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M Boscaro

Publications and source records attributed to M Boscaro.

At least 37 records · Page 2Linked to original sources
PubMed2001

Scintigraphic patterns of adrenocortical carcinoma: morpho-functional correlates.

OBJECTIVE: Adrenocortical scintigraphy has demonstrated clinical utility in the morpho-functional characterization of adrenal tumors. The aim of this study was to identify possible relationships between the scintigraphic pattern and endocrine and/or morphological data in a series of adrenocortical carcinomas. DESIGN AND METHODS: Twenty-one patients with adrenocortical carcinoma (11 nonfunctioning and 10 hormone-secreting) were investigated with 75Se-methyl-nor-cholesterol scintigraphy. Clinical, hormonal, radiological, and pathological data were analyzed. RESULTS: The adrenal mass showed no radiocholesterol uptake in 18 cases (11 nonfunctioning and 7 functioning lesions). Contralateral normal adrenal gland was visualized in all patients with nonfunctioning tumors, whereas classic bilateral nonvisualization was observed in the 7 cases with hyperfunctioning masses. Three patients with cortisol-producing carcinomas showed radiotracer uptake by the mass, without visualization of the contralateral gland. At histology, the tumors were shown to be undifferentiated adrenocortical carcinomas; they had an aggressive clinical behavior. CONCLUSIONS: Radiocholesterol scintigraphy has an important role in diagnosing adrenocortical carcinomas, which typically are not visualized. However, 30% of hypersecreting adrenocortical carcinomas show an atypical increased tracer uptake, not predictive of the biochemical and histological features of the tumor.

Adolescent↗
PubMed2001

Multiple endocrine neoplasia type 1 and adrenal lesions.

PURPOSE: We investigated the relationship of long-term pancreatic hormone hypersecretion with adrenal lesions in patients with multiple endocrine neoplasia type 1 and in those with sporadic pancreatic endocrine tumors. MATERIALS AND METHODS: We assessed the prevalence of adrenal lesions in 20 patients with multiple endocrine neoplasia type 1 and in a control group of 12 with sporadic pancreatic endocrine tumors. We also performed genetic testing for germline mutations of MEN1, the multiple endocrine neoplasia type 1 gene. RESULTS: Adrenal lesions were common in multiple endocrine neoplasia type 1, accounting for 35% of cases. All adrenal lesions were nonfunctioning and benign. The relative risk of adrenal tumors was higher in patients with multiple endocrine neoplasia type 1 than in controls (p <0.05). No apparent relationship was observed of hormonal pattern or genotype with adrenal disease. CONCLUSIONS: Hormone hypersecretion by pancreatic endocrine tumors is not the primary cause of the development of adrenal lesions and the role of the MEN1 gene in adrenal tumorigenesis remains unclear. Adrenal lesions follow a benign course in most multiple endocrine neoplasia type 1 cases but careful morphological and functional followup is advisable.

Adolescent↗
PubMed2000

The diagnosis of Cushing's syndrome: atypical presentations and laboratory shortcomings.

In the last 3 decades, there have been several advances in understanding the pathogenesis of Cushing's syndrome and in testing for the diagnosis and differential diagnosis of its various forms. Advanced diagnostic techniques provide useful tools in discovering ectopic adrenocorticotropic hormone sources. However, the occurrence of unusual clinical presentations, laboratory shortcomings, and exogenous compound interference may lead to wrong conclusions. This article reviews the atypical presentations of hypercortisolism and some laboratory shortcomings that may confuse the diagnosis of Cushing's syndrome. Comments and suggestions are given with the aim of helping the clinician avoid diagnostic mistakes.

Cushing Syndrome↗
PubMed2000

Effect of the serotonin antagonists ritanserin and ketanserin in Cushing's disease.

