 5 years preceding cancer diagnosis. Individual comorbid conditions were identified using ICD-10 codes, and overall burden of comorbidity attributed using a cancer-specific measure of comorbidity (C3 Index).Results:We observed that the presence of patient comorbidity (a) increases the odds of being diagnosed with distant metastases, (b) does not lead to earlier diagnosis and (c) increases the likelihood of a patient receiving no stage of disease at diagnosis.Conclusions:Patient comorbidity has a substantial impact on cancer stage at diagnosis; however, this impact varies considerably by cancer type, individual comorbid condition and overall comorbidity burden.

BackgroundThe aetiology of testicular cancer remains elusive. In this manuscript, we review the evidence regarding the association between cannabis use and testicular cancer development.MethodsIn this systematic review and meta-analysis, we reviewed literature published between 1st January 1980 and 13th May 2015 and found three case–control studies that investigated the association between cannabis use and development of testicular germ cell tumours (TGCTs).Results/ConclusionsUsing meta-analysis techniques, we observed that a) current, b) chronic, and c) frequent cannabis use is associated with the development of TGCT, when compared to never-use of the drug. The strongest association was found for non-seminoma development – for example, those using cannabis on at least a weekly basis had two and a half times greater odds of developing a non-seminoma TGCT compared those who never used cannabis (OR: 2.59, 95 % CI 1.60–4.19). We found inconclusive evidence regarding the relationship between cannabis use and the development of seminoma tumours. It must be noted that these observations were derived from three studies all conducted in the United States; and the majority of data collection occurred during the 1990’s.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1905-6) contains supplementary material, which is available to authorized users.

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Acute rheumatic fever (ARF) and its sequela, rheumatic heart disease (RHD), have largely disappeared from high-income countries. However, in New Zealand (NZ), rates remain unacceptably high in indigenous Māori and Pacific populations. The goal of this study is to identify potentially modifiable risk factors for ARF to support effective disease prevention policies and programmes. A case-control design is used. Cases are those meeting the standard NZ case-definition for ARF, recruited within four weeks of hospitalisation for a first episode of ARF, aged less than 20 years, and residing in the North Island of NZ. This study aims to recruit at least 120 cases and 360 controls matched by age, ethnicity, gender, deprivation, district, and time period. For data collection, a comprehensive pre-tested questionnaire focussed on exposures during the four weeks prior to illness or interview will be used. Linked data include previous hospitalisations, dental records, and school characteristics. Specimen collection includes a throat swab (Group A Streptococcus), a nasal swab (Staphylococcus aureus), blood (vitamin D, ferritin, DNA for genetic testing, immune-profiling), and head hair (nicotine). A major strength of this study is its comprehensive focus covering organism, host and environmental factors. Having closely matched controls enables the examination of a wide range of specific environmental risk factors.

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