[Clinical case of the month. MELAS syndrome]. / Le cas clinique du mois. Le syndrome MELAS.

A patient, born in 1961, was first examined for autoimmune hyperthyroïd at the age of 25. Then, several episodes of serious dehydration and alteration of general condition were followed by a severe encephalopathy with a symptomatology of stroke-like episodes, and during a hospitalization, a volvulus of the colon. Epilepsy developed also. A MELAS syndrome was diagnosed when she was 32 years old, based on her clinical metabolic history of the presence of Ragged-Red-Fibers at muscular biopsy and of the genetical analysis. At the age of 37, after a new episode of encephalopathy, the patient fell into a rapidly evolving coma and deces.

A novel messenger ribonucleic acid homologous to human MAGE-D is strongly expressed in rat Sertoli cells and weakly in Leydig cells and is regulated by follitropin, lutropin, and prolactin.

We have cloned a novel complementary DNA whose expression was decreased in rat Sertoli cell cultures after treatment with FSH. This complementary DNA encodes a protein of 570 amino acids and shares 92% homology with the human MAGE-D protein. In contrast to other MAGE genes (A, B, or C), we have shown that MAGE-D expression was ubiquitous in healthy rat tissues. In the seminiferous tubules, the MAGE-D was expressed in Sertoli cells but not in germ cells as demonstrated by RT-PCR and in situ hybridization, whereas for the other MAGE genes, expression has been shown to be restricted to germ cells. Interestingly, MAGE-D was also detected for the first time in the female gonad by Northern blotting. In MLTC-1 cells (mouse Leydig tumor cell line-1), LH and PRL stimulated MAGE-D expression. Using hypophysectomized rats, it was confirmed that FSH decreased MAGE-D expression, whereas LH and PRL increased MAGE-D messenger RNA level in the whole testis most probably through a direct action on Leydig cells. As MAGE-D is present in both the seminiferous compartment and interstitium and hormonally regulated in each, it is possible that it has specific functions in each compartment during the development and the maintenance of the testis.

[Cushing syndromes due to aberrant expression of functional receptors other than ACTH. A new organic hypercorticism syndrome entity]. / Syndromes de Cushing dus à l'expression aberrante de récepteurs fonctionnels à des entités autres que l'ACTH. Une nouvelle entité d'hypercorticisme organique.

The diagnosis of Cushing's syndrome remains a challenge in clinical endocrinology. Cushing's syndromes are usually classified as dependent or independent from ACTH. In the first class are Cushing's disease, the ectopic corticotropin syndrome and the rare ectopic CRH syndrome. These ACTH-dependent Cushing's syndromes usually present diffusely hyperplastic adrenal glands. In the second class, are cortisol producing unilateral adrenocortical adenomas or carcinomas. New entities have recently emerged as bilateral adrenal hyperplasia not dependent from ACTH; their etiopathogenies are heterogeneous with illicit expressions at the adrenal level of functional receptors to various ligands: GIP, catecholamines, lutropin... The knowledge of such entities has to be taken into consideration in the diagnostic and management of ACTH independent Cushing syndromes.

[Radioiodine (131I) as the only treatment of hyperthyroidism. Results of 10 years of experience]. / Radioiode (131I) comme seul traitement de l'hyperthyroïdie. Résultats d'une expérience de 10 années.

This work present the results of the use of 131I, as first line and only, antithyroid treatment, applied to 120 patients suffering from autoimmune hyperthyroidism, compared to 64 patients with toxic goiter and adenoma. The diagnostic weight of the determination of the various antithyroid antibodies was assessed in the identification of autoimmune hyperthyroidism, for which TRAb and TPO Ab are the most significant. The evolution after treatment of a preexisting ophthalmopathy (i.e. Graves'disease) was never found to be alarming and in most cases regularly improved with time. A single case (out of 72) of autoimmune hyperthyroidism with no preexisting sign developed a severe ophthalmopathy after treatment, which was well controlled thereafter. Mean cumulated 131I doses to control hyperthyroidism were 22.8 mCi for toxic goiter, 21.6 mCi for adenoma, 14.1 mCi for autoimmune hyperthyroidism and 16.7 mCi for Graves'disease. Post 131I hypothyroidism was found in 28.2% of toxic goiters, 12.1% of adenomas, 66% of autoimmune hyperthyroidisms and 70% of Graves'disease. No relapse was observed after treatment. A surgical indication was proposed for cases requiring more than two 131I doses to control hyperthyroidism.