Central serotonergic regulation could have a role in the course of pituitary-dependent Cushing's disease. We studied the effects of ritanserin and ketanserin, two related selective 5HT2 receptor antagonists, in 11 patients with Cushing's disease. Treatment lasted from 1 month to 1 year (up to 4 years in one patient). Daily doses were 10-15 mg for ritanserin, and 40-80 mg for ketanserin. Since the two drugs share the same mechanism of action and no qualitative or quantitative differences in response to their administration were observed, the results were pooled together. Patients were assessed by clinical and hormonal evaluation. Urinary cortisol and ACTH were considered the parameters of interest. Short-term response: after 1 month, there was a significant decrease of urinary cortisol from 781 (160) to 331 (215) nmol/d (P < 0.02) while ACTH was 9.8 (1.5) pmol/L baseline and again 8.8 (2.2) pmol/L at 1 month (P = NS). For 9 patients, hormonal parameters were available after 1 week of treatment. In this case, also ACTH levels were significantly decreased (from 9.6 (1.7) to 5.2 (1.3) pmol/L; P < 0.01) together with urinary cortisol (from 781 (194) to 372 (165) nmol/d; P < 0.01). Long-term response: in 3 patients, hormonal parameters failed to respond to serotonin receptor antagonists, which were thus discontinued. An improvement was recorded in the remaining 8 patients, that was prolonged in 3, and transient in 5. In 3 of these latter patients, a marked increase of ACTH was observed before treatment discontinuation. Ketanserin was given to 2 patients with Nelson's syndrome, with only transient ACTH decrease in one, and no changes in ACTH response to CRH after 1 month treatment in both cases. An inhibitory effect of ritanserin and ketanserin on ACTH and cortisol production in Cushing's disease appeared to be limited both in terms of duration of response and number of patients with a satisfactory outcome. However, the results may provide a better understanding of serotonergic modulation in Cushing's disease and lead to therapeutic developments.

Adolescent↗
PubMed2000

New perspectives for gene therapy in endocrinology.

Gene therapy for endocrine diseases represents an exciting new type of molecular intervention that may be a curative one. Endocrine disorders that might be treated by gene therapy include monogenic diseases, such as GH deficiency and hypothalamic diabetes insipidus, and multifactorial diseases, such as diabetes mellitus, obesity and cancer. Premises seem promising for endocrine tumours, but many combined approaches of cell and gene therapy are foreseeable also for other endocrine disorders. This review outlines the principles of gene therapy, describes the endocrine disorders that might take advantage of gene transfer approaches, as well as the gene therapy interventions that have already been attempted, their major limitations and the problems that remain to be solved.

Animals↗
PubMed2000

Diagnosis and management of adrenal incidentalomas.

PURPOSE: The incidental discovery of adrenal masses has become a common clinical problem. We address current trends in clinical, endocrine, radiological and scintigraphic evaluation, and strategies for management of adrenal masses. A diagnostic and therapeutic algorithm is suggested. MATERIALS AND METHODS: A comprehensive review of the literature was performed using MEDLINE, bibliographies of select articles, current issues of peer reviewed general medicine, endocrinology, diagnostic imaging and surgical journals, and meeting abstracts of recent international congresses. RESULTS: Most adrenal incidentalomas are benign and nonhypersecreting but all should be evaluated to exclude from diagnosis hypersecretory syndromes or malignancy. In all cases hormonal screening for pheochromocytoma, hyperaldosteronism and subclinical hypercortisolism should be performed. Attenuation values on computerized tomography, chemical shift magnetic resonance imaging and scintigraphy reveal the nature of the mass in most cases. Fine needle aspiration biopsy should be reserved for cases suspected of extra-adrenal malignancy. CONCLUSIONS: A multidisciplinary approach, including hormonal screening, radiological evaluation and scintigraphy, is required to identify and remove adrenal masses with endocrine and oncological morbidity. Long-term morphofunctional followup is suggested for nonoperated cases.

Adrenal Gland Diseases↗
PubMed1999

Medical therapy for Cushing's disease.

