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Biomedical subjects

J Seth

Publications and source records attributed to J Seth.

90 records · Page 5Linked to original sources
PubMed1976

Simple solid-phase radioimmunoassays for total tri-iodothyronine and thyroxine in serum, and their clinical evaluation.

1. Simple solid-phase radioimmunoassay methods for total tri-iodothyronine and thyroxine in serum or plasma are described. By using antibodies that are covalently coupled to microcrystalline cellulose, virtually identical assay procedures can be used for the determination of both hormones. An alkaline sodium glycinate buffer provides better assay conditions than the buffers often recommended for thyroid hormone radioimmunoassay. 2. Assay results are unaffected by moderate sample haemolysis. Plasma samples stored at room temperature for more than nine days often show an apparent increase in concentration of both thyroid hormones. 3. Serum tri-iodothyronine and thyroxine concentrations in healthy euthyroid subjects, and in euthyroid pregnant women are reported. In a series of 100 consecutive patients referred to a thyroid clinic the tri-iodothyronine assay discriminated better than the thyroxine assay between hyperthyroid and euthyroid patients. The thyroxine assay was much better than the tri-iodothyronine assay in discriminating between hypothyroid and euthyroid patients.

Anilino Naphthalenesulfonates↗
PubMed1976

Hypothalamic/pituitary/adrenal function in patients treated with intermittent high-dose prednisolone and cytotoxic chemotherapy.

Hypothalamic/pituitary/adrenal (H.P.A.) function was assessed in ten patients receiving intermittent high-dose prednisolone and cytotoxic chemotherapy for myeloma of lymphoma in order to predict their possible requirement for additional steroid therapy between and at the end of treatment courses. Standard insulin hypoglycaemia tests performed 36 hours after the last dose of prednisolone often demonstrated impairment of corticotrophin (adrenocorticotrophic hormone, A.C.T.H.) and growth-hormone responses, indicating hypothalamic/pituitary suppression; plasma-corticosteroid responses to endogenous A.C.T.H. and tetracosactrin were abnormal in two patients, indicating secondary adrenal suppression. Such hypothalamic/pituitary and adrenal suppression may make these patients susceptible to acute adrenal insufficiency in times of stress. H.P.A. function should be fully assessed on completion of chemotherapy.

Adrenal Cortex Hormones↗
PubMed1976

Propranolol in the treatment of thyrotoxicosis by subtotal thyroidectomy.

Subtotal thyroidectomy was performed in 40 patients with thyrotoxicosis in whom propranolol alone was used as preparation for surgery. Propranolol was given orally in a dose of 40 mg every 6 h for a mean preoperative period of 17 days (range 4-60 days) and continued for seven days after operation. The mean +/- SE blood loss at operation was only 160 +/- 20 ml. The period of follow-up was from three to nine months. Recurrent thyrotoxicosis has not occurred in any patient. Low levels of total serum triiodothyronine (T3) and total serum thyroxine (T4) were observed in the early postoperative weeks in some patients and were associated with symptoms of mild hypothyroidism, but by six months in the presence of a raised serum thyrotropin (TSH) the thyroid hormone levels returned to normal. Permanent hypothyroidism developed in only two patients. Despite normal or low total serum T3 and T4 levels, the TSH response to thyrotropin-releasing hormone (TRH) was absent in all patients one week after operation. At four weeks and at eight weeks, the response was absent or sub-normal in 70% and 20% of the patients respectively, indicating a delay in the recovery of the hypothalamo-pituitary axis previously exposed to high levels of T3 and T4. It is considered that subtotal thyroidectomy for thyrotoxicosis in patients prepared with propranolol is an acceptable procedure which has some advantages over the conventional preparation with carbimazole and potassium iodide, not the least of which are the potential reduction in preparation time, the more flexible timing of operation, and the reduced operative blood loss.

Female↗
PubMed1975

Thyroid function in the long-term follow-up of patients treated with iodine-131 for thyrotoxicosis.