A novel gene overexpressed in the prostate of castrated rats: hormonal regulation, relationship to apoptosis and to acquired prostatic cell androgen independence.

We have identified a novel complementary DNA (cDNA) corresponding to a gene overexpressed in the rat ventral prostate after castration. This cDNA displays 89.4% identity with 453 bp of a mouse EST and 81.5% identity with 157 bp of a human EST and was named PARM-1 for prostatic androgen-repressed message-1. The complete cDNA is 1187 bp long and codes for a protein of 298 amino acids that contains four potential glycosylation sites and three half cystinyl residues. The PARM-1 gene was found to be expressed at quite low levels in most rat tissues including those of the urogenital tract. The kinetic of induction of PARM-1 gene in the prostate was highly correlated to the development of apoptosis in the whole organ. Supplementation of castrated animals with androgens reversed both the process of apoptosis and the overexpression of PARM-1 gene. Supplementation with estrogens did not result in an increase in the PARM-1 messenger RNA levels when compared with the castration alone. However, the treatment resulted in a more rapid return to intact levels in the castrated plus estrogen group. When apoptosis of testis and prostate was induced in vivo by hypophysectomy, it was found that PARM-1 was only overexpressed in the prostate. Therefore, PARM-1 seems to be regulated by androgens only in the prostate. Using in situ hybridization and immunohistological techniques, we have shown that PARM-1 gene product is found exclusively in the epithelial cells of involuting prostate. Analysis by flow cytometry of MAT LyLu epithelial cells transiently expressing PARM-1 protein did not allow us to demonstrate a direct effect of PARM-1 gene overexpression on the programmed death of the transfected cells. Treatment of MAT LyLu cells by transforming growth factor-beta induced apoptosis but had no effect on PARM-1 production. However PARM-1 protein has been detected by Western blotting in various cell lines such as MAT LyLu, MAT Lu, and PIF, which are androgen independent. This would suggest that PARM-1 gene product would be a marker for acquired androgen-independence of these tumor cells.

Lymphoid cell apoptosis induced by trophoblastic cells: a model of active foeto-placental tolerance.

To test the hypothesis that CD95-L (Fas-L) present on trophoblastic cells plays a part in establishing foeto-placental tolerance by inducing apoptosis of immune defence cells, we cocultured trophoblasts with lymphoid cells and scored the frequency of cell death in these cultures. We prepared human trophoblastic cells from term placentas removed by C-section and placed them in culture for 48 h before introducing the lymphoid cells. We added Jurkat cells, a CD3 + lymphoid cell line, or purified T cells from human blood to the cultured trophoblasts and monitored apoptosis by electron microscopy and flow cytometry after TUNEL or annexin V labelling. The frequency of cell death in the CD3 + cell population was higher when the lymphoid cells were cocultured with trophoblastic cells than when they were cultured alone. This frequency increased with time but was reduced when anti-CD95-L antibodies were added to the culture medium. Cell death was less frequent in the lymphoid cell population when trophoblasts were replaced with human fibroblasts not expressing CD95-L.

Effects of pituitary hormones on the prostate.

BACKGROUND: Although essential, androgens alone are not sufficient to induce normal growth and functionality of the prostate. Nonandrogenic hormones must also be involved in the proliferation of the prostate cancer cells which do not respond to antiandrogenic therapy and which thus become androgen-independent. Prolactin, but also growth hormone and luteinizing hormone, are potentially able to act on both normal and abnormal prostatic cells. METHODS: In this review we summarize data from the literature concerning the physiological and pathological implications of prolactin, growth hormone, and luteinizing hormone on the prostate. RESULTS: In rodent prostates, prolactin and growth hormone can induce a variety of effects independently of androgens (e.g., transactivation of certain genes, or synthesis of the major secretion products). Moreover, hyperprolactinemia is responsible for inflammation and dysplasia of the gland, while growth hormone promotes the development of prostate tumors in vivo in the mouse and rat. Growth hormone acts on the gland directly, through prostatic growth hormone receptors, and/or indirectly via the stimulation of insulin-like growth factor-I (IGF-I) synthesis in the liver. Luteinizing hormone receptor is expressed in rat and human prostates. Luteinizing hormone increases the amount of various transcripts in the rat prostate through an androgen-independent pathway. CONCLUSIONS: Prolactin, growth hormone, and luteinizing hormone, alone or synergistically with androgens, play physiologically significant roles in the normal prostate. The involvement of these hormones in the development of benign prostatic hyperplasia and prostatic carcinoma is an issue that needs to be addressed.

