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Biomedical subjects

A Querido

Publications and source records attributed to A Querido.

At least 19 recordsLinked to original sources
PubMed1993

[Theory and practice of medicine: levels of knowledge and clinical medicine as a cultural institution].

The author discusses the contents of his book "The inside of medicine" which appeared at the end of 1990 (it is written in dutch). The book aims to acquire a view how the metamorphosis of theory and practice of medicine as to size and diversity in the past fifty years came about. Also health care developed into a social right, and became a cultural institution. The book is not meant as a history of medicine of that period, but rather as a history of ideas illustrated with examples. The author feels qualified to do so, because he was actively involved with research during those years. Before World War II his activities were during ten years limited to laboratory research (biomedical) in the Netherlands, U.S.A. and finally at the Pasteur Institute in Paris. Residencies in internal medicine followed and qualification for this specialty. From 1948-1983 he held a chair at Leiden University in Internal medicine and concentrated his research on endocrinology and metabolic diseases (patient centered research). He was Founding Dean of the Rotterdam Medical Faculty for 5 years. Since the beginning of the 20th century it is accepted that illness in general is multifactorially determined. However research about illness is still dominated by the Newtonian unidirectional paradigm of cause to effect, which leads to mechanistic thinking. Obtained data are followed further by the same method, through different levels of knowledge from symptom to morphology and to pathophysiology, and finally to the molecular level. Undoubtedly much has been achieved. The integrated approach, reflecting reality, often characterized by the term of the bio-psycho-social view, was hardly used. It is frequently suspected that advances are disappointing in diseases like atherosclerosis, or the deviating course of disease and recovery in advanced age etc. because of that reason. Molecular biology is at a too early stage of development that reasoning upwards to the "lived human body" is possible. The author feels that there are signs of changing the approach and paradigm at present. Some examples will be discussed.

Culture↗
PubMed1984

Direct and quantitative measurement by immunoprecipitation assay of anti-thyrotrophin receptor antibodies in sera of patients with Graves' disease.

The presence of anti-TSH receptor antibodies in the sera of 32 patients with untreated Graves' disease, 21 patients with euthyroid autonomous multinodular goitre, nine patients with Hashimoto's disease and 22 normal controls, was investigated by means of a direct and quantitative immunoprecipitation assay (IPA). A comparison was made between the IPA anti-TSH receptor antibody titres, the thyrotrophin-binding inhibitor immunoglobulins (TBII) index determined by radio-receptor assay and the presence of circulating immune complexes (CIC); no correlation was found. Twenty-six (81%) of the 32 untreated patients with Graves' disease were IPA-positive; 16 (50%) had a positive TBII index. None of the patients with euthyroid autonomous multinodular goitre and none of the normal controls were IPA-positive and their TBII index was normal in all cases. Of the nine patients with Hashimoto's disease seven were IPA-positive and three had a positive TBII index. Of ten patients with Graves' disease still in remission none was IPA-positive and their TBII index was normal. Of 18 patients who relapsed after treatment, 13 were IPA-positive and only five had a positive TBII index. In seven patients with Graves' disease studied serially, anti-TSH receptor antibodies remained present in the sera of four, although the TBII indices normalized. For the five patients who relapsed, a rise in the anti-TSH receptor antibody titre at the time of the relapse was observed. It is concluded that not all anti-TSH receptor antibodies cause TSH-binding inhibition in the radio-receptor assay, and further evidence has been obtained that anti-TSH receptor antibodies are the cause of the hyperfunctioning of the thyroid gland in Graves' disease.

Adolescent↗
PubMed1982

Thyrotrophin binding inhibition by anti-thyrotrophin receptor antibodies in Graves' disease which is not reflected by 1.6 M ammonium sulphate precipitates.

In ten patients with Graves' disease before, during and after treatment and three patients in remission, we have compared the TSH-binding inhibition caused by serum, 1.6 M ammonium sulphate precipitates from serum and by the fractions (19S, 7S and 4S) obtained after G-200 gel chromatography of serum and ammonium sulphate precipitates. Five out of ten patients had a positive thyrotrophin-binding inhibitor immunoglobulin (TBII) index before treatment, three of whom relapsed. The binding inhibition caused by 7S fractions from ammonium sulphate precipitates of ten untreated patients could be correlated with their TBII index (r=0.9, P less than 0.001). By contrast, the 7S fractions prepared directly from the sera of the same ten patients all showed marked TSH-binding inhibition (P less than 0.001) when compared with normal plasma 7S, and no correlation with the TBII index could be demonstrated (r=0.21, P less than 0.05). It is concluded that ammonium sulphate precipitates, which are used to calculate the TBII index, do not reflex the presence of anti-TSH receptor antibodies in serum accurately in all patients.