Various drugs have been employed in the management of pituitary-dependent Cushing's disease. The neuromodulatory compounds used thus far have demonstrated true clinical efficacy only occasionally when employed as sole treatment. Steroid synthesis inhibitors are effective in the majority of cases in a dose-dependent manner. By their ability to correct hypercortisolism and its severe complications quickly, they are suitable for critical cases and in preparation for surgery. The clinical experience with the only glucocorticoid receptor antagonist that can be administered to humans is still too limited to assess its therapeutic validity. No medical strategy can be standardized for this complex condition. Different therapeutic tools should be selected according to the form of disease to be treated (hypothalamic/pituitary) and the peculiar clinical situation of each patient. Combined treatments may achieve better therapeutic efficacy.

Adrenal Glands↗
PubMed1999

Abnormalities of von Willebrand factor are also part of the prothrombotic state of Cushing's syndrome.

Glucocorticoids are known to increase plasma concentrations of factor VIII (FVIII) and von Willebrand factor (vWF), and their administration is associated with an increased incidence of thrombotic complications. Because Cushing's syndrome is characterized by an endogenous increase in glucocorticoids, we studied levels of FVIII and vWF in 20 patients with Cushing's syndrome. Plasma levels of FVIII and vWF were found to be markedly increased. Moreover, the molecular organization of plasma vWF appeared to have been altered by the presence of unusually large multimers, normally present only in the cellular compartments. Spontaneous platelet aggregation and hyperresponsiveness to ristocetin were also observed. All patients underwent therapeutic surgery. Within 1 month of the intervention, regardless of its efficacy as evaluated by the assay of plasma and urinary cortisol, an additional significant increase in levels of FVIII and vWF was observed, with a concomitant more pronounced representation of abnormally large vWF multimers in circulation. In the cured patients, a progressive decrease in the levels of FVIII and vWF was observed, beginning in the third month after surgery, with complete normalization of the pattern within 12 months of surgery; a concomitant improvement in the plasma vWF multimer pattern was also observed. In contrast, no significant changes in FVIII or vWF were found in patients with persistent Cushing's syndrome. Our findings emphasize that vWF abnormalities are also part of the prothrombotic state of Cushing's syndrome. Moreover, this study also identified a period of additional thrombotic risk immediately after surgery, as a result of the worsening of the hemostatic pattern.

Adolescent↗
PubMed1999

Slow-release lanreotide treatment in acromegaly: effects on quality of life.

BACKGROUND: It is not known whether medical treatment to lower growth hormone (GH) and insulin-like growth factor (IGF)-1 levels may improve the compromised quality of life of patients with acromegaly. METHODS: We studied the effects on quality of life of the slow-release somatostatin analogue lanreotide, 30 mg i.m., every 14 days for 2 months in 10 patients with active acromegaly (8 females/2 males, mean age 57.3 +/- 11.4). Hormone measurements and psychometric evaluation by means of self-rating scales were carried out in baseline conditions and after 1 and 2 months. The Symptom Questionnaire (SQ), the Cognitive Scale of the Screening List for Psychosocial Problems by Kellner and the Social Situation Questionnaire by Marks were employed. RESULTS: Together with a significant decrease in GH and IGF-1, treatment with lanreotide significantly improved SQ psychological distress, SQ well-being and Social Situation Questionnaire social fears. CONCLUSION: Medical treatment with lanreotide may improve the quality of life of patients with acromegaly. Being an open trial, changes could be due to nonspecific effects. However, they did not fade at 2 months. Improvement involved fears of social situations that have been linked to GH abnormalities.

Acromegaly↗
PubMed1999

Corticotropin-releasing effect of hexarelin, a peptidyl GH secretagogue, in normal subjects pretreated with metyrapone or RU-486, a glucocorticoid receptor antagonist, and in patients with Addison's disease.