Expression of growth hormone receptors by lymphocyte subpopulations in the human tonsil.

The ability of human tonsillar lymphoid cells to express growth hormone receptor (hGH-N-R) was analyzed by flow cytometry. FITC-coupled recombinant human growth hormone (hGH-N) was used to reveal the receptors, in combination with phenotype markers. Unlike T cells, tonsillar B cells constitutively express the hGH-N receptor. Quiescent cells separated from activated cells by Percoll-gradient centrifugation bear fewer receptors than activated ones. Activated T cells express hGH-N-R, but the typical germinal centre CD4+ CD57+ T cells do not. These latter thus appear not to be fully activated. Inside the lymph follicles, the germinal centre CD38+ B-cell population and the mantle-zone CD39+ B-cell population display similar levels of hGH-N-R expression, but receptor density is lower on dividing dark-zone CD38+ CD10+ B cells. Different lymphoid-cell populations thus differ markedly in their ability to express the growth hormone receptor, in relation notably to their activation status. This highlights the link between the neuroendocrine system and the active immune defense.

Placental hormones during induced hypoglycaemia in pregnant women with insulin-dependent diabetes mellitus: evidence of an active role for placenta in hormonal counter-regulation.

OBJECTIVE: To study the effect of induced hypoglycaemia on serum levels of the placental hormones oestriol, human placental lactogen, placental growth hormone and progesterone in the third trimester of pregnancy. DESIGN: A prospective experimental investigation. SETTING: High risk pregnancy unit and diabetes research unit at Karolinska Institutet Danderyd Hospital, a university hospital. PARTICIPANTS: Ten women with insulin-dependent diabetes mellitus in the third trimester of pregnancy. METHODS: Venous blood samples were collected every 15 minutes for analyses of oestriol, progesterone, human placental lactogen and placental growth hormone, during the 150 min of a hyperinsulinaemic hypoglycaemic clamp, which maintained arterial blood-glucose level of about 2.2 mmol/l. MAIN OUTCOME MEASURES: Levels of analysed placental hormones during hypoglycaemia. RESULTS: A statistically significant increase was observed in placental growth hormone during hypoglycaemia (P < 0.0001), whereas the placental hormones progesterone, human placental lactogen and oestriol did not show changes of clinical significance. CONCLUSIONS: The increase in placental growth hormone indicates that the placenta is an endocrine organ which may take an active part in acute metabolic processes, such as here in the hormonal counterregulation of hypoglycaemia.

Demonstration of the expression of CD95 ligand transcript and protein in human placenta.

Tolerance of the fetal allograft enables the human conceptus to implant itself into the maternal uterus and survive and grow there. This tolerance phenomenon remains largely obscure, notably because it appears to be controlled by multiple mechanisms. CD95 ligand (CD95-L), which can trigger death of CD95-positive cells by apoptosis, may participate in inducing anti-fetus-sensitized CD95-positive T lymphocytes to enter apoptosis. Using immunohistochemistry (first trimester and term placentae), FACS assays (term placenta) and RT-PCR assays (term placenta), the presence of CD95-L protein and mRNA has been shown in crude placental tissue preparations and isolated placental cells. Among the latter, CD95-L expression was detected in trophoblastic cells, fetal blood cells (mRNA only) and also the Hofbauer macrophages. No CD95-L was detected in fibroblasts or fetal endothelial cells. Thus trophoblastic cells, Hofbauer macrophages, and perhaps also fetal blood cells could form a sequential barrier blocking maternal activated defence cells bearing CD95 molecules.

Surgical management of amiodarone-associated thyrotoxicosis: too risky or too effective?

Amiodarone-associated thyrotoxicosis, often clinically mild and resolutive after amiodarone discontinuation or under medical therapy, is sometimes drug unresponsive and not uncommonly follows a dramatic, even fatal course. Therefore, we considered a surgical solution in 15 severely amiodarone-associated thyrotoxic patients. Twelve men and three women (mean age 68 years, range 50-84 years) underwent radical thyroidectomy for clinical and biologically proved amiodarone-associated thyrotoxicosis. In six surgery was the first-line therapeutic option. In the other nine thyroidectomy seemed unavoidable considering the unresponsiveness to medical therapy and rapid deterioration of the patients' clinical condition, with life-threatening cardiac failure in three. In every patient surgery was conducted without immediate or delayed complications. Total thyroidectomy proved uniformly, definitively, and rapidly effective in controlling thyrotoxicosis in all patients, with a spectacular reversal of cardiac failure in the three most critical cases. Surgery was beneficial to our 15 patients and undoubtedly life-saving in the three most worrying cases. These results suggest that thyroidectomy should be more liberally regarded as an interesting alternative to conventional, but unpredictably effective, medical therapies.

