[Riedel's thyroiditis and lymphoma. Diagnostic difficulties]. / Thyroïdite de Riedel et lymphome. Difficultés diagnostiques.

Two cases of Riedel's thyroiditis demonstrated the difficulties encountered in diagnosis. In the first case, subtotal thyroidectomy was performed due to compressive goiter. The intraoperative macroscopic aspect suggested Riedel's thyroiditis. The pathology report also discussed the diagnosis, despite a major lymphoid component, as dense fibrosis had multilated the thyroid parenchyma. Subsequent clinical course led to the diagnosis of lymphoma. The clinical presentation in the second case was classical with rapid increase in size of a hard thyroid gland. Histology was however atypical showing calcifications and liquid cysts within the fibrous thyroid tissue. The initial signs of Riedel's thyroiditis, a very rare disease, usually suggest neoplasia: ligneous compressive goiter with deep adherences. Histologically, there is invasive fibrous thyroiditis with highly suggestive occlusive phlebitis in certain cases. The origin of the disease remains obscure. The differential diagnosis between a sclerosing form and lymphoma is particularly important for therapeutic management.

Administration of RU 486 for 8 days in normal volunteers: antiglucocorticoid effect with no evidence of peripheral cortisol deprivation.

New therapeutic indications based on the antiprogesterone action of RU 486 (Mifepristone) are emerging which require long term administration and raise the question of its safety because of the antiglucocorticoid action of the drug. A trial was designed to assess the antiglucocorticoid effect of RU 486, possible manifestations of peripheral cortisol deprivation, and the adrenocortical and corticotroph reserves. Ten normal male volunteers (aged 21-29 yr) were given RU 486 (200 mg/day) or placebo between 0800-0900 h for 8 consecutive days in a randomized, double blind, cross-over design, with a 1-month interval between the two periods. RU 486 induced overactivation of the pituitary-adrenal axis; baseline values (mean +/- SEM) before and at end of treatment were, respectively: 0800 h plasma cortisol, 147.3 +/- 15.5 and 257.6 +/- 8.8 ng/mL; 0800 h salivary cortisol, 5.8 +/- 1.2 and 15.2 +/- 0.8 ng/mL; nocturnal (2200-0800 h) urinary cortisol, 8.4 +/- 1.5 and 33.7 +/- 11.1 micrograms; and 0800 h plasma ACTH, 29.2 +/- 3.7 and 60.2 +/- 8.4 pg/mL. All of these variations were significantly different from those during placebo treatment (0.0001 < P < 0.03) and disappeared within 4 days after the end of treatment. A daily record of subjective clinical symptoms, body weight and temperature, blood pressure, and heart rate showed neither side-effects nor any significant variation during treatment. Blood electrolyte and eosinophil counts were unchanged; fasting blood glucose was slightly higher at the end of treatment (5.0 +/- 0.2 vs. 4.7 +/- 0.1 mmol/L; P = 0.04). The adrenocortical response to Cortrosyn (0.25 mg, im) was exaggerated during RU 486 treatment (P < 0.006): peak values before and at the end of treatment were, respectively: plasma cortisol, 272.5 +/- 15.2 and 347.1 +/- 20.6 ng/mL; and salivary cortisol, 17.0 +/- 2.2 and 31.1 +/- 3.1 ng/mL. Direct pituitary stimulation (100 micrograms ovine CRH, followed by 1 IU lysine vasopressin over 15 min) also induced exaggerated corticotroph and adrenocortical responses (P < 0.005); peak values before and at the end of treatment were, respectively: plasma ACTH, 147.7 +/- 24.6 and 254.0 +/- 41.3 pg/mL; and plasma cortisol, 231.6 +/- 7.3 and 319.2 +/- 12.3 ng/mL. These data show that 8-day treatment with 200 mg RU 486 daily induces a hormonally detectable antiglucocorticoid effect without clinical symptoms. This state results from reversible cortisol overproduction with preservation of adrenocortical and pituitary reserves.