GH secretagogues (GHS) are peptidyl and nonpeptidyl molecules which possess strong GH-releasing activity but also stimulatory effect on hypothalamo-pituitary-adrenal axis. The ACTH and cortisol responses to Hexarelin (HEX), a peptidyl GHS, are abolished by low-dose dexamethasone pretreatment in normal subjects but are exaggerated and higher than those after hCRH in patients with pituitary ACTH-dependent Cushing's disease, in spite of their hypercortisolism. Based on the foregoing, we studied the ACTH, cortisol and GH responses to HEX (2.0 microgram/kg i.v. at 0 min) alone and after metyrapone (2 g p.o. at 23:00 h the night before) or RU-486 (400 mg p.o. at 02:00 h), a glucocorticoid receptor antagonist, in 6 normal women (NS, age 26-34 years). The endocrine responses (mean +/- SEM) to HEX alone were also studied in 8 patients with Addison's disease (AD, 6 males, 2 females, age 30-77 years; last hydrocortisone administration the day before testing). In NS, HEX stimulated basal ACTH (peak, mean +/- SEM: 26.0 +/- 7.8 vs. 10.7 +/- 2.0 pg/ml, p < 0. 05), cortisol (163.2 +/- 18.3 vs. 137.4 +/- 15.4 microgram/l, p < 0.05) and GH (72.6 +/- 23.5 vs. 3.7 +/- 1.3 microgram/l, p < 0.01) levels. Metyrapone markedly increased basal ACTH (294.4 +/- 61.6 pg/ml, p < 0.05), reduced basal cortisol (19.6 +/- 7.2 microgram/l, p < 0.05), while it did not modify GH levels. After metyrapone pretreatment the ACTH response to HEX was clearly increased (DeltaAUC: 2,857.4 +/- 901.9 vs. 367.3 +/- 274.0 pg/ml/h, p < 0.05), while the GH response was not modified. HEX did not stimulate the low cortisol levels after metyrapone pretreatment. RU-486 significantly increased basal ACTH (76.6 +/- 12.5 pg/ml, p < 0.05) and cortisol (312.7 +/- 22.2 microgram/l, p < 0.05), while it did not modify basal GH levels. RU-486 pretreatment did not modify the ACTH, cortisol and GH responses to HEX. In AD, HEX elicited a marked ACTH response (6,619.4 +/- 3,365.8 pg/ml/h; p < 0.01), which was clearly higher (p < 0.01) than that in NS after HEX alone but not significantly different from that after HEX+MET. The GH response to HEX in AD (1,325.6 +/- 284.1 microgram/l/h) was similar to that in NS (1,519.7 +/- 483.8 microgram/l/h). In conclusion, our present data demonstrate that the ACTH-releasing activity of HEX is increased in primary hypoadrenalism as well as in normal subjects after metyrapone but not after RU-486 pretreatment. These findings indicate that in normal subjects as well as in hypocortisolemic patients the ACTH-releasing activity of GHS is enhanced by the lack of negative glucocorticoid feedback.

Addison Disease↗
PubMed1999

Mutations in CYP11B1 gene converting 11beta-hydroxylase into an aldosterone-producing enzyme are not present in aldosterone-producing adenomas.

In the human adrenal cortex, cortisol and aldosterone are synthesized by the isozymes 11beta-hydroxylase and aldosterone synthase, respectively, encoded by the 93% identical CYP11B1 and CYP11B2 genes. In vitro mutagenesis of CYP11B1 complementary DNA, resulting in the replacement of CYP11B1 codons by those encoding the corresponding amino acid residues of CYP11B2 enzyme (exon 5, Ser288Gly; exon 6, Val320Ala), yields a complementary DNA encoding a mutant enzyme with an efficient aldosterone synthase activity. Identical somatic mutations in the CYP11B1 gene in vivo would produce a gene encoding an enzyme with C18 activity and that would preserve ACTH responsiveness due to the retained 5'-promoter in the mutated CYP11B1 gene. An ACTH-responsive aldosterone synthase activity of this type is commonly seen in patients with aldosterone-producing adenomas (APA). We examined the occurrence of mutations in exons 5 and 6 of the CYP11B1 gene in APA from 10 patients with primary aldosteronism. Patients were selected on preoperative evidence of a 50% or greater plasma aldosterone decrease after short term dexamethasone trial and no aldosterone response to upright posture. DNA from adenomas was amplified by PCR using two pairs of primers spanning the regions of CYP11B1 gene, i.e. exons 3-5 and exons 6-9, where mutations could be located. Targeted regions were screened for mutations by automated sequencing of PCR products. No point mutations of the CYP11B1 gene over the two regions examined were found in APA. This argues against involvement of mutations in the pathogenesis of ACTH-responsive APA.