Serum level of placental growth hormone is raised in pregnancy rhinitis.

OBJECTIVE: To describe any relationship between pregnancy rhinitis and weight gain or serum levels of estradiol, progesterone, placental growth hormone, or insulinlike growth factor I. PATIENTS: Twenty-seven nonsmoking healthy pregnant women aged 22 to 38 years (mean age, 28 years) who had no history of respiratory allergy or chronic nasal or sinus problems volunteered to enter the study. They had no nasal complaints at entry. METHODS: Nasal patency was registered daily from early pregnancy until 1 month after delivery. Nasal and oral peak expiratory flow rates were established, and the subjective blockage was scored from 0 to 4, with 0 indicating no blockage. Serum samples were collected and weight was measured on 4 occasions during pregnancy and again at the end of the study. Pregnancy rhinitis was diagnosed if the subjective nasal obstruction score was 1 or higher every morning for at least 6 weeks immediately preceding delivery, then returned to 0 within 2 weeks and remained at 0 until the end of the study. If on any day other signs of respiratory tract infection occurred, that day was excluded. RESULTS: Pregnancy rhinitis was diagnosed in 5 women. These 5 women showed significantly higher levels of placental growth hormone than the women without the diagnosis. No significant difference was found between the 2 groups regarding body weight or any of the other serum levels studied. CONCLUSIONS: Serum level of placental growth hormone is raised in pregnancy rhinitis and may be involved in its pathogeny. Pregnancy rhinitis does not significantly raise weight gain or serum levels of estradiol, progesterone, or insulinlike growth factor I.

Expression of somatostatin receptor SST4 in human placenta and absence of octreotide effect on human placental growth hormone concentration during pregnancy.

In pregnancy, the human placenta GH acts as a growth-promoting hormone and appears to be the main stimulator of insulin-like growth factor I (IGF-I) secretion. In a woman with a TSH-secreting macroadenoma, successful treatment with the somatostatin analog octreotide was conducted during the first month and the second half of pregnancy without side-effects on placental and fetal development. As observed in normal pregnancy, both serum placental GH and IGF-I levels increased throughout pregnancy and dropped sharply after delivery. In placental membranes from both treated and healthy untreated patients, we demonstrated the presence of high affinity binding sites for somatostatin-14 (Kd, 4.6 and 5.3 nmol/L; binding capacity, 1.53 and 1.35 pmol/mg protein, respectively). These receptors displayed low affinity for octreotide (IC50, 1.2-2 mumol/L), suggesting the presence of SST1 and/or SST4 receptors. We found that messenger ribonucleic acids of these two subtypes were expressed in both human placental tissue and purified human cytotrophoblast cells. Finally, the SST1-selective analog, des-AA1,2,5[D-Trp8,IAmp9]S-14 had low affinity for placental somatostatin receptors. These results argue in favor of the presence of the SST4 subtype in human placenta. At the doses administered, octreotide did not bind to placental somatostatin receptors. Our results may explain the absence of changes in both human placental GH and IGF-I concentrations that we observed during octreotide treatment.

Pituitary control of proliferation and differentiation of Leydig cells and their putative precursors in immature hypophysectomized rat testis.