PIP: At Cochin Hospital in Paris, France, ten 21-29 year old normal male volunteers received either 200 mg RU-486 per day or a placebo for 8 consecutive days between 8:00 and 9:00 in the morning, then went through a 28-day washout period before receiving what they did not receive the first time for 8 days. The researchers wanted to examine the antiglucocorticoid effect of RU-486, any evidence of peripheral cortisol deprivation, and the adrenocortical and corticotroph reserves. An assessment of potential risk of longterm administration of RU-486 is needed to determine whether it can be used to treat chronic diseases (e.g., meningioma and breast cancer). RU-486 was responsible for overreaction of the pituitary-adrenal axis (8:00 am plasma cortisol, 147.3 ng/mL vs. 257.6 ng/mL; 8:00 am salivary cortisol, 5.8 ng/mL vs. 15.2 ng/mL; nocturnal urinary cortisol, 8.4 mcg vs. 33.7 mcg; and 8:00 am plasma adrenocorticotropic hormone [ACTH] 29.2 pg/mL vs. 60.2 pg/mL). All these changes differed significantly from those during placebo treatment (0.0001 p 0.03). These changes no longer existed 4 days after the end of treatment. The men kept a daily record of subjective clinical symptoms, body weight and temperature, blood pressure, and heart rate, which did not indicate any side effects or any considerable variation during treatment. RU-486 did not affect blood electrolyte and eosinophil counts. Blood glucose levels during fasting were somewhat higher at the end of treatment (p = 0.04). During RU-486 treatment, the adrenocortical response to 0.25 mg of intramuscularly injected Cortrosyn was amplified (peak values before and after, plasma cortisol, 272.5 ng/mL vs. 347.1 ng/mL; 17 ng/mL vs. 31.1 ng/mL) (p 0.006). Direct stimulation of the pituitary resulted in exaggerated corticotroph and adrenocortical responses (p 0.005). These findings showed that a daily dose of 200 mg RU-486 causes a hormonally detectable antiglucocorticoid effect but no clinical symptoms.

Comparison of computerized tomography and magnetic resonance imaging for the examination of the pituitary gland in patients with Cushing's disease.

OBJECTIVE: The vast majority of patients with Cushing's disease have a corticotroph adenoma, the selective removal of which, through the transsphenoidal route, has the potential to offer a definitive and complete cure. This study was designed to compare the diagnostic accuracy of computerized tomography (CT) and magnetic resonance imaging (MRI) to identify the presence, evaluate the size, and assess the topographic characteristics of pituitary corticotroph adenomas. METHODS: Forty-two patients with Cushing's disease were included in this prospective study, of whom 16 were subsequently explored transsphenoidally. Computerized tomography used a CE 12,000 CGR apparatus with 1.5-mm coronal slices and a 2-mm interslice gap. Magnetic resonance imaging used an MR Max 0.5T GE apparatus; adjacent 3-mm slices were obtained with a T1-weighted gradient echo before and after gadolinium injection. RESULTS: Lesions compatible with an adenoma were identified in 29 patients by MRI and in 21 patients by CT (69 vs 50%, P < 0.02). Seven macroadenomas were identified as well by the two methods. Eight of the 22 microadenomas detected by MRI were not identified by CT. Evidence for intracavernous tumour extension was found in nine patients: it was more frequently detected by MRI (8 patients) than by CT (4 patients). Fourteen patients with positive MRI had a pituitary examination: in one case the adenoma could not be reached because of purely suprasellar location; of the other 13 all were found by the surgeon and the surgical outcome was successful in 12 cases. CONCLUSION: MRI is superior to CT for the examination of the pituitary gland in patients with Cushing's disease.

[Bilateral adrenal tumoral formation. Regressive spontaneous evolution]. / Formation tumorale surrénalienne bilatérale. Evolution spontanée régressive.

A case of bilateral adrenal tumoral formation associated with Addison's disease is reported, and the possible cause of this association is discussed. The short-term deleterious course of metastatic malignancies, hemopathies or severe infections when left without specific treatment, and the long-term course of our patient's tumoral pathology excluded these diagnoses. The spontaneous regression of a bilateral pseudotumoral mass was suggestive of 2 causes: haematoma or tuberculosis. Haematoma was unlikely in the absence of causal factors, and this, combined with the slow regression of the adrenals, made tuberculosis the most probable diagnosis. The few similar cases found in the literature are reviewed.

Suppression of ectopic adrenocorticotropin secretion by the long-acting somatostatin analog octreotide.

The long-acting somatostatin analog (octreotide) was administered to a 37-yr-old woman with the ectopic ACTH syndrome. The patient had diffuse metastatic spread of a nonpituitary tumor, presumably of pancreatic origin, and severe and rapidly progressive hypercortisolism with extreme myopathy, hypokalemia, and diabetes mellitus. Plasma ACTH and lipotropin levels and 24-h urinary cortisol excretion were greatly elevated [218 pg/mL (48 pmol/L), 1340 pg/mL (220 pmol/L), and up to 830 micrograms/24 h (2290 nmol/day), respectively]. Urinary cortisol excretion decreased to normal within 3 days after the initiation of octreotide therapy (150, 300, and 600 micrograms/day), and plasma ACTH and lipotropin levels also decreased. Urinary cortisol excretion remained normal for 2 months during chronic octreotide therapy, and her general condition improved dramatically. The only side-effect was a slight increase in the number of bowel movements. Tumor progression, however, was not controlled, and she eventually died of hepatic insufficiency. These data indicate that octreotide can be a highly effective treatment for patients with the ectopic ACTH syndrome.