Adenoma↗
PubMed1999

Risk factors and long-term follow-up of adrenal incidentalomas.

The natural course of adrenal incidentalomas and the risk that such lesions evolve toward hormonal hypersecretion or malignancy are still under evaluation. Of 246 consecutive patients with adrenal incidentaloma studied at our institution in the last 15 yr, 91 underwent surgery. Of the remaining patients, a group of 75 (52 females and 23 males; median age, 56 yr; range, 19-77 yr) with incidentally discovered asymptomatic adrenal masses (60 unilateral and 15 bilateral; median diameter, 2.5 cm; range, 1.0-5.6) was enrolled in an endocrine and morphological follow-up of at least 2 yr after diagnosis (median, 4 yr; range, 2-10). During follow-up, no patients developed malignancy; 9 showed mass enlargement, with appearance of a new mass in the contralateral gland in 2; 3 developed adrenal hyperfunction (overt Cushing's syndrome in 2, nonclinical hypercortisolism in 1); and 3 showed adrenal mass enlargement associated with adrenal hyperfunction (nonclinical hypercortisolism in 2, pheochromocytoma in 1). The estimated cumulative risks to develop mass enlargement and hyperfunction were 8% and 4%, respectively, after 1 yr, 18% and 9.5% after 5 yr, and 22.8% and 9.5% after 10 yr. Nine risk factors for adrenal mass enlargement or hyperfunction were arbitrarily selected and evaluated: sex, age, presence of obesity, hypertension, diabetes, abnormal endocrine tests, mass size, mass location, and scintigraphic uptake pattern. Three of them attained statistical significance: mass size of 3 cm or more at diagnosis and exclusive radiocholesterol uptake by the mass at scintigraphy had relevance for the occurrence of adrenal hyperfunction, whereas the presence of endocrine test abnormalities at diagnosis had predictive value for mass enlargement. It is concluded that subtle hormonal abnormalities are risk factors for mass size increase, which is not a sign of malignant transformation. Both mass size of 3 cm or more at diagnosis and exclusive radiocholesterol uptake, indicating higher risks of hyperfunction, should be considered to plan a more thorough endocrine follow-up.

Adolescent↗
PubMed1999

Inactivation of the p16 tumor suppressor gene in adrenocortical tumors.

The mechanisms of adrenocortical tumorigenesis are still unknown. Evidence that the majority of adrenocortical tumors are monoclonal in origin suggests that a progressive accumulation of genetic aberrations, due to activation of protooncogenes and/or inactivation of tumor suppressor genes, leads to abnormal cell proliferation through a multistep process. Inactivation of the p16 tumor suppressor gene (p16INK4A), which encodes the cell cycle protein p16, was investigated in a series of 14 adrenocortical tumors. Using 11 polymorphic microsatellite markers spanning the short arm of chromosome 9, we demonstrated that three of seven adrenocortical carcinomas and one of seven adrenocortical adenomas had loss of heterozygosity (LOH) within chromosome 9p21, the region containing p16NK4A. Immunohistochemistry showed the absence of p16 nuclear staining in all adrenocortical tumors with LOH within 9p21, and positive staining in all remaining tumors without LOH. In conclusion, LOH within 9p21 associated with lack of p16 expression occurs in a considerable proportion of adrenocortical malignant tumors, but is rare in adenomas. Inactivation of p16INK4A may contribute to the deregulation of cell proliferation in this neoplastic disease.