Adult↗
PubMed1982

Propranolol improves the impaired TSH response to TRH in patients with autonomously functioning euthyroid multinodular goitre.

Ten patients with autonomously functioning euthyroid multinodular goitre received propranolol (Inderal Retard 160 mg daily) for 4 weeks in order to investigate whether normalization of the TRH test or an increased TSH response to TRH could be obtained by decreasing serum T3 levels. Serum T3 decreased significantly after 2 and 4 weeks of propranolol administration. Serum T4 increased during this period, although the change was only significant after 4 weeks of propranolol. T3 resin uptake did not change. The TSH response to TRH increased significantly during the administration of propranolol. Mean delta TSH basally was 1.0, range 0-3.9 mU/l, and mean delta TSH after 4 weeks of propranolol was 2.4, range 0-9.3 mU/l. A strong correlation was found between the increase in delta TSH and the decrease in serum T3 after 4 weeks of propranolol. After withdrawal, delta TSH and T3 returned to premedication levels. Our data suggest that T3 is an important factor in the impairment of the TSH response to TRH in our patients. Normalization of the TRH test was, however, not obtained. These findings support the concept of subclinical hyperthyroidism in 'euthyroid' multinodular goitre with autonomous function.

Adult↗
PubMed1980

Circulating immune complexes and thyroid-stimulating immunoglobulins before, during, and after antithyroid drug therapy in patients with Graves' disease.

Sera from patients with Graves' disease were assayed for thyroid-stimulating immunoglobulins (TSI) and circulating immune complexes (CIC) before, during, and after antithyroid drug treatment. 41 (72%) of 57 untreated patients had a positive TSI index and 17 (30%) had CIC. In untreated patients CIC were significantly more common in patients with a negative TSI index than in those with a positive one. It is suggested that because CIC prevent TSI from being detected the TSI index may be negative in Graves' disease. Early in the course of the treatment CIC developed in 85% of the patients; in all of these patients TSI disappeared. Later in the course of treatment when CIC could no longer be detected TSI did not reappear. These findings indicate that the development CIC could be the manifestation of the re-establishment of a natural tolerance to thyroid-stimulating hormone receptors in patients with Graves' disease.

Antibodies, Anti-Idiotypic↗
PubMed1980

Effects of iodine deficiency on mental and psychomotor abilities.

Severe iodine deficiency may lead to endemic cretinism, which is characterized by a number of abnormalities, such as mental retardation, neurological abnormalities and hearing disorders. These abnormalities may occur in various combinations, but impaired mental development is always a component. The present study was attempted to determine whether there is also evidence of mental retardation, perhaps to a lesser degree, in that part of the population that manifest no symptoms of cretinism, the non-cretins, in an iodine-deficient area. Results of an extensive test battery have been collected in two village populations: one village in an area with severe iodine deficiency and a control village in a non-iodine-deficient area. Both villages were situated in Central Java, Indonesia. In the selected villages the total population between the ages of 6 and 20 years participated in this study. No evidence of significant mental retardation has been detected in the non-cretin group in the severely iodine-deficient area. Significant differences between the two populations, however, have been found with regard to a number of perceptual and neuro-motor abilities.

Adolescent↗
PubMed1979

Exchange of triiodothyronine derived from thyroxine with circulating triiodothyronine as studied in the rat.

