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Good practice guide for cervical ultrasound scan and echo-guided techniques in treating differentiated thyroid cancer of vesicular origin. American, European and French Recommendations for the treatment of differentiated vesicular thyroid cancer were recently published. Cervical ultrasound scanning is now considered a key examination in the follow-up of these cancers. This examination is noninvasive, easy to perform and to obtain, is not costly, but remains operator-dependent. To date, there are no recommendations published that assemble all the technical aspects, results, indications and the limits of this examination in the initial medical report and the follow-up of these cancers. In order to standardise the procedure and validate the quality of the examination, a workgroup made up of a panel of experts particularly involved in carrying out ultrasound scans was set up. The aim was to draw up a good practice guide for performing cervical ultrasound scans and echo-guided techniques in treating patients with differentiated thyroid cancer of vesicular origin. The main objectives are to: (a) standardise the procedure and reports, (b) define the criteria for establishing whether lesions identified during a cervical ultrasound scan are malignant or benign, (c) standardise the indications for carrying out cytological tests and an in situ assay of markers, (d) help doctors to select the patients who ought to receive a cervical ultrasound scan and or cytological tests, (e) discuss how frequently the examinations should be carried out depending on the risk of recurrence., (Copyright © 2011 Elsevier Masson SAS. All rights reserved.)

TSH-secreting adenomas are rare tumors, representing only 0.5 to 2.5% of pituitary adenomas. Their main clinical characteristics include signs of thyrotoxicosis, diffuse goiter and a compressive syndrome. Biologically, free T4 and T3 serum levels are elevated, contrasting with inadequate serum TSH levels and increased alpha chains. Magnetic resonance (MR) imaging shows a pituitary tumor, the main differential diagnosis being resistance to thyroid hormones. Treatment is based on surgery, possibly associated with somatostatin analogs and radiotherapy. Though the long-term evolution of this rare pathology seems to have improved, some clinical situations are still a challenge to treat. We report one such case that was resistant to both stereotactic radiotherapy and somatostatin analogs, but surprisingly improved with cabergoline. We suggest that cabergoline should be considered as an alternative treatment in cases of pituitary adenomas that resist traditional treatments.

Anaplastic thyroid carcinoma may represent the ultimate dedifferentiation step of thyroid tumorigenesis and is one of the poorest cancers in human. It accounts for less than 2% of thyroid cancers and affects older patients in their sixth to eighth decade. Usual clinical presentation is a rapidly growing thyroid mass invading surrounding structures with compressive symptoms. Cervical lymph nodes enlargement and distant metastases occur frequently. Though cytological results obtained by fine needle aspiration may be suggestive of diagnosis, tissue biopsy for immunohistochemical study can be necessary to exclude lymphoma and to validate aggressive therapies. Patients developing anaplastic thyroid cancer must be referred urgently in cancer centers to plan multimodality therapeutic approach depending on their performance status. The treatment regimen combines surgery when feasible, hyperfractionated and accelerated external beam radiotherapy and doxorubicin based chemotherapy. Such treatment can provide control of locoregional disease but does not impact on overall survival in patients with distant metastases. The prognosis is dismal with a mean survival of four to nine months after diagnosis. Long survivors are patients with emerging disease presenting a resectable tumor and receiving adjuvant radiotherapy and/or chemotherapy. Therapeutic researches investigate redifferenciation strategies and targeted therapies to inhibit EGF receptors and neoplastic angiogenesis. Primary prevention of this lethal disease may consist of adequate treatment of differentiated thyroid cancers and goiters in elderly.

We present the case of a 17-year-old male who was diagnosed at birth with hereditary fructose intolerance (HFI). The patient complained of morning-time asthenia and post-prandial drowsiness despite a correct sleep pattern. The physical examination and biological check-up only showed severe vitamin C deficiency (<10 mol/l; normal range: 26-84). The patient's tiredness was attributed to this vitamin C deficiency, which is a frequent side-affect of the fructose-free diet. A change in diet associated with a supplementation in vitamin C was advised, with an increase in vegetable intake, principally avoiding carrots, onions, leaks and tinned sweet-corn. This case offers the opportunity for a review of this rare disease. Two kinds of fructose metabolism disorders (both autosomal recessive) are recognized: 1) essential fructosuria caused by a deficiency of fructokinase, which has no clinical consequence and requires no dietary treatment; 2) HFI, linked to three main mutations identified in aldolase B gene that may be confirmed by fructose breath test, intravenous fructose tolerance test, and genetic testing. In HFI, fructose ingestion generally induces gastro-intestinal (nausea and vomiting, abdominal pain, meteorism) and hypoglycemic symptoms. Fasting is well tolerated. If the condition remains undiagnosed, it leads to liver disease with hepatomegaly, proximal tubular dysfunction, and slow growth and weight gain. In conclusion, endocrinologists should be aware of this rare metabolic disease in order to provide careful follow-up, particularly important when the patient reaches adulthood. Moreover, hypoglycemia induced by fructose absorption, unexplained liver disease, irritable bowel syndrome or familial gout in an adult is suggestive of the diagnosis.

