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Biomedical subjects

J How

Publications and source records attributed to J How.

At least 37 records · Page 2Linked to original sources
PubMed1984

A search for the mechanism underlying the altered MCV in thyroid dysfunction: a study of serum and red cell membrane lipids.

The mean red cell volume (MCV) is increased in hypo- and decreased in hyperthyroidism but the underlying cause(s) is unknown. In view of the well recognised alterations in serum lipids in thyroid dysfunction, we have examined the possibility that a corresponding alteration in the amount or distribution of lipids in the red cell membrane may account for the red cell volume changes. Our findings however do not support this hypothesis.

Adult↗
PubMed1983

Evidence for cell-mediated immunity and specific suppressor T lymphocyte dysfunction in Graves' disease and diabetes mellitus.

Migration inhibition of purified peripheral T lymphocytes in response to pancreatic islet cell antigen or thyroid antigen was used to study cell-mediated immune mechanisms in patients with diabetes mellitus (IDDM) and Graves' disease (GD). In response to islet cell antigen, T lymphocytes of subjects with IDDM for less than 3 yr exhibited migration inhibition, whereas those of normal subjects, noninsulin dependent diabetics, and subjects with IDDM for longer than 3 yr did not. Admixture of T lymphocytes from normal subjects with T lymphocytes from patients with IDDM for less than 3 yr substantially ameliorated the migration inhibition of the IDDM subjects to islet cell antigen. Migration of T lymphocytes from GD subjects was markedly inhibited by thyroid antigen and marginally inhibited by islet cell antigen. Admixture of GD T lymphocytes significantly ameliorated the migration inhibition of IDDM T lymphocytes to islet cell antigen, despite sensitization to thyroid antigen of the GD T lymphocytes. We conclude: 1) sensitization to islet cell antigen in IDDM of recent onset is confirmed; 2) the ability of normal and GD T lymphocytes to ameliorate the migration inhibition of IDDM T lymphocytes strongly suggests correction of deficient suppressor T lymphocyte function; 3) the ability of GD T lymphocytes to ameliorate migration inhibition of IDDM T lymphocytes to islet cell antigen is evidence for an antigen-specific rather than a generalized suppressor T lymphocyte defect in GD; and 4) similarly, the normalization of migration index of GD T lymphocytes in response to thyroid antigen by those IDDM T lymphocytes not sensitized to thyroid antigen is again evidence for an antigen-specific and not a generalized suppressor T lymphocyte defect in IDDM.

Antigens↗
PubMed1982

Successful pregnancy after cyproheptadine treatment for Cushing's disease.

A patient with active Cushing's disease who became pregnant following treatment with cyproheptadine is described. Despite stopping the cyproheptadine treatment at 3 mth gestation, the previous amelioration of the clinical and biochemical features of the adrenal hyperfunction was maintained and the pregnancy progressed satisfactorily. Moreover, serial evaluation of maternal glucose tolerance proved to be normal and it is suggested that this matabolic aspect is an important determinant in the outcome of pregnancies occurring in patients with Cushing's syndrome.

Adult↗
PubMed1981

Suppressor T lymphocyte dysfunction in Graves' disease: role of the H-2 histamine receptor-bearing suppressor T lymphocytes.

The allo-suppressor effect of normal T lymphocytes on the production of migration inhibition factor by sensitized T lymphocytes of Graves' disease in response to human thyroid antigen has been studied further by a modified migration inhibition factor test employing purified T lymphocyte preparations. The production of migration inhibition factor was consistently abolished when normal T lymphocytes were mixed with the Graves' disease lymphocytes in various ratios (1:9, 2:8, and 5:5). However, pretreatment of the normal T lymphocytes with cimetidine (an H-2 histamine receptor antagonist) led to a demonstrable loss in their allo-suppressor properties, whereas pretreatment with chlorpheniramine (an H-1 histamine receptor antagonist) had no such effect. These studies indicate that a subset of normal T lymphocytes bearing H-2 histamine receptors suppresses the production or release of migration inhibition factor by sensitized T lymphocytes, and further suggest the possibility that there may be an abnormality in the H-2 receptors on Graves' disease suppressor T lymphocytes. It is conceivable that this defect is fundamental in the pathogenesis of Graves' disease.

Adult↗
PubMed1980

Masked giant-cell arteritis.

Five bipsy-proven cases of giant-cell arteritis illustrate some of the lesser known, but not uncommon, masquerades of this disease. The delay in reaching the diagnosis, which is common with these presentations, was a major factor in the emergence of serious sequelae including arotic regurgitation, stroke, and death. To increase awareness of the variety of clinical presentation of giant-cell arteritis, a classification of these variants into cachectic, febrile, and other forms is suggested.

Aged↗
PubMed1980

The effect of atenolol on serum thyroid hormones in hyperthyroid patients.

The effect of the beta-1-adrenoceptor blocking agent, atenolol, on serum levels of thyroxine (T4), triiodothyronine (T3) and reverse triiodothyronine (rT3) was studied in twelve hyperthyroid patients. While all patients improved symptomatically after treatment with atenolol 100 mg twice daily for 2 weeks, there were no significant changes in the serum T3 or rT3 concentrations. The serum T4 level showed a small but statistically significant fall. These data do not support the hypothesis that the beneficial clinical effects of beta-adrenoceptor blocking drugs in thyrotoxicosis are mediated by an action on the peripheral metabolism of thyroid hormones.

Adult↗