[Asymptomatic nodular thyroiditis].
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Biomedical subjects
Publications and source records attributed to S Charmion.
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BACKGROUND: The aim of the present study was to investigate the inflammatory reaction and its evolution in patients who underwent a prosthetic vascular procedure. Moreover the participation of this chronic process, during the follow-up, as a promoting or a consequence of vascular injury must be discussed. METHODS: Thirty-four patients were enrolled in the study. All patients had an aortic disease and underwent a prosthetic vascular procedure. Preoperative exclusion criteria were an emergency situation, diabetes, infection, chronic inflammatory disease, cancer and hemopathy. Postoperative exclusion criteria were the same together with abdominal complications and additional surgery during the follow-up. The inflammatory process was investigated with the measurement of blood acute phase proteins, haptoglobin, alpha1-glycoprotein acid, C-reactive protein and interleukin-6, before, immediately after surgery and several months after surgery. RESULTS: An increase in acute phase proteins was not observed to the same extent for all the studied patients. Before the surgical procedure, chronic inflammatory process was revealed by an increase in haptoglobin (52.9 p 100) and alpha1 glycoprotein acid (52.9 p 100) whereas increase in C-reactive protein (26.4 p 100) and interleukin-6 (92 p 100) are related to an acute process. Later after surgery, the chronic inflammatory process remained but differed from the observed process before surgery only by haptoglobin (61.7 p 100) and interleukin-6 (47 p 100). CONCLUSIONS: The presented results, observed during the follow-up of vascular surgery focused on persistent inflammatory process and the surgical procedure did not modify the time course of this process. The evolutionary disease could be considered as chronic and independent of the local effect.
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The term "chronic fatigue syndrome" (CFS) applies to a condition of unknown aetiology characterized clinically by an association of subjective symptoms, the most constant being an invalidating tiredness. The diagnostic criteria in current use do not permit to isolate an homogeneous subgroup among patients consulting for chronic asthenia. In the present state of research no infectious or immunological cause has been demonstrated conclusively, although a persistent enterovirus or herpesvirus type 6 infection or a state of chronic immune activation seem to play a role in some cases. Patients who fulfill the criteria of CFS present with psychiatric overmorbidity, essentially depressive, and in 50% of the cases with the mental disorders preceding CFS. The various theoretical models linking CFS to psychopathology are discussed, and finally the syndrome is regarded as a social construction reproducing or renovating the neurasthenia of the late 19th century. There is no specific treatment of CFS, but antidepressants, cognitive-behavioural therapy and perhaps certain immuno-modulators can be useful. The future lines of research should endeavour to isolate a subgroup of patients with prolonged asthenia after a recognized episode of infection and to identify the immunological, psychological and behavioral characteristics of this particular group as well as their reciprocal interactions.
The binding capacity of serum TeBG (testosterone-estradiol binding globulin), the plasma concentrations of thyroid hormones and the TSH response to TRF (200 micrograms i.v.) have been measured in female patients with a solitary autonomously functioning thyroid nodule (n = 26) or with a cold thyroid nodule (n = 20). It was found that TeBG was higher than the upper limit for normal (1.77 micrograms/dl) in the patients (n = 10) with increased serum concentrations of thyroid hormones and in 5 patients among 16 with normal thyroid hormone levels. After surgical removal of the nodule, the increased TeBG levels fell down within the normal, while the response of TSH to TRF which was suppressed before surgery, was recovered. In patients with a cold nodule, the administration of dl-Thyroxine (200-300 micrograms/daily) suppressed the response of TSH to TRF and increased slightly TeBG from 0.97 +/- 0.08 to 1.29 +/- 0.10 micrograms/dl (p less than 0.05) with a value higher than 1.77 micrograms/dl in 5. These data suggested that the pituitary secretion of TSH and the liver production of TeBG have a different threshold of sensitivity to thyroid hormones action. It is proposed that the measure of TeBG is a tool for the diagnosis of thyrotoxicosis in patients with autonomous thyroid nodules.
To ascertain the responsibility of renal artery thrombosis for the genesis of arterial hypertension, the methods available are not sufficiently sensitive and reproducible, and the residual revascularization maintained by a vicarious arterial network is not easy to demonstrate. Renal scintigraphy with technetium 99m-labelled mercaptoacetyltriglycine (MAG3) was performed in 4 old and severely hypertensive male patients with chronic thrombosis of one renal artery. With this tracer the thrombotic kidney was detected lately and weakly at the vascular and nephrographic stages. When the functions of both kidneys were compared, that of the affected kidney was always estimated at less than 5%. At the excretory stage a residual activity could be detected in the kidney with renal artery thrombosis. Owing to the specific biophysical behaviour of the tracer, MAG3 scintigraphy coupled with arteriography and assays of plasma renin activity in the veins contribute to the decision concerning nephrectomy.
Among the thrombotic events associated with a circulating anticoagulant of the antiprothrombinase type, myocardial infarction is exceptionally reported, which justifies the presentation of two cases. In both patients, myocardial necrosis occurred some time after the antiprothrombinase was discovered, and there was nothing special in its clinical features. No obvious atherosclerotic lesion and no image suggestive of vasculitis were found at coronary arteriography, which suggested that the antiprothrombinase played a predominant role in the genesis of infarction. Relationships between antiprothrombinase, arterial thrombosis (particularly of the coronary arteries) and the presence or absence of systemic lupus erythematosus (SLE) are discussed. As observed in thrombosis of other arteries, it is not certain that the presence of SLE constitutes an additional risk factor, except in cases with unquestionable vasculitis or if the treatment of SLE requires prolonged corticosteroid therapy. On the other hand, the appearance of an antibody directed against phospholipids is not necessarily related to the presence of SLE; in fact, this antibody itself might be a risk factor of myocardial infarction, as has recently been suggested.
Among the atypical forms of phaeochromocytoma the isolated inflammatory form is rare and difficult to diagnose clinically. The authors report such a case, where computerized tomography and magnetic resonance imaging contributed enormously to the diagnosis.