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B Luttrell

Publications and source records attributed to B Luttrell.

5 recordsLinked to original sources

Computerized method for validating laboratory reference ranges for triiodothyronine and thyroxin immunoassays.

We used a computer-based method to help validate the reference ranges of assays for triiodothyronine (T3) and thyroxin (T4). A retrospective search of a database of laboratory results for the previous six months identified all patients with apparent euthyroid status, as defined by methods independent of the immunoassay under review. A computer-generated reference group (CGR Group) of 2001 records had a gaussian distribution of T4 values and a reference range (mean +/- 2 SD) of 56-161 nmol/L, compared with the supplier's suggested range for euthyroid subjects (58-148 nmol/L) and an in-house range of 60-144 nmol/L for a group of 97 normal subjects. A similar CGR Group of 1902 records gave a reference range for T3 of 0.7-2.1 nmol/L (manufacturer's range 0.8-2.8; normal subjects 0.8-2.2). An attempt to devise a reference range for thyrotropin failed when we found that its concentration in the population of patients with normal values for thyroid hormones was distributed differently from that in the normal population. The method is intended to be used in addition to conventionally derived ranges based on results for healthy subjects. It allows the laboratory to conveniently verify the reference ranges for T3 and T4 assays at regular intervals by using very large samples with appropriate age, sex, and weight distribution, drawn from the population of patients' samples submitted for analysis.

Computers

Susceptibility in vitro of Nocardia species to antimicrobial agents.

Fifty-four clinical isolates of Nocardia spp. were tested in vitro for susceptibility to several antimicrobial agents. Of these, 89% were susceptible to ciprofloxacin, 86% to imipenem, 85% to fusidic acid, and 71% to cefotaxime. Some of the agents may be suitable alternative or adjunctive drugs to sulfonamides and aminoglycosides for chemotherapy of Nocardial infections.

Anti-Bacterial Agents

Clinical experiences with human parathyroid hormone 1-34.

Human parathyroid hormone (PTH) 1-34 was given to nine normal subjects and to 10 patients with hypoparathyroidism. There were no side effects associated with the protocol employed. In normal subjects, five statistically significant changes occurred during the period of observation: plasma cyclic adenosine monophosphate (cAMP) rose by a factor of 3 (at 30 min), nephrogenous cyclic AMP rose approximately 40-fold (at 60 min), urinary phosphate rose by a factor of 2 (at 120 min), urine calcium levels fell by 50% between 60 and 120 min, and plasma prolactin rose by a factor of 1.4 (at 60 min). The cAMP responses were significantly blunted in five patients with chronic hypocalcemia, chronic hyperphosphatemia, and detectable serum immunoreactive PTH levels. On the basis of this test these patients were designated as suffering from pseudohypoparathyroidism. The acute phosphaturic and hypocalciuric responses were apparently intact in these five individuals. Human PTH 1-34 is likely to replace bovine material in the delineation of syndromes associated with PTH resistance.

Adult

Metabolism of cortisol-21 glucosiduronate in man.

The metabolism of cortisol-21-glucosiduronate has been studied in two subjects. Urinary excretion was about 65% in both subjects, with cortisol glucosiduronate as the principal metabolite accompanied by small amounts of 11 beta, 17,21-trihydroxypregnane-3,20-dione (THF) glucosiduronate. The absence of the other normal metabolites of cortisol [17,21-dihydroxypregnane-3,11-20-trione (THE), 3 alpha, 11 beta, 17, 20xi, 21-pentahydroxypregnane, and 3 alpha, 17, 20xi, 21-tetrahydroxypregnan-11-one] indicates that negligible hydrolysis at C-21 occurred and that an unoccupied C21 position is required for oxidation at C-11 and reduction at C-20. The limited conversion to THF suggests that a pathway through cortisol-21-glucosiduronate does not contribute significantly to the differences in specific activity of urinary THF and THE observed after administration of labeled cortisol.

Humans