The objective of this study was to determine the effects of pituitary hormones (luteinizing hormone [LH], follicle-stimulating hormone [FSH], growth hormone [GH], and prolactin [PRL]) on interstitial cell proliferation and differentiation in the testis of immature hypophysectomized rats. Macrophages, Leydig cells, precursor mesenchymal cells, endothelial lymphatic cells, and myoid cells were studied. Our experimental approach was aimed at determining whether changes in a cellular subpopulation observed after pituitary hormone treatments were the result of division of existing cells in the population, of differentiation of interstitial precursor cells, or both. In this context, it must be stressed that our data reflected the effects of hormones to prevent the decline of cells due to hypophysectomy rather than their recovery. Macrophage proliferation was taken into account because macrophages closely resemble Leydig cells and are known to proliferate after hormonal treatment. A double-labeling procedure (acid phosphatase and anti-bromodeoxyuridine [anti-BUdR]) revealed that LH, FSH, and PRL increased the number of testicular macrophages 105-, 104-, and 103-fold, respectively, in hypophysectomized rats compared to hypophysectomized control animals. BUdR incorporation in testicular macrophages was greater after PRL treatment than after LH and FSH supplementation. In contrast, we were unable to demonstrate any effect of rat GH on the macrophage population. Light microscopic analysis of plastic embedded sections of treated rat testis revealed that LH increased the numbers of Leydig, precursor mesenchymal, and myoid cells 6-, 4-, and 1.3-fold, respectively. LH also stimulated BUdR incorporation into all interstitial cell types. PRL administration increased both the number of Leydig and precursor mesenchymal cells (each 3-fold) but decreased the number of endothelial lymphatic cells (1.5-fold) when compared to the control animals. In contrast, FSH did not increase the number and proliferation of Leydig cells but exerted a slight proliferative effect on the other interstitial cell populations. In GH-treated rats, the number of precursor mesenchymal cells increased two fold above the control rats. GH also exerted slight proliferative effects on both precursor mesenchymal and myoid cells. Immunohistochemical studies of steroidogenic enzymes in the testicular interstitium of treated rats demonstrated the presence of steroidogenic enzymes, not only in Leydig and precursor mesenchymal cells, but also in some (1%-2%) endothelial lymphatic cells and myoid cells. This may indicate that both of these cell types are also constitutively equipped to perform steroidogenesis or that they are precursor cells undergoing differentiation. Taken together, changes in the number of Leydig cells in our animal model appeared more likely to be dependent on the transformation of precursor cells than on division of preexisting mature Leydig cells.

Growth hormone directly affects the function of the different lobes of the rat prostate.

In this study, we investigated the involvement of GH in rat prostate function. First, we demonstrated that specific transcripts corresponding to the GH receptor (4.5 kilobases) and to the GH-binding protein (1.2 kilobases) were expressed in the normal rat prostate, but also in all prostatic carcinoma cell lines tested (LNCaP, PC-3, MAT-Lu, MAT-LyLu, and Pif-1). Moreover, these transcripts were much more abundant in the human and rat carcinoma cells than in the normal tissue. One-year-old dwarf rats were supplemented for 7 days with saline (group DR1) or highly purified rat GH (group DR2). Northern blotting and quantitation of prostatic messenger RNAs (mRNAs) revealed that GH increases the steady state levels of transcripts coding for androgen receptor (2.4-fold), type I and II 5 alpha-reductases (2.6- and 2.2-fold), and several androgen-dependent proteins [prostatein C3 subunit (3.6-fold), probasin (11.0-fold), and R. W. B. (Royal Winnipeg Ballet) (12.5-fold)]. This suggests that GH might either potentiate the action of androgens on the prostate or act directly on this gland by a mechanism that does not depend on testicular androgens. To address this question, we supplemented hypophysectomized and castrated adult rats for 7 days with saline (group HC1), rat GH (group HC2), testosterone propionate (group HC3), or GH plus testosterone (group HC4), starting 3 days after castration. In this animal model, the abundance of C3 mRNA increased in all hormone-treated rats; the stimulation factors were 3.5 (group HC2), 25.5 (group HC3), and 9.5 (group HC4) compared to group HC1. Analysis of prostatein synthesis by Western blotting confirmed these results at the protein level. The same trend was observed for probasin and RWB mRNA levels. Probasin mRNA increased 4.5-fold in group HC2 and 12-fold in group HC3, but did not increase in group HC4 (both hormones combined); enhancement of RWB mRNA was, respectively, 5.0-, 28.0-, and 15.0-fold in groups HC2, HC3, and HC4. GH did not affect the abundance of androgen receptor mRNA. As described previously, the level of this mRNA dropped significantly in group HC3. GH alone did not significantly alter the level of either 5 alpha-reductase mRNA, whereas testosterone, alone or with GH, produced a 2-fold increase in type II 5 alpha-reductase mRNA (groups HC3 and HC4). Type I isoenzyme mRNA reached 1.6 times the control level (group HC1) in groups HC3 and HC4.(ABSTRACT TRUNCATED AT 400 WORDS)

Glucose inhibits human placental GH secretion, in vitro.

