Intraoral and pulmonary tuberculosis following dental treatment.
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Biomedical subjects
Publications and source records attributed to D Davies.
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A 51-year-old female was thought to have Conn's syndrome because she had hypertension, hypokalaemia and low plasma renin activity. The cause was not aldosterone excess, but there was an adrenal cortical carcinoma producing 11-deoxycorticosterone (DOC) in extremely large quantities, with ineffective 11 beta-steroid hydroxylation. Plasma and urinary aldosterone levels were within the normal range. Blood levels of other steroids including those on the pathways of formation of glucocorticoids and sex steroids were unaffected. The tumor was cultured in vitro and shown by high performance liquid chromatography (HPLC) to produce predominantly DOC from tritiated pregnenolone, with no detectable aldosterone, in agreement with the in vivo results.
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Fifty pregnancies occurred in 37 women with hyperprolactinaemia. Thirty women (81%) initially attended with infertility and 24 (65%) had secondary amenorrhoea. Twelve women (31%) had pituitary macroadenomas, of whom seven (19%) were treated with neurosurgery and/or external radiotherapy before conception. Forty-one conceptions (82%) followed treatment with bromocriptine. There were no unusual obstetric or endocrinological complications. Serum prolactin measured at least 6 months post partum when under basal conditions, without bromocriptine and not breast feeding, showed no significant trends compared with initial values. Tumour growth was not stimulated by the high oestrogen levels of pregnancy.
Budesonide is a highly potent non-halogenated glucocorticoid intended for the local treatment of lung disease. Budesonide is designed to have a high ratio between local and systemic effects. The biotransformation of 3H-budesonide was studied in vitro and compared to the biotransformation of 3H-triamcinolone acetonide and 3H-beclomethasone dipropionate. Budesonide was degraded 3--6 times as rapidly as triamcinolone acetonide in human and rat liver, respectively. Beclomethasone dipropionate was immediately hydrolyzed to the monopropionate in human liver. The degradation of beclomethasone monopropionate is the step that represents the major loss in biological activity and this step was only about one fourth as fast as the degradation of budesonide. 6 beta-hydroxy budesonide and 16 alpha-hydroxy prednisolone are two of the main metabolites of budesonide in human liver. The formation of these metabolites are important inactivation steps. The pharmacokinetics of 3H-budesonide was studied in healthy male volunteers after inhalation, oral and intravenous administration. The plasma half-life was 2.8 +/- 1.1 h (mean +/- SD), distribution volume 301.3 +/ 41.7 1 and plasma clearance 83.7 +/- 27.5 1/h. The systemic availability was 10.7 +/- 4.3% after oral administration and 72.8 +/- 42.0% after inhalation, corrected for the amounts of substance deposited in the inhalation device and oral cavity.
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Ipratropium bromide was given to patients admitted to hospital with acute asthma. A cumulative-dose-response technique in six patients showed that 500 micrograms given by nebuliser produced a maximal increase in peak expiratory flow rate. This dose of ipratropium bromide was included in a regimen in which it was given either two hours before or two hours after nebulised salbutamol to 22 patients. Ipratropium bromide given on admission was as effective as nebulised salbutamol. The two drugs in sequence produced greater bronchodilatation than either used alone, and the mean peak expiratory flow rate rose by 96% in four hours. Thus giving ipratropium bromide in addition to salbutamol in severe asthma enhances the bronchodilator effect. Further studies are needed to determine whether the same effect may be obtained by giving two maximal doses of salbutamol two hours apart.
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