In February, 1972, 58% of patients euthyroid after iodine-131 therapy for thyrotoxicosis between 1954 and 1966 had a raised plasma thyroid-stimulating-hormone (T.S.H.) (greater than 7-4 mU/l) and 42% a normal T.S.H. level. A group of 69 of the euthyroid patients with a raised plasma T.S.H. (25-0 +/- 2-0 mU/l) in 1972 was re-examined annually for three years. There was no apparent change in the mean plasma T.S.H. level between 1972 and 1975 in the patients remaining euthyroid, but overt hypothyroidism developed in 3 patients in 1973, in a further 3 patients in 1974, and in 1 patient in 1975. In contrast, none of a group of 61 patients, euthyroid with a normal plasma T.S.H. (4-0 +/- 0-2 mU/l) in 1972, developed overt hypothyroidism over the next three years, although slightly raised T.S.H. levels were recorded in 3 patients in 1974 and in a further 6 patients in 1975. Both the mean serum T-4 and T-3 in the euthyroid patients with a raised plasma T.S.H. were significantly lower, but still in the respective normal ranges, than those in the euthyroid patients with a normal plasma T.S.H. No significant difference in the fasting serum-cholesterol or triglyceride levels could be demonstrated between the two groups. Since no patient with a normal plasma T.S.H. after iodine-131 treatment for thyrotoxicosis six to eighteen years earlier developed overt hypothyroidism over a three-year period, the follow-up of such patients need not be so frequent as that of similarly treated euthyroid patients with a raised plasma T.S.H. in whom overt hypothyroidism develops at the rate of 2-5% per year.

Cholesterol↗
PubMed1975

Solid-phase radioimmunoassay of thyroxine in untreated serum.

We describe a simple, convenient solid-phase radioimmunoassay of total thyroxine in unextracted serum. Serum samples are added directly to the assay incubation mixture, interference in the antigen/antibody reaction by the thyroxine-binding serum proteins being almost completely eliminated by the addition of 8-anilino 1-naphthalene sulfonic acid and incubation at pH 10.5. Residual interference is compensated for by including thyroxine-free serum in the standards. Use of thyroxine antibodies that are coupled to a solid support permits separation of free and antibody-bound hormone by a single washing step, followed by centrifugation. The method is specific, accurate, and reasonably precise. The results obtained compare well with those for radioimmunoassay of thyroxine in serum freed of protein by gel filtration, and with results of a competitive protein-binding method. The technical simplicity of the procedure should readily permit automation. These features suggest that the technique should be well suited for routine clinical laboratory use.

Anilino Naphthalenesulfonates↗
PubMed1974

Plasma TSH and serum T-4 levels in long-term follow-up of patients treated with 131-I for thyrotoxicosis.

In February 1972 58% of patients euthyroid after iodine-131 therapy given for thyrotoxicosis between 1954 and 1966 had a high plasma TSH (>7.4 muU/ml) and 42% a normal plasma TSH level. A group of 69 of the euthyroid patients with high plasma TSH levels (25.0+/-2.0 muU/ml) in 1972 were re-examined 15 and 24 months later. The mean plasma TSH in the 66 patients remaining euthyroid at 15 months was 22.6+/-1.8 muU/ml, while three patients had become hypothyroid. At 24 months 64 of the patients were still available for study, of whom 61 remained euthyroid with a mean plasma TSH of 21.6+/-2.0 muU/ml, and a further three had become hypothyroid.All of a group of 61 of the euthyroid patients with normal plasma TSH levels (4.0+/-0.2 muU/ml) in 1972 remained euthyroid at 24 months with a mean plasma TSH of 4.1+/-0.3 muU/ml, though the plasma TSH level had become slightly raised in three.The mean serum T-4 level in the euthyroid patients with a high plasma TSH was significantly lower, though still in the normal range, than that in the euthyroid patients with a normal plasma TSH both in 1972 and in 1974.Since no patient with a normal plasma TSH level after iodine-131 treatment six to 18 years earlier for thyrotoxicosis developed hypothyroidism over a two-year period, the follow-up of such patients need not be so rigorous as that of similarly treated euthyroid patients with raised plasma TSH levels in whom hypothyroidism developed at the rate of 5% per year.

Follow-Up Studies↗