Human placenta specifically expresses the GH-V gene leading to the production of placental Growth Hormone (PGH). During pregnancy, PGH levels increase progressively in maternal blood, but its regulation remains unknown. In this study the effect of glucose on PGH secretion by human term placenta was tested, in vitro, by means of two different experimental models: organ culture of villous tissue and primary culture of isolated cytotrophoblasts. PGH was assayed in the culture medium by an immunoradiometric assay using a specific PGH monoclonal antibody. The presence of glucose (25 mmol/L) in the culture medium significantly inhibited (p < 0.001) the secretion of PGH by either placental villous explants or by cultured trophoblast cells. This inhibitory effect of glucose on PGH secretion was dose-dependent. More than 50% inhibition being observed with 5.5 mmol/L. In the same conditions, the daily production of hPL and hCG, were unmodified. Furthermore, the glucose-induced inhibition of PGH secretion was more effective when cultured trophoblast cells are differentiated into syncytiotrophoblast. This study demonstrates, for the first time, that among the gestational polypeptide hormones secreted by the human placenta, only PGH secretion is modulated by glucose, suggesting a key metabolic role for this hormone during pregnancy.

Expression and functionality of luteinizing hormone/chorionic gonadotropin receptor in the rat prostate.

In addition to androgens that are essential for maintenance of prostate growth and function, nonandrogenic hormones must also be considered to explain some regulatory events occurring in the prostate. The detection of LH/CG receptor (LH/CG-R) gene expression in some nongonadal tissues, has led us to consider LH as a potential regulatory factor of prostatic development and function. In this study, we have demonstrated by RT-nested polymerase chain reaction and Northern blotting that the rat prostate contains the same LH/CG-R transcript as the gonads. Western immunoblotting, ligand blotting, and binding analysis have shown that rat prostate also contains a 93-kDa receptor protein that is able to bind [125I]hCG specifically and with a high affinity (6.0 x 10(9) M-1). Our results also indicated that the concentration of binding sites was lower in the prostate than in the gonads. LH/CG-R sites of expression have been localized in the prostate by immunohistochemistry: specific staining was observed in all the epithelial cells of the gland, but the ventral lobes are much more immunoreactive than the lateral and dorsal lobes. Finally, the ability of this prostatic LH/CG-R to induce a physiological response was evaluated in an explant culture system. A time course experiment was carried out, and we observed a significant dose-dependent stimulation of cAMP production after 3 h of treatment: 3.0 +/- 0.4, 4.2 +/- 0.4, and 5.0 +/- 0.5 pmol/ml of cAMP for 0, 100, and 500 ng/ml of LH, respectively. In conclusion, LH is able to act directly on the prostatic gland through specific receptors that are structurally and functionally very similar to those expressed in the gonads and are mainly localized in the ventral lobe of the organ. These data suggest that LH plays a significant physiological role in the prostate.

The treatment of amiodarone-induced hyperthyroidism. Is there a place for surgery?

In many instances amiodarone-induced hyperthyroidism has been reported as mild, thyroid functions returning to normal after discontinuation of the drug. Nevertheless, life-threatening amiodarone-induced thyrotoxicosis has also been described. Conventional treatments such as with antithyroid drugs (Thionamide) and corticosteroids are essentially ineffective or fail to stop the dramatic course of the thyroid crisis. This limited efficacy of medical therapy, particularly in patients with previously--neglected or unknown--thyroid disease, prompted us to intervene surgically. We report a series of six patients who underwent total or nearly total thyroidectomy as first line therapy for four of them. Surgery resulted in rapid resolution of thyrotoxicosis with an uneventful postoperative course. This approach has the advantage of immediate and safe efficacy, low risk of relapse and finally, appears to be the only antithyroid treatment that permits continued therapy with amiodarone.

Cancer of the thyroid--explorations of clinical biology.

A brief review of the cancers derived from the follicular thyroid epithelium and parafollicular cells (medullar cancer) is made. The contribution of clinical biology to the diagnosis has little significance in the case of thyroid cancer. On the other hand, the quantitative analysis of thyroglobulin is very important for the detection of recurrence in the course of the follow-up of a patient who has been treated by complete thyroidectomy. The biological markers of medullar cancer are most specific. The observation of pathological secretion of thyrocalcitonin is determining for the diagnosis of medullary carcinoma. It must lead to a parathyroid and medulloadrenal exploration as well as to systematic investigation of family history. These steps are essential for the diagnosis of the syndromes of multiple endocrine neoplasias types 2a and 2b.