At present it is widely assumed that T3 derived from T4 is rapidly and totally exchangeable within the volume of distribution of T3 secreted by the thyroid into the bloodstream. This concept is implied when conclusions are drawn from comparisons between a biological effect in a responsive tissue and circulating T3 and T4 levels. Such conclusions are often in conflict with those derived by comparing the biological effect with the concentrations of T3 and T4 in the responsive tissue itself. Thus, it appeared important to test the above assumption directly. Thyroidectomized rats have been treated for 4-4 1/2 days with a mixture of 131I labelled T4 (131T4) and 125I labelled T3 (125T3), which was either injected twice daily or administered by continuous i.v. infusion. The rats were bled, perfused, and their plasma and tissues submitted to extraction and paper chromatography. If the tested assumption were correct, the ratio between the T3 derived from T4 and the T3 injected as such (namely, the 131T3/125T3 ratio) should be the same in plasma, liver, kidney, heart, muscle, etc. It was evident that the 131T3/125T3 ratio was not the same for different tissues. The differences were not merely due to artefactual deiodinations. The presence of small amounts of 131I and 125I containing compounds in the T3 spot was considered as highly unlikely, though not totally excluded. The data thus suggest that T3 derived from T4 and the injected (or thyroidally secreted) T3 might not be totally exchangeable within an observation period which is considerably longer than the one for which complete equilibrium was previously assumed. If so, changes in the size of the T4 pool, or in the rate of T4 conversion to T3, might affect the concentration of T3 in a given tissue to an extent not disclosed from the circulating T3 levels alone. Several possible consequences of the present findings are discussed.

Animals↗
PubMed1977

Hypothyroidism in an area of endemic goiter and cretinism in Central Java, Indonesia.

In an area of severe endemic goiter in Central Java, Indonesia, clinical overt or mild hypothyroidism appeared to be present in 7 out of 20 cretins and also in 12 out of 94 non-cretinous subjects, all 5-20 years of age, living in the village of Sengi. Hypothyroidism was not found in a control group of 70 subjects of the same age living in Londjong just outside the edemia. In hypothyroid subjects the plasma PBI-concentration was 0.98+/-0.32 mug/100 ml (mean+/-SD) vs. 2.72+/-1.24 mug/100 ml in euthyroid subjects from Sengi and 4.86+/-0.80 mug/100 ml in controls from Londjong. Values for T3 were 56.3+/-3.17 ng/100 ml in hypothyroids, 140.5+/-38.5 ng/100 ml in euthyroids from Sengi and 121.6+/-27.4 ng/100 ml in controls. The TSH levels (geometric mean and range) in these 3 groups were, respectively, 210.1 (108.0-342), 15.6 (3.0-372) and 4.1 (0.8-7.0) muU/ml. The differences between the mean concentration of PBI, T3 and TSH in the hypothyroid and euthyroid groups were highly significant (P less than 0.001). These data strengthen the clinical diagnosis of hypothyroidism in cretins as well as in non-cretinous subjects. All hypothyroid subjects had a PBI less than 1.8 mug/100 ml and T3 less than 120 ng/100 ml and TSH greater than 100 muU/ml. In 8 hypothyroid subjects, restudied 18 months after iodized oil injection, hypothyroidism was either corrected or markedly improved. It therefore appears that iodine deficiency per se in postnatal life may lead to (juvenile) hypothyroidism, which can be corrected by iodine therapy. Our findings have implications for the definition and diagnosis of endemic cretinism. Not all hypothyroid subjects in an area of endemic iodine deficiency should be classified as cretins.

Adolescent↗
PubMed1975

Studies on hearing loss in a community with endemic cretinism in Central Java, Indonesia.

An audiometric study was carried out in a community of 642 subjects severly affected by endemic goitre and cretinism. Hearing loss was measured in 34 out of 41 subjects diagnosed as cretins, 92 normal subjects aged 5-20 years from the same community and 54 subjects (also of 5-20 years) living in a nearby control area without endemic goitre. The excess number of hearing defects in the endemic area seems to be entirely due to the process that leads to cretinism. There is no reason to describe deafness and deafmutism in an area with severe endemic goitre as a separate entity. The hearing defect showed a definite greater loss in the higher frequencies than in the lower frequencies and was found in 92% of the cretins. Deafmutism was present in 5, a loss of more than 60 db in 8, a loss of 40-60 db in 10 cretins. A loss of 20-30 db was found in 2.2% of normal subjects in the endemic area and 1.8% of those living in the control area. It is concluded that audiometry is a simple and significant test to establish the presence of the neurological form of endemic cretinism, which is the most prevalent form in most endemias. The differential diagnosis and pathogenesis of the described hearing defect are discussed.

Adolescent↗