Clinical medicine (London, England)
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The differential diagnosis of haematological abnormalities, such as leucocytosis, erythocytosis, thrombocytosis or indeed anaemia, is wide and disarming. Here we report on significant updates in the differential diagnosis of erythrocyosis and thrombocytosis presenting a simplified schema for the clinician. We then move to discuss significant advances in this field which have followed a series of key molecular findings, most specifically those affecting the JAK/STAT pathway.
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Treatment resistance affects around 20% of people with epilepsy and carries a significant comorbidity. It is important to ensure that the diagnosis of epilepsy is secure and the underlying cause of the epilepsy is investigated thoroughly. Management involves early referral for epilepsy surgery when suitable, optimisation of pharmacological treatment, and consideration of comorbidities such as depression.
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The last 20 years have seen a transformation in the landscape of rheumatoid arthritis, which has changed from being a life limiting condition to a chronic but often remitting illness. The importance of early disease control, the better use of existing therapies, and the development of new therapies have all been key to this success. The future of therapy now lies in the identification of stratifying biomarkers, to allow more rational delivery of treatment. The ultimate goal remains the reintroduction of immune tolerance to potentially achieve a 'cure.'
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Barretts oesophagus represents the most significant risk factor for the development of oesophageal adenocarcinoma (OAC), although the majority of patients will not develop cancer. However, early detection of OAC and its precursors significantly improves outcome and underlines the importance of endoscopic surveillance programmes. Clearly there is a discrepancy between the small number of people who need to undergo surveillance because they are at significant progression risk, and the large number that do. ⋯ Currently such stratification is currently based on clinical findings, endoscopic diagnosis and histopathological grade. Histopathology can be imperfect and is likely to require molecular confirmation of different grades, thus molecular stratification is becoming more important in this regard and p53 immunohistochemistry is already clinically useful, with other molecular biomarkers likely to prove beneficial in the future. The hope is that non-endoscopic methods, such as the Cytosponge may be able to combine molecular biomarkers with histopathology and therefore perhaps benefit a population screening as well as a surveillance programme.
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Many patients with heart failure (HF) have a normal left ventricular ejection fraction, and are labelled as having HF with preserved left ventricular ejection fraction (HFPEF). Hypertension, atrial fibrillation and age are important contributors to the development of HFPEF and, therefore, its prevalence is likely to increase in the next few decades. The pathophysiology of HFPEF is heterogeneous but with a final common pathway leading to congestion. ⋯ No treatment has been shown conclusively to alter the prognosis of HFPEF. However, treatments directed at congestion and hypertension, such as diuretics, mineralocorticoid receptor antagonists (MRAs) and angiotensin converting-enzyme inhibitors, may improve symptoms and probably do improve outcomes. No treatment has yet been shown to reverse the underlying myocardial pathology of HFPEF, although there is some hope that MRAs might.