Seasonal variation in mortality from myocardial infarction and haemopericardium. A postmortem study

BACKGROUND: Seasonal variation in the incidence of and mortality from myocardial infarction (MI) has been well recognised for many years. Haemopericardium (HP) is usually a fatal complication of MI. No data exist in the literature with regard to the seasonal variation in mortality from HP. AIMS: To perform a necropsy based study to confirm seasonal variation in mortality from MI in a London population and to determine whether seasonal variation in mortality from HP can be established. METHODS: Postmortem causes of death issued by several pathologists, working in two public London mortuaries over a five year period from 1999 to 2004 were analysed. Deaths caused by HP secondary to traumatic or iatrogenic causes were specifically excluded, as were deaths caused by HP secondary to bicuspid aortic valve and aortic dissection. The results were subdivided into winter (1 November to 31 March) and summer (1 April to 31 October). RESULTS: In total, there were 2266 cases of MI and 135 cases of HP. Significantly more deaths from HP (83 of 135; 61.5%; p = 0.004) and MI (1051 of 2266; 46.4%; p = 0.016) occurred in the five month winter period. Furthermore, there was a significantly higher incidence of HP compared with MI during the winter (83/1051; 7.9%) than the summer (52/1215; 4.3%; p<0.001). There was no significant difference in the age or sex of patients dying in either the winter or summer. CONCLUSION: There is seasonal variation in mortality from both MI and HP in the London population, as confirmed by a postmortem study

Molecular and kinetic features of transitional cell carcinomas of the bladder: biological and clinical implications.

This paper sets out the molecular basis for the suggestion that the molecular evolution of invasive TCC is distinct to that of In situ carcinoma of the bladder. In particular Dr Naase set out the molecular pathways

Phaeochromocytoma crisis presenting with profound hypoglycaemia and subsequent hypertension.

A patient was presented with four days of vomiting, abdominal pain and sweating. At presentation the Capillary Blood Glucose (CBG) was 1.7 mmol/L, the Blood Pressure (BP) was 182/102 mmHg, and the pulse 100 bpm. On examination, he was sweaty, pale and cold. The initial differential diagnosis was hypoglycaemia secondary to insulin abuse, hypoadrenalism or insulinoma, the transient hypertension being considered a consequence of sympathetic stimulation. He remained clinically well overnight with a CBG of 10-14 mmol/L following intravenous glucose. The next morning he complained of nausea and abdominal pain. The BP had risen to 203/127 mmHg when he was later reviewed, having been given 10mg intramuscular metoclopramide. Shortly afterwards, he developed acute pulmonary oedema and had become hypoglycaemic again; a phaeochromocytoma crisis was suspected. Treatment with alpha-adrenoceptor blockade with intravenous phenoxybenzamine was advised. However, the patient deteriorated and died in the Intensive Care Unit within two hours. Autopsy examination confirmed a phaeochromocytoma in the left adrenal, with haemorrhage within the head of pancreas, but no evidence of a pancreatic tumour