Does lats cause hyperthyroidism in Graves' disease?

McKenzie, J. M.

doi:10.1016/0026-0495(72)90012-1

Cited by 35 publications

(10 citation statements)

References 44 publications

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“…Several laboratories have now reported that serum and immunoglobulin fractions from patients with Graves' disease can inhibit the binding of labeled thyroid-stimulating hormone (TSH) to thyroid membranes (23,24,37,38). In addition, these same preparations stimulate the adenylate cyclase activity in thyroid tissue (23,24,(39)(40)(41) and, when administered in vivo, stimulate thyroid hormone secretion (42,43). As with the anti-insulin receptor antibodies described in this report, immunoglobulins from patients with Graves' disease show heterogeneity with respect to titer, differing specificity for TSH receptors of various species, and ability to stimulate adenylate cyclase once bound to the receptor (23,24,40).…”

Section: Discussionmentioning

confidence: 99%

Effects of Autoantibodies to the Insulin Receptor on Isolated Adipocytes

Kahn¹,

Baird²,

Flier³

et al. 1977

J. Clin. Invest.

243

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A B S T R A C T Autoantibodies to the insulin receptor have been detected in the sera of several patients with the Type B syndrome of insulin resistance and acanthosis nigricans. In this study we have used three of these sera (B-1, B-2, and B-3) as probes ofthe insulin receptor in isolated rat adipocytes. Preincubation of adipocytes with each of the three sera resulted in an inhibition of subsequent [1251]insulin binding. 50% inhibition of binding occurred with serum dilutions of 1:5 to 1:7,500. As in our previous studies with other tissues, Scatchard analysis of the insulin-binding data was curvilinear consistent with negative cooperativity. Computer analysis suggested that in each case the inhibition of binding was due to a decrease in receptor affinity rather than a change in available receptor number.In addition to the effects on insulin binding, adipocytes pretreated with antireceptor sera also showed alterations in biological responses. All three sera produced some stimulation of basal glucose oxidation. With serum B-3, maximal stimulation of glucose oxidation occurred at a serum concentration that inhibited binding by only 10-15%, whereas with serum B-2 the dilution curves for inhibition of binding and stimulation of glucose oxidation were superimposable. Serum B-1 behaved as a partial agonist; that is, it inhibited binding more effectively than it stimulated glucose oxidation. Cells pretreated with this serum in a concentration which inhibited binding by 80% also showed a five-fold shift to the right in the dose response of insulin-stimulated glucose oxidation, whereas sperminestimulated glucose oxidation was unaffected. Serum B-2, which contained the highest titer of antireceptor

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Section: Discussionmentioning

confidence: 99%

Effects of Autoantibodies to the Insulin Receptor on Isolated Adipocytes

Kahn¹,

Baird²,

Flier³

et al. 1977

J. Clin. Invest.

243

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show abstract

“…GroBes Interesse land zungchst der als pathogenetische Faktor (oder Indicator ?) angesehene LongActing-Thyroid-Stimulator (LATS), ein Gamma-Globulin (IgG)yon AntikSrpercharakter [38,60]. Dieser stimuliert die Schflddriise ghnlich dem TSH --allerdings mit zeitlicher VerzSgerung --und wird auf Grund seiner Placentaggngigkeit auch fiir die passagere Hyperthyreose Neugeborener hyperthyreoter Miitter verantwortlich gemacht.…”

Section: Diskussionunclassified

“…]:)as korrespondierende Antigen liegt in der Schilddriise, mSglicherweise in der Mikrosomenfraktion [60]. Allerdings ist LATS nicht in Seren aller Hyperthyreose-Kranker zu finden [38], soll jedoch besonders hgufig bei Patienten mit Hyperthyreose, die mit e.O. und prgtibialem Myxoedem vergesellschaftet ist, vorkommen (Ubersicht [60]).…”

Section: Diskussionunclassified

“…Die pathogenetische Beziehung zwischen LATS und e.O. wurde jedoch mehrfach bezweffelt [38,39,43]. Auch Horster [22] war es im Tierexperiment unmSglich, eine exophthalmogene Wirkung durch LATS-haltige Seren zu erzielen.…”

Section: Diskussionunclassified

“…[53] im Experiment eine Bindung des LATS an Retroorbitalgewebe. Die alleinige Rolle des LATS war schon deshalb zweifelhaft, da LATS bei schwerer Ophthalmopathie oft fehlte [38,39] 58], wie neuere mittels des ,,migration inhibition factor"-Tests (MIF) gewonnene Ergebnisse vermuten lassen [32]. Mit diesem Veffahren wird eine durch thymusabhgngige Lymphocyten vermittelte Immunreaktion nachgewiesen, wie sic in der Genese des Morbus Basedow und der Hashimoto-Thyreoiditis eine Rolle spielt [i2].…”

Section: Diskussionunclassified

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Zur Problematik der subtotalen Strumaresektion bei Hyperthyreose mit endokriner Ophthalmopathie

Schümann

Grabs

1975

Langenbecks Arch Chiv

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Observation of 39 patients who had undergone surgery for hyperthyroidism with or without endocrine ophthalmopathy between 1965 and 1972 indicate that this type of therapy involves no higher risk than do medication of radiological measures as far as the course of ophthalmic changes is concerned. Examination of the basal and the TRH-stimulated TSH concentrations i.s. argues against any primarily pituitary cause for progressive ophthalmopathy after surgery. In addition, it elucidates the almost inevitable postoperative development of preclinical hypothyroidism while the clinical condition is still euthyroid, and indicates the necessity of constant postoperative hormone substitution.

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Humoral and Genetic Factors in Thyrotoxic Graves Disease and Neonatal Thyrotoxicosis

Green¹

1976

JAMA

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Does lats cause hyperthyroidism in Graves' disease?

Cited by 35 publications

References 44 publications

Effects of Autoantibodies to the Insulin Receptor on Isolated Adipocytes

Effects of Autoantibodies to the Insulin Receptor on Isolated Adipocytes

Zur Problematik der subtotalen Strumaresektion bei Hyperthyreose mit endokriner Ophthalmopathie

Humoral and Genetic Factors in Thyrotoxic Graves Disease and Neonatal Thyrotoxicosis

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