Pneumocystis thyroiditis.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
D Perry-Keene
Publications and source records attributed to D Perry-Keene.
Screening for thyroid malignancy: the role of fine-needle biopsy.
Cytological examination of the aspirate of fine-needle biopsy is becoming more widely accepted as a screening test for malignancy in thyroid nodules. However, it tends to be used in addition to, rather than instead of, more traditional methods. In this five-year prospective evaluation we performed fine-needle biopsy in 618 euthyroid patients with nodular thyroid enlargement, 86% of whom also underwent radionuclide scans and 55% of whom underwent ultrasound scans. In 19% of patients fine-needle biopsy yielded insufficient material for diagnosis, and in 14% of patients normal follicular cells were found (which indicated that the clinical lesion was not sampled). To date, a histological diagnosis has been obtained in 258 (42%) patients, 44 of whom had malignancies. The results of the radionuclide and ultrasound scans did not alter the odds in favour of the detection of malignancy. The cytological diagnosis of malignancy was falsely-positive in two patients and falsely-negative in four patients (three cases of which probably were sampling errors). If, in addition to overtly-malignant cells, atypical Hürthle cells and follicular neoplasms were considered to be potentially malignant, fine-needle biopsy alone had a sensitivity of 87% and a specificity of 72%. This good accuracy would be reduced by sampling failures, but a policy of operating on all patients with potentially-malignant cells, or on those in whom satisfactory aspirates could not be obtained, would yield high rates of the diagnosis of malignancy and would reduce the number of operations. Our data indicate that the most-appropriate method of screening thyroid nodules for malignancy is fine-needle biopsy without pertechnetate scanning or ultrasound examinations.
Australia↗
Phaeochromocytoma in Queensland--1970-83.
A statewide survey was conducted in Queensland to record all cases of phaeochromocytoma between the years of 1970 and 1983 inclusive. There were 46 cases giving an incidence of 1.55/million population per year. Twenty-nine patients (63%) were successfully treated while 10 patients (22%) died of the tumour effects. Seven cases (15%) were found incidentally at autopsy, though at least one showed diagnostic clinical features before death. Five patients (11%) had extra adrenal phaeochromocytoma, five patients (11%) had multiple tumours, four patients (9%) had multiple endocrine neoplasia and three patients (7%) had clinically malignant tumours. Of 13 patients suffering a major adrenergic crisis only six survived. Five patients with unsuspected phaeochromocytoma suffered crisis under anaesthesia and only one survived. Only one of the patients dying of benign phaeochromocytoma had adequate ante mortem adrenergic blockade. Of all patients in the series 35% were not diagnosed in life.
Adolescent↗
Chronic diphenylhydantoin therapy does not reduce plasma 25-hydroxy-vitamin D.
A randomized controlled study was performed to investigate the effect of 2 years' monitored diphenylhydantoin (DPH) therapy on plasma 25-hydroxyvitamin D (25-OHD) in non-epileptic, non-institutionalized subjects. Mean +/- SEM plasma 25-OHD of 18 DPH-treated subjects at the end of 2 years' drug treatment was 59 +/- 8 nmol/l (23.6 +/- 3.2 ng/ml), which was not decreased compared to that of eighteen control subjects (54 +/- 8 nmol/l, 21.6 +/- 3.2 ng/ml). In addition, mean plasma 25-OHD had not changed 1 month after ceasing DPH. The treated group had a higher mean serum alkaline phosphatase (SAP) during DPH treatment, attributable to hepatic enzyme induction. It is concluded that therapeutic doses of DPH without other anticonvulsants do not have a clinically significant effect on plasma 25-OHD.
Adult↗
Thyroid hormone levels and protein binding in patients on long-term diphenylhydantoin treatment.
The effect of long-term diphenylhydantoin (DPH) treatment on thyroid hormone concentrations and protein binding was determined in a randomized controlled trial. As has been demonstrated previously, total thyroxine (T4) concentrations were significantly depressed in patients on DPH. There was no significant effect on indirect indices of protein binding of thyroid hormones, and the free thyroxine index (FTI) was also significantly depressed. Triiodothyronine (T3) and thyrotrophin (TSH) concentrations were either unaffected, or only very slightly affected by DPH. Significant effects on the FTI were still apparent 4 weeks after discontinuing treatment. It is concluded that the depression of total T4 levels observed in vivo is not due solely to diminished protein binding, but may instead be largely explained by reports suggesting enhanced degradation of T4 following DPH therapy.
Adult↗