Are the PBS guidelines for lipid-lowering treatment appropriate for patients with CHD?
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Biomedical subjects
Publications and source records attributed to G A Tallis.
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We have compared the lipid and apolipoprotein values and the frequency of DNA polymorphisms of the apolipoprotein B gene detected with the restriction enzymes, Xba I and Eco RI in 122 patients with coronary heart disease (CHD) and 80 control subjects. The patients with coronary heart disease (CHD) were defined by > 70% stenosis in at least one major coronary artery whereas the controls showed no signs of coronary artery narrowing at angiography. When males and females were considered separately, differences in triglyceride, total cholesterol and high density lipoprotein-cholesterol (HDL-cholesterol) between CHD and control subjects were significant only for females. The polymorphism studies showed no significant differences between the control and CHD subjects except for a difference in the frequency in the females of the Xba I polymorphism (p < 0.05). The X1 allele (absence of the restriction enzyme cutting site) occurred significantly more often in the patient group than in the controls. Individuals with the X1X2 genotype had the highest serum total cholesterol whereas those with the X1X1 genotype had the lowest HDL-cholesterol value. Generally, the associations between the Xba I and Eco RI alleles and serum lipid levels were weak and inconsistent. Furthermore, even after careful selection of disease and control groups, a useful role for restriction fragment length polymorphism studies in assessing CHD risk in individual patients was not demonstrated.
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Lactate dehydrogenase (LD) activity is often increased in malignancy, and may occasionally be a useful tumor marker. In the case reported here, a persistently increased LD activity led to an extensive search for a neoplasm. Results of routine investigations were normal, but LD electrophoresis followed by gel filtration and immunofixation confirmed the presence of a circulating macromolecular LD, comprising IgAK bound to LD. Altogether it may provoke unnecessary investigations, the LD-IgA complex currently has no diagnostic significance.
We describe hyperparathyroidism in an 18-year-old man with Wilson's disease--the first report in the English literature of the simultaneous occurrence of these two conditions.
Four cases of symptomatic hyponatraemia in psychiatric patients are described. All patients exhibited varying degrees of the compulsive intake of water. The initial urinary osmolalities in all cases suggested impaired clearance of free water. This may be related to an exacerbation of the psychotic state. All patients demonstrated a marked diuresis after treatment with a hypertonic (1.8%) saline solution. The underlying pathophysiology is discussed. This clinical syndrome may be associated with significant morbidity and occasional mortality that are related to the rapid development of hyponatraemia.
Three cases of acute lead arsenate poisoning which occurred in South Australia during a 12 month interval are described. The case reports demonstrate a number of features of the characteristic clinical syndrome which may follow ingestion of lead arsenate. The recommended management is immediate gastric lavage and subsequent chelation therapy with calcium EDTA and dimercaprol. Early gastric lavage may prevent significant lead absorption. However, arsenic acid (produced in the stomach when lead arsenate reacts with hydrochloric acid) is relatively water soluble and prompt gastric lavage is unlikely to prevent extensive arsenic absorption. It remains controversial as to whether chelation with dimercaprol prevents arsenical neuropathy.
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OBJECTIVE: To present a case of lead poisoning following ingestion of Indian herbal medicine. CLINICAL FEATURES: A 37-year-old man presented with a history of abdominal pain, anorexia and malaise. He had recently returned from a trip to India where he had been taking two different herbal tonics. Investigation revealed low-grade hepatitis and normocytic anaemia with prominent basophilic stippling. The blood lead concentration was high, and analysis of the herbal tablets revealed a very high lead content. INTERVENTION AND OUTCOME: The patient required narcotic analgesia for abdominal pain and was treated with chelation therapy with calcium ethylenediaminetetra-acetate (calcium EDTA) for five days which resulted in a high urinary excretion of lead and resolution of his symptoms over a period of several days. CONCLUSION: Lead poisoning in Australia is usually the result of chronic industrial exposure, but practitioners should be aware of the possibility of poisoning from other domestic sources such as unglazed pottery, cosmetics and herbal remedies, especially those from Asia and India, in which lead may be present in high concentration. Patients from Asia who present with unexplained anaemia or abdominal symptoms should be asked about exposure to such sources.