26099246
Expression profiling and individualisation of treatment for ovarian cancer.
Ovarian cancer is the commonest cause of gynaecological cancer-related mortality. Patients with this disease generally undergo surgery followed by platinum-taxane chemotherapy, with additional chemotherapy at relapse. Although the prognosis for patients with advanced cancer is poor--a five-year survival of only 30-40%--there is a wide range of outcomes for individual patients. To date, clinico-pathological variables such as age, stage, grade, histology, debulking status and response to chemotherapy continue to provide the basis on which treatment decisions are made for individual patients. Immunohistochemical markers and information on p53 mutation status have been extensively evaluated in ovarian cancer, but have not yet been shown to be sufficiently informative to influence clinical decisions on a routine basis. The recent advent of expression profiling has provided a new impetus to identifying clinically useful prognostic markers. The ambition of personalised medicine through microarray-based profiling appears to be realistic, but further studies on large uniform cohorts are needed before this potential is fully realised.
8134220
Prognostic factors in ovarian cancer: how close are we to a complete picture?
Prognostic factors in ovarian cancer: how close are we to a complete picture? Ovarian cancer is the fourth most common cause of cancer-related death in women, but is the most lethal of the gynaeco-logical malignancies with 30–40% overall survival at 5 years [1]. This is in part because the majority of patients with ova-rian cancer present with advanced disease, and treatment options at presentation are confined to a combination of debulking surgery and platinum based chemotherapy, which are only partially effective [2]. Consequently, almost all patients with advanced disease ultimately relapse and die of their disease. Advances in the management of these patients are therefore urgently required. Prognostic factors are defined as phenotypes which correlate with overall survival. In general prognostic factors reflect the intrinsic biology of a tumour (e.g. histological subtype, grade), disease extent (e.g. stage) and/or the capacity of a patient to cope with the morbidity associated with the tumour and treatment (e.g. performance status). As well as these pretreatment factors, others which may impact on outcome include the treatment received by a patient (e.g. optimal surgical cytore-duction, platinum-based chemotherapy), and the effect of treatment on the tumour (e.g. complete response) or the patient (e.g. myelosuppression). As clinical tools, prognostic factors can potentially help in individualising treatment for patients. In properly staged early disease (stage Ia/b), patients have a better prognosis and the benefits of adjuvant chemotherapy may be confined to those with adverse features (e.g. histological subtype or grade) [3]. In this context a prognostic factor with a good positive or negative predictive value for individual patients, would be useful in deciding which patients should receive chemotherapy and those for whom the toxicity was not justified. In contrast, in advanced disease, the majority of patients benefit from paclitaxel –carboplatin chemotherapy and debulking surgery. As there are no established alternatives for patients with either good or poor prognosis, pretreatment prognostic stratification has little influence on clinical management [2]. Instead, pre-treatment markers predictive of response or resistance to individual cytotoxic drugs would be more useful in this context for treatment selection. As research tools, prognostic factors can help identify subgroups of patients with especially poor prognosis and alert us to the need to develop alternative treatment strategies for these patients, while in clinical trials prognostic factors are used to balance patients between treatment arms to minimise the risk of confounding. Prognostic factor studies can also provide useful insights into …
9771743
Home and ambulatory blood pressure monitoring in chronic kidney disease.
PURPOSE OF REVIEW
Whereas blood pressures (BPs) obtained in the clinic have formed the basis of diagnosis and treatment of hypertension among patients with chronic kidney disease (CKD), home and ambulatory BP monitoring obtained outside the physician's office have emerged as viable alternatives for the surveillance of hypertension. The purpose of this review is to discuss the recent advances in out-of-office BP recordings in the management of patients with CKD including those on hemodialysis.


RECENT FINDINGS
In patients with CKD not yet on dialysis, hypertension is often seemingly difficult to control in part because of 'white-coat hypertension'. Masked hypertension is seen in about 8% of patients. Nondipping ambulatory BP manifests early in the course of CKD but may not be independently associated with end-stage renal disease. Out-of-office measured BPs better predict end-organ damage and mortality outcomes in CKD and hemodialysis patients. The analysis of patterns of ambulatory BP monitoring has revealed that elevated BP in these patients is associated with increased arterial stiffness and a blunted rate of rise in BP between dialysis with volume overload.


SUMMARY
It is recommended that the diagnosis and treatment of hypertension among patients with CKD is best done with home (or ambulatory) BP monitoring.
27121062
The anatomy of the split ear lobe.
20409600
Hypertension in chronic kidney disease and dialysis: pathophysiology and management.
Hypertension affects 24% of the adult US population. In the United States, 3% of the adult population has an elevated serum creatinine level, and 70% of these patients have hypertension. The prevalence of hypertension in chronic kidney disease (CKD) depends on the patient's age and the severity of renal failure, proteinuria, and underlying renal disease. As patients with CKD progress to end-stage renal disease (ESRD), 86% are diagnosed with hypertension. It has long been recognized that kidney function affects and is affected by hypertension. This article discusses the pathophysiology and management of hypertension in patients with CKD.
7762587
The role of statins in chronic kidney disease.
Chronic kidney disease is associated with cardiovascular event rates that are at least as high as in patients with established atherosclerotic cardiovascular disease or in those with diabetes mellitus. Chronic kidney disease is therefore considered a cardiovascular disease risk equivalent. Treatment of dyslipidemia, which is very common in this population and reflects the pattern seen in the metabolic syndrome, reduces cardiovascular events in patients with chronic kidney disease. Thus, patients with chronic kidney disease should be evaluated and treated for dyslipidemia. Dyslipidemia is a risk factor for the development of impaired kidney function. Dyslipidemia is also associated with progressive renal disease in subjects with no overt renal disease, as well as those with diabetic and nondiabetic kidney disease. Although definitive randomized controlled trials are lacking, the collective evidence suggests that treatment of dyslipidemia is associated with less decline in renal function. The use of potent statins in high doses can lead to transient proteinuria via impairment of proximal tubular receptor--mediated endocytosis, in a dose-dependent manner. Over the long term, however, the use of statins results in a reduction in proteinuria and in the rate of decline of renal function. Several large definitive trials that are currently underway to examine the safety and efficacy of statins in cardiovascular and renal protection should provide more definitive answers on the role of these drugs in this very high risk population.
34997993
Iron, oxidative stress, and clinical outcomes
It is well known that iron is pro-oxidant. Chronic kidney disease (CKD) is a pro-oxidant state, and intravenous administration of iron is frequently used to correct anemia. On one hand, there is little doubt that iron causes oxidative stress. On the other, it is far from clear whether oxidative stress, so generated, leads to poor clinical outcomes. Iron has benefits that may be independent of the correction of anemia. Furthermore, concerns surround the use of high doses of erythropoietin in causing excess heart failure and death in patients with CKD. Thus, it would be prudent if iron were to continue to be used judiciously in patients who require erythropoietin. Iron, given orally, would be the preferred first-line agent in patients not on hemodialysis. In patients with sepsis, intravenous treatment with iron should be avoided, because, in animal experiments, intravenous administration of iron can compound the inflammatory response and increase mortality. Clinical trials are needed to ascertain the risk and benefits of the intravenous administration of iron in patients with CKD.