Adrenal Cortex Neoplasms↗
PubMed1999

Regression of cardiac abnormalities after replacement therapy in Addison's disease.

OBJECTIVE: To evaluate by echocardiography the cardiac structure and function in patients with primary adrenocortical insufficiency. DESIGN AND METHODS: Two-dimensionally guided M-mode echocardiograms and spectral Doppler studies were performed in seven consecutive patients with newly diagnosed autoimmune primary adrenal failure before and 4-8 months after an adequate regimen of steroid substitution. Echocardiographic parameters were also studied in ten healthy controls. RESULTS: In the cases with untreated Addison's disease, both left ventricular end-systolic and end-diastolic dimensions were significantly reduced in comparison with those in controls (P<0.01). Four patients had echocardiographic signs of mitral valve prolapse (MVP) at the anterior leaflet, with no evidence of mitral regurgitation by Doppler echocardiography. Systolic clicks characteristic of MVP were present on auscultation in two of these cases. Left ventricular chamber size normalized, i.e. significantly increased (P<0.01), and both echocardiographic and physical signs of MVP resolved after steroid substitution in all patients. All other echocardiographic indices were normal before and after treatment. CONCLUSIONS: Patients with untreated Addison's disease have cardiac abnormalities which regress after steroid substitution. A valvular-ventricular disproportion due to the hypovolemic state could explain these findings.

Addison Disease↗
PubMed1998

Effect of octreotide on 24-h blood pressure profile in acromegaly.

The aim of the study was to investigate the effect of octreotide, a somatostatin analog drug potentially able to inhibit growth hormone (GH), on the circadian blood pressure profile in a group of patients with acromegaly. Ten patients with GH-secreting pituitary adenoma were studied before and 6 months after treatment with subcutaneous octreotide 0.2 to 0.6 mg/day. Twenty-four hour blood pressure and heart rate were measured every 15 min at daytime (07:00 to 22:59) and every 30 min at nighttime (23:00 to 06:59) using a TM-2420 recorder. No correlation was found between GH levels and 24-h blood pressure in baseline conditions. Untreated patients had a significant nocturnal decrease of both systolic and diastolic blood pressure (P < .01), and all showed a circadian systolic or diastolic blood pressure rhythm. During octreotide treatment, 24 h as well as nighttime systolic and diastolic blood pressures significantly increased (P < .05), whereas daytime systolic and diastolic blood pressures did not change. Treated patients did not have a nocturnal decline in both systolic and diastolic blood pressures (P = NS), and eight lost their systolic or diastolic blood pressure rhythm. In conclusion, blood pressure circadian rhythm seems to be maintained in acromegaly. Octreotide treatment is associated with an increase of 24-h and nighttime blood pressure, and with loss of circadian blood pressure rhythm. Splanchnic vasoconstriction by this drug, shifting blood to peripheral vessels, may explain this phenomenon.

Acromegaly↗
PubMed1998

Zona fasciculata-like histotype and aldosterone response to upright posture are not related in aldosterone-producing adenomas.

Two distinct subtypes of patients with primary aldosteronism due to aldosterone-producing adenomas (APA), based on different aldosterone responses to angiotensin, have been identified. We evaluated the relationship between adrenal zona fasciculata-like histotype and response of plasma aldosterone to upright posture in a series of patients with APA. Twenty-five patients were retrospectively divided in two groups according to aldosterone response to posture, i.e., a first group without postural change of aldosterone (n = 19) and a second group with at least 30% aldosterone increase after standing (n = 6). The percentage of zona fasciculata-like cells was calculated at histology in all adenoma tissues removed at adrenalectomy. The two groups of patients were similar in sex, age, systolic/diastolic blood pressure, supine/upright plasma renin activity, supine/