11beta-hydroxysteroide dehydrogenase (11beta-OHSD) enzymes exhibit a regulating action upon cortisol metabolism before access to its receptors. Two types of isoenzymes have been described, type 2 being the most anciently known. Type 2 11beta-OHSD, which changes cortisol into cortisone, is a unidirectional dehydrogenase mainly located in kidney, that protects mineralocorticoid receptors from illicit activation by glucocorticoids. Mutations of the gene coding for this enzyme has been demonstrated in apparent mineralocorticoid excess, which induces hypertension and hypokalemia with low renin and aldosterone levels. Polymorphisms of this gene could modulate essential hypertension and also be responsible for certain forms of acquired apparent mineralocorticoid excess especially after liquorice intoxication, in hypothyroidism, Cushing syndrome, and chronic renal insufficiency. Type 1 11beta-OHSD, which changes cortisone into cortisol, is a reductase, mainly located in liver and adipose tissue. Functional defects of this enzyme have been shown in polycystic ovaries and cortisone reductase deficiency. By contrast, metabolic syndrome, corticoid-induced osteoporosis, and glaucoma are linked to a local over-activity of this enzyme. The understanding of action mechanisms of these two enzymes currently leads to 11beta-OHSD inhibitors development, therefore opening new therapeutic strategies, especially in metabolic syndrome.

We report two cases of thyrotoxicosis-revealing functional metastases of a follicular carcinoma that extended to the bones, liver and kidneys in one case and to the lungs in the other. Both patients had undergone surgical intervention for a thyroid nodule more than 15 years before the diagnosis of thyrotoxicosis and metastatic dissemination. In both the cases, the carcinoma was not recognized by the pathologist after the first surgical intervention, but was finally diagnosed several years later due to the occurrence of thyrotoxicosis. Iodine-131 therapy was effective at suppressing the thyrotoxicosis in both the patients. The effectiveness on the metastatic extension was very different for each patient: in the first case, the patient died a few years later without any control of the metastatic tissue. For the second patient, the metastases disappeared a few months after radioiodine treatment, with the patient still in remission more than 10 years later. The physiopathology and the evolution of these two cases are discussed with the data available in the literature.

Calcium is a major ion in human metabolism and its level is highly controlled. This regulation is performed via the Calcium Sensing Receptor, a discovery which ten years ago led to the explanation of a number of clinical disorders. The syndromes caused by CaSR abnormalities are characterized by hypercalcemia or hypocalcemia, associated with inappropriate calciuria. An underlying genetic or auto-immune cause may be demonstrated. High blood calcium levels linked to mutations of the CaSR gene lead to familial hypocalciuric hypercalcemia and the neonatal and non neonatal forms with severe hypercalcemic. Hypocalcemia determined by mutations in the CaSR gene include autosomal dominant hypocalcemia and its sporadic form. Another clinical presentation similar to Bartter syndrome has been reported. Auto-antibodies directed against CaSRs, seen in auto-immune diseases, can lead to similar clinical presentations. Finally, CaSR polymorphisms modulate the range of blood calcium levels. With diagnosis of these diseases deleterious therapeutics can be avoided. The discovery of this receptor has led to new therapeutic prospects such as calcimimetics for hyperthyroidism.

Renal proximal tubular reabsorption of phosphate and intestinal absorption both regulate phosphate homeostasis. Brush-border membrane Npt2a cotransporter is the key element in proximal tubular P (i) reabsorption. Inactivating mutations of Npt2a cause bone demineralisation and urolithiasis. An excess of a phosphaturic factor, called "Phosphatonin", could modulate phosphate reabsorption by inhibition on Npt2a. Inactivating mutation of PHEX, an endopeptidase-membrane coding gene, is responsible for X-linked Hypophosphatemia (XLH), because of an impaired degradation of phosphatonine by PHEX product. Autosomic Dominant Hypophosphatemic Rickets (ADHR) is explained by a mutation preventing FGF23 (one of the best identified phosphatonines) from cleavage. According recent data, FGF23, MEPE (Matrix Extracellular Phosphoglycoprotein) et FRP4 (frizzled related protein-4) are 3 putative "phosphatonines".

Between 1971 and 2002, 80 patients underwent surgery for insulinoma at the Department of General and Endocrine Surgery of the Lille University Hospitals. The present report deals with 13 patients with proven multiple endocrine neoplasia type I (MEN I) or supposed genetic-related insulinomas. This entity differs from spontaneous insulinoma by the presence of multiple foci in the pancreas. Enucleation is not advised in this setting due to the strong likelihood of persistence or recurrence. Various studies suggest different strategies for preoperative localization and surgical approach. We analyzed retrospectively the surgical strategy proposed by the A.F.C.E. and G.E.N.E.M. The purpose of this study was to validate the strategy, integrate the contribution of genotypic diagnosis, simplify preoperative imaging studies, and re-evaluate the value of intraoperative baseline secretin-stimulated insulin measurements. We recommend preoperative endoscopic ultrasonography of the pancreatic head only and routine left pancreatectomy with enucleation of cephalic tumors under intraoperative hormone monitoring. Preoperative invasive localization studies are proposed only if the endoscopic ultrasonography is negative for the pancreatic head. Intraoperative secretin stimulation test can be useful in difficult cases, especially with concurrent nesidioblastosis or in case of secondary surgery. All but one of the 13 patients achieved long-term cure with this strategy.

The typical manifestations of severe hypercalcemia with osteitis fibrosa cystica have become exceedingly rare. We describe the case of a woman hospitalized for a tibial tumor with functional impotence, leading to a diagnosis of primary hyperparathyroidism (HPT I) associated with profound vitamin D deficiency. This 31-year-old woman was admitted, after two pregnancies complicated by the HELLP syndrome. Preoperative laboratory values were as follows: calcemia 4.05 mmol/l (2.2-2.6); urinary calcium 30 mmol/24 h (1.25-7.5); parathormone (PTH) 1 195 pg/ml (10-60); and 25 OH-vitamin D 13 nmol/l (22-120). Specific MIBI uptake by the tibial lesion oriented the diagnosis towards a brown tumor. After surgical excision of a parathyroid adenoma and the brown tumor (associated with tibial fracture), calcemia fell to 1.55 mmol/l and normalized after three months. Urinary calcium fell to 0.1 mmol/24 h and remained low during the 2 years following surgery. Vitamin D levels rapidly normalized on supplementation (87 nmol/l). PTH levels fell markedly after surgery but remained higher than normal till 2 years after surgery despite normalization of calcemia three months after. Bone repair, estimated by means of bone densitometry, improved from preoperative Z-score values of - 6.54, - 5.20 and - 3.50 in the left femoral neck, right femoral neck and lumbar spine, respectively, to - 0.20, - 1.55 and - 0.28, respectively, one year after surgery. In conclusion, this case illustrates: 1) the severe osseous expression of HPT probably related to vitamin D deficiency; 2) specific MIBI uptake by the bone lesion, orientating the diagnosis towards a brown tumor; 3) the consequences of vitamin D deficiency on postoperative outcome, with transient severe initial hypocalcemia related to bone calcium avidity; 4) a possible link between HPT and the HELLP syndrome.

Thyroid hormones are involved in vertebrate development and metabolic homeostasis. Their actions are mediated through several nuclear receptors encoded by TRalpha and TRB genes. The interspecies conservation of 3 functional receptors (TRalpha1, TRB1 and TRB2) and their partially distinct tissue distribution suggest that they serve non-redundant physiological functions. The exclusive TRB gene involvement in the resistance to thyroid hormone (RTH) reinforces the hypothesis of a functional specificity. Recent mouse knock-out and transgenesis methods allow invalidation or overexpression of a gene of interest, respectively. They therefore provide powerful means to determine the specific function of a gene and have been applied to the thyroid hormone receptor genes. Mice TRB(-/-) represent a model of the recessive form of RTH. They have been shown to develop goiter and high thyroid hormone and TSH (Thyroid Stimulating Hormone) levels, suggesting an unique role for TRB in the negative regulation of TSH pituitary secretion. The associated disorder in audition maturation also showed that TRB plays an essential role in the development of audition. By contrast, mice TRalpha(-/-) exhibited thyroid gland atrophy along with decreased thyroid hormones and TSH levels. Clinical phenotype included growth interruption and retardation of both intestine and bone maturation, but no hearing loss. Mice TRalphaB(-/-) combined the disorders, including delayed neonatal development despite hyperactive hypothalamus-pituitary axis. Finally, transgenic overexpression of a mutant TRB gene reproduced the dominant form of RTH and confirmed the major role of dominant negative activity in the occurrence of some phenotypic key-features such as high circulating hormone levels despite high TSH levels, hyperactivity and lack of severe hearing loss. From these studies, it is suggested that TRalpha and TRB receptors are to some extent able to cooperate or substitute for each other. However some organs constitute TR-specific T3 target-tissues such as inner ear, pituitary, heart, liver, bone and small intestine.

Objective: The aim of the study was to assess the economic consequences of the early screening and management for overt hypothyrodism in elderly women suffering from hypercholesterolaemia., Methods: A cost analysis was performed using screening decision tree followed by a Markov model, targeted on an hypothetical cohort of elderly women (i.e. > or = 55 years of age) suffering from hypercholesterolaemia. Two arms were compared, "no diagnosis", patients being treated by lipid lowering drugs in the long run, "diagnosis", patients being screened for thyroid disturbance and proposed adequate correction by hormone treatment. Relevant clinical data introduced into the model were obtained from published data and from experts. At the end of the initial diagnostic, patients could enter three different health states: euthyroidism, subclinical hypothyroidism or overt hypothyroidism. During 30 years, patients were assumed to be seen each year by a general practitioner for clinical examination and cholesterol dosage, plus, according to the health state evolution, TSH and T4 screening. In the baseline analysis, euthyroidian patients who had a inexplicable degradation of hypercholesterolaemia control were tested for TSH and, if abnormal, T4 serum; for subclinical hypothyroidian patients, TSH and T4 were measured every year. The direct costs taken into account were concerning medical supervision, drug treatment and biologic exams. Costs were analysed from the societal perspective and were expressed in 1998 French Francs (FF) with an accounting rate of 5% by year. A sensitivity analysis was also performed., Results: The total cost at 30-year was equal to 25,006 F for "diagnosis" strategy, to 24,390 F for "no diagnosis" strategy. The incremental cost of the first strategy decreased according to the time horizon. It was 6.8% at 5-year and 2.5% at 30-year. Results were sensitive to variation in response rate of hypercholesterolaemic patients to hormone treatment of hypothyroidism (0.25 in base-case)., Conclusion: The investment cost in screening and treatment of hypercholesterolemic female patient aged 55 and more can be considered offset in the long run (30 years). Considering the other important outcomes in favour of hormonal drug treatment of hypothyroidism, such as enhancement of well-being, functional capacities and quality of life, the "diagnosis" strategy can be recommended in the ambulatory medical practice.

Aim of the Study: Evaluation of frequency and outcome of loco-regional persistance and recurrences of differentiated thyroid carcinomas after surgery., Material and Methods: from 1964 to December 1990, we operated and followed up more than 5 years (from 5 to 31 years): 589 thyroid cancers (309 papillary, 262 follicullar et 18 Hürthle cells); 145 patients were lost to follow-up (24%), 33% of them were microcarcinomas. Surgery consisted ultimately in 411 total thyroidectomies, 51 sub-total thyroidectomies, 113 lobectomies with isthmusectomies, 9 isthmusectomies or tumorectomies and 4 tracheotomies. Neck dissection was not routinely performed but rather selectively (n = 137). All Patients were put under suppressive hormone therapy. After total thyroidectomy, ablative 131 iodine was almost routinely done. All patients have been controlled by clinical examination, radio-iodine scanning and, since 1983, by sequential thyroglobulin assays. We have analysed the course of patients according to L. J. Degroot's staging (Stage I: Patient with intrathyroidal disease. Stage II: Patient with cervical node involvement. Stage III: Patient with extra-thyroidal neck invasive disease. Stage IV: Distant metastasis)., Results: Stage I, n = 383, Stage II, n = 96. Total = 479. Local recurrences in the bed of total thyroidectomy were exceptional: n = 2/323 (0.6%). Recurrences in the thyroid remnant after non total thyroidectomy were rare: n = 3/156 (2%). Cervical nodal recurrences were also rare: n = 7/479 (1.5%). Stage III (n = 73): 34/306 papillary, 9/78, well differentiated follicular, 25/175 poorly differentiated follicular. 2/9 follicular of other type and 3/18 hurtle cell. In 67 patients, the loco-regional sterilization was achieved, 5 of which were reoperated for nodal cervical metastasis. 6 patients died from continuing loco-regional disease and 10 presented distant metastases. 4 of which died from. Among opered patients are still alive (52/73 = 71,2%) no loco-regional recurrence persisted., Conclusion: The true problem is not recurrence but the persistance after surgery in stage III patients, despite the application of 1131. The determining factor of the persistance and recurrence is the initial stage of the carninomatous disease at the time of treatment.

Since TSH favors thyroid cells growth and proliferation, thyroid hormone administration is widely used to reduce TSH secretion in patients treated for thyroid cancers. But what degree of TSH suppression is required to inhibit tumorgenesis and prevent recurrences remains unknown. High doses of thyroid hormone can determine undesirable effects on quality of life, bone mass, or cardiac function. These effects have to be evaluated and eventually prevented by specific therapies. Probably the degree of TSH suppression has to be adjusted to the prognosis of the thyroid cancer and the specific risks for every patient.

Sustained remission can be observed among 30-50% of the patients long-term treated with antithyroid drugs for Graves' disease. Many parameters have been proposed as predictors of remission of relapse of hyperthyroidism. Initial thyroid volume and its evolution during therapy, T3/T4 ratio, TSH to TRH responsiveness, serum thyroglobulin concentration, and Technetium or Iodine uptake under T3 appeared as the most sensitive indicators of intensity or permanence of thyroid stimulation activity. Few studies only demonstrated a relation between prognosis and HLA B8 or DR3. Those markers predict more accurately the relapse than the remission. Their interest and their management in clinical practice remain still imperfectly determinated.

The appropriateness of treating thyroid nodules with thyroid hormone is being debated: in fact, the development of nodules is not caused by an iodothyronine deficiency or a desuppression of TSH, and T4 seems to be able to regain control on cell proliferation. A very great number of authors have reported their experience with suppression of thyroid nodules with thyroid hormone, but treatment efficacy has been variably appreciated (9 to 69% regression). On the other hand, the four randomized prospective studies available at present, which analyze the evolution of nodules, especially on ultrasonography, have not demonstrated that hormone therapy is more effective than a placebo. The methodology of these studies is not free from criticism, and other prospective surveys are required, especially to establish whether this treatment is innocuous and whether some varieties of nodules may be more amenable to hormone therapy than others.

Reduction of hyperprolactinemia by Methysergide (4.4 mg p.o.) and Bromocriptine (2.5 ng p.o.) was studied in 20 patients (7 subjects with pituitary macroadenoma and 13 hyperprolactinemic patients with normal sella turcica). No difference was observed between the effects of the two drugs 4 hours after their administration, with and without respect of the aetiologies of hyperprolactinemia. However the serum prolactin levels were significantly lower 6 hours (n = 11 p = 0,01) and 12 hours (n = 10 p less than 0,01) after Bromocriptine than after methysergide. The difference observed between the two drugs seems to be inherent to their different half-lives.

Twelve patients (2 with only bone metastases, 3 with only soft tissues metastases and 7 with bone and soft tissues metastases) were treated with 131-I-MIBG (specific activity: 20 mCi/mg), 100 to 200 mCi every 3-6 months. A dosimetric study was carried out before each administration. The follow-up ranged from 6 to 24 months and the number of doses ranged from 1 to 8, with 1.85-9 GBq per administration and a cumulative activity of 1.85-62. 2 GBq according to patients. The cumulative absorbed activity ranged from 850 to 9700 cGy. The following side effects were observed: a bone marrow hypoplasia (1 patient) and a transient increase in catecholamines (3 patients). The treatment was successful in 7 patients (3 with soft tissue metastases, 3 with bone and soft tissue metastases and one with bone metastases). This success consisted in clinical improvement and a decrease greater than 50% of hormonal values in the 7 patients and a decrease greater than 50% of tumoral masses in only 3 patients. No complete remission was obtained at this stage of the study. The disease recurred in 1 patient after a year of partial remission. There was no clear-cut relation between the number of doses and the results. This study shows that 131-I-MIBG can give encouraging though limited results.

T3 serum concentrations (RIA) was low in 25 cases and normal low in 10 among 57 patients with serious systemic illnesses. These 35 patients were in clinical euthyroid state and had a normal T4 serum concentration and F.T.I. T.S.H. serum concentration was normal in 28 cases of 31 low T3 syndrome observed.

Thyroid explorations were made in 57 patients complaining of serious illnesses in order to identify "low T3 syndrome". All these patients were clinically euthyroid as assessed by normal values of T4 concentration, RT3U ratio and FT4I. However, all the patients included in this study had significantly low serum T3 (42 +/- 29 ng/100 ml) and FT3I (0,44 +/- 0,30). Low T3 syndrome was particularly frequently seen in patients with cancer (8/10), hepatic cirrhosis (5/6), renal failure (6/7), old age (5/8) and in serious systemic diseases (6/12). Nevertheless, at adverse with other authors, we have observed less frequently the low T3 syndrome in anorexia nervosa (4/6) as well as during fasting (1/8). In 31 out of 35 patients with low or normal low T3 concentrations, the serum TSH values observed were within the normal limits in 28 cases. The etiologies of isolated decreased T3, mainly the deviation of peripheral conversion of T4 to reverse T3, are discussed. Normal metabolic state and normal TSH concentration encountered in the low T3 syndrome are equally commented.

The very diverse clinical expressions of pheochromocytoma are dependent upon type of catecholamine secreted and excreted by the tumor. The role of each of the three amines (adrenaline, noradrenaline, dopamine) is reviewed in relation to physiologic regulation of blood pressure: adrenaline and noradrenaline are pressor hormones and act on almost all blood pressure factors. They possess chronotropic and positive inotropic effects by their action on cardiac beta 1 adrenoceptors, a peripheral vasoconstricting action by interaction with vascular alpha 1 receptors and a direct effect on renin production and tubular resorption of sodium. Inversely, dopamine presents as a hypotensive agent, opposing effects of adrenaline and noradrenaline and possessing numerous sites of action: central hypotensive action on cardiovascular integration structures, inhibitory effect on sympathetic ganglionic neurotransmission, action on specific presynaptic receptors at nerve endings, reducing sympathetic vasoconstrictor tone and finally a direct vasodilator effect. Based on these recent physiologic data the role is discussed of hypersecretion of each amine in the cardiovascular expression of pheochromocytoma. Attention should be concentrated on the nature of hormonal hypersecretion of pheochromocytoma, and a determining role given to the type of catecholamine secreted by the tumor and to the relation between the different amines with respect to the blood pressure symptomatology of pheochromocytoma.

Studies were conducted in 14 patients with pheochromocytoma over a 3-year period. Circumstances of detection of these tumors varied greatly and were sometimes misleading, hypertension being an inconstant finding in the clinical history and was not always the predominant feature. Biologic exploration involved assay of excretion of free urinary noradrenaline (NA), adrenaline (AD) and dopamine (DA) using a HPLC technique as well as assay of total methoxy derivatives and urinary vanilmandelic acid. Validity of each assay in the diagnosis of pheochromocytoma could be evaluated and only the total free methoxy derivatives gave false negative results. Hormonal secretion of pheochromocytoma is often mixed, but sometimes predominant or exclusive for a single catecholamine. Relative increases of the different catecholamines, evaluated from the ratios DA/NA and DA/NA + AD, are an important factor since a relation exists between blood pressure induced symptomatology and equilibrium between hypotensive hormone (DA) and pressor amines (NA + AD); 3 types of pheochromocytoma can be described: NA-induced with paroxysmal or permanent hypertension but without typical metabolic and cardiac disorders, and with a very reduced DA/NA + AD ratio during hypertensive crises; AD-induced without permanent hypertension but with a mainly orthostatic hypotension and episodes of cardiovascular collapse following hypertensive attacks and with an AD/NA ratio greater than 1; finally the DA-induced lesion in which hypertension is never associated and manifestations are misleading and atypical with an elevated DA/NA + AD ratio.

By using immunohistoenzymatic techniques, cells of 4 pituitary adenomas are revealed with beta MSH, alpha and beta endorphins antisera but do not react with 1--24 and 17--39 ACTH antisera. These data suggest that adenomatous cells are able to synthesize and LPH-like molecule without ACTH. The levels of plasmatic LPH and beta MSH, studied by RIA, stay normal. These results are discussed.