Dina Matias

Glutathione S-transferase mu polymorphism and susceptibility to lung cancer in the Portuguese population†

Epidemiological studies have led to the suggestion that a genetic basis may exist in the individual variation in predisposition to cancer. Interindividual differences in human toxicological response to carcinogenic exposure have been attributed to heritable polymorphisms in metabolism, namely glutathione S-transferases (GSTs) coding for enzymes that are known to be detoxifiers of carcinogens. Within the human GST mu class, there is a specific isozyme that is frequently lacking. To check whether or not this association exists in the Portuguese population with lung cancer, we used polymerase chain reaction (PCR)-based genotyping to examine GSTM1 polymorphism (nulled and non-nulled) in 84 individuals as a control healthy population and a group of 98 lung cancer patients. In this study we were able to find a frequency of the GSTM1 phenotype among our healthy control subjects consistent with earlier genotyping studies in other Caucasoid populations. For the group of individuals with lung cancer as a whole, or in subsets of histological subtypes, our data for the Portuguese population did not show a positive correlation between the null allele and this neoplasm. In contrast, we found a slight increase in the frequency of the wild-type allele in our lung cancer group.

Doentes com neoplasia do pulmão de não pequenas células submetidos a tratamento com erlotinib – Casos clinicos

Resumo Apresentam-se quatro casos clinicos, da nossa expe-riencia do IPO, de doentes com neoplasia do pulmao nao pequenas celulas, tratados em segunda e terceira linhas com erlotinib. Sao doentes seleccionados em que se salienta a boa resposta ao tratamento instituido e a presenca de efeitos secundarios predo-minantemente cutâneos. Rev Port Pneumol 2008; XIV (Supl 3): S65-S69

Tuberculose das Cordas Vocais

Platelet derived serotonin (5HT) contributes to blood pressure elevation and the development of thromboembolic complications. Among the pathophysiological mechanisms involved in these vascular events, derangements in 5HT kinetics and exaggerated platelet response to 5HT may be part of the major triggering factors. An age-dependent attenuation platelet 5HT kinetics was revealed in normotensive control subjects but not in patients with essential hypertension. In older hypertensive patients, particularly in men, platelet 5HT uptake was decreased. In parallel, platelet reactivity was increased with advancing age as shown by a greater 5HT induced platelet aggregation and higher plasma concentration of beta-thromboglobulin. Antihypertensive treatment with the 5HT2-receptor antagonist ketanserin attenuated platelet 5HT turnover and inhibited 5HT induced platelet aggregation; the latter was more pronounced in older patients. The clinical efficacy and tolerability of ketanserin 20-40 mg twice daily given as mono- or combination therapy was evaluated in 188 patients with mild to moderate essential hypertension for a period of 12 weeks. A greater fraction of patients greater than or equal to 60 years achieved diastolic target pressure of less than or equal to 95 mgHg. Complaints related to the central nervous system or the peripheral circulation were greatly reduced in patients older than 60 years. In older patients, over and above the antihypertensive effect, 5HT2-receptor blockade may play an important role in the prevention of thromboembolic complications by inhibition of 5HT induced platelet activation.