Rising incidence of oesophageal adenocarcinoma in men in Australia

Adenocarcinomas of the oesophagus and of the gastric cardia have been reported to be increasing in incidence in many countries, while the incidence of squamous cell carcinoma of the oesophagus is stable and non-cardia gastric cancers are decreasing in incidence. Age-standardized incidence rates for the years 1982–93 for oesophageal adenocarcinoma and non-adenocarcinoma, and gastric cardia and non-cardia cancers were calculated based on state cancer registry incidence data. Time trends in the age-standardized rates were assessed using linear regression. A consistent increasing trend in the incidence of oesophageal adenocarcinoma in men was seen in all states of Australia and was statistically significant in all states except South Australia. There were no consistent nationwide trends in the incidence of oesophageal adenocarcinoma in women, although a trend towards an increase in the incidence of this cancer reached statistical significance ( P < 0.05) in three states (New South Wales, Victoria, Queensland). There were no important trends in the incidence of oesophageal non-adenocarcinoma in either men or women. There were no consistent nationwide changes in the incidence of gastric cardia cancer in either men or women, although this cancer was significantly increasing in Tasmania in both men and women. The incidence of cancer of the stomach not arising at the gastric cardia was significantly decreasing in men in all states and was also decreasing in women in all states, although in women this decrease was statistically significant only in New South Wales, Victoria and Western Australia. There has been a dramatic increase in the incidence of oesophageal adenocarcinoma in men in Australia. The incidence of this cancer in men is now approximately equal with that of non-adenocarcinoma of the oesophagus. The incidence of non-cardia stomach cancer continues to fall.     

Simplified sensitive method for the detection of B‐cell clonality in lymphoid malignancies

Molecular response and monitoring of minimal residual disease (MRD) is becoming an essential part of most protocols for treating leukemia and lymphoma patients. Detection of abnormal clones by PCR analysis of complementarity determining regions (CDRs) in immunoglobulin genes is currently standard practice for diagnosis, but is not widely used to monitor MRD because of the low sensitivity of assays that use consensus primers. Use of specific primers can improve the sensitivity of the assay, but is a cumbersome, expensive, and time‐consuming process. We developed a simple and cost‐effective approach to detect MRD in B‐cell malignancies that is usable in clinical laboratories. The new assay uses ligase chain reaction (LCR) to detect clonality. The sensitivity of the LCR assay is 1 per 500 000 cells, and it can detect all subclones that were present in the pretherapy diagnostic sample.     

LUMBOSACRAL FACETAL 'JOINT ANGLES' ASSOCIATED WITH LEG ENGTH INEQUALITY

Differences in the right and left lumbosacral facetal ‘jointangles’ are compared in non-acute low back pain patientswith a leg length discrepancy of greater than 9 mm and a controlgroup with a 0–3 mm leg length discrepancy. The methodof erect-posture lumbosacral oblique radiography is described,as well as the method of measuring the lumbosacral facetal jointangles.     

The effects of lithium on vascular development in the chick area vasculosa

The effects of lithium on vascular development were examined using the chick embryo area vasculosa in shell-less culture as an experimental model. Embryos were explanted after 48 h in ovo and LiCl (50, 100, 150 and 200 μg in 10 μl water) was applied to the centre of the blastodisc. Controls were untreated or given equimolar amounts of NaCl. At 24 h and 48 h after treatment, untreated and NaCl controls were identical, having well developed extraembryonic vessels. At doses of 100 μg and greater, LiCl significantly inhibited normal vascular development and expansion of the area vasculosa in the majority of explants. In many specimens blood islands continued to form but their assembly into primitive vessels was prevented, indicating that lithium affects the mechanism regulating the assembly of vascular endothelium. At the same time the embryos were alive but retarded in development compared with controls. When LiCl (150 μg) was applied to cultures explanted after 72 h in ovo (when the primary vascular network had already formed through vasculogenesis) no adverse effects were seen. This suggests that lithium affects vasculogenesis but not angiogenesis. Treatment with myo-inositol completely reversed the effects of lithium in a time dependent manner indicating that the phosphatidylinositol second messenger cycle may be involved in the cellular events of vasculogenesis. Finally the results of this study show that the yolk sac vasculature is particularly vulnerable to lithium and the consequent effects of this interference on embryonic development are discussed.     

Intravascular coagulation in gestational hypertension and pre-eclampsia: the value of haematological screening tests

Summary. Routine investigations designed to detect excessive intravascular coagulation in patients with gestational hypertension and pre-eclampsia have been analysed in 936 cases. Reticulocyte counts did not differ significantly from those in normal controls and abnormal red cell morphology was detected in only two patients. Fibrinogen degradation products and thrombocytopenia were found in about 10% of all hypertensive women and macrothrombocytosis in 32%. Neither reticulocyte counts nor the scanning of stained blood films for evidence of microangiopathic haemolysis have a place in the routine investigation of preeclampsia and it is doubtful whether any of the other screening tests can influence the management of patients with uncomplicated gestational hypertension. In fully developed pre-eclampsia, macrothrombocytosis is found in about 50% of patients, fibrinogen degradation products and thrombocytopenia in about 15%. All three parameters reflect the degree of clinical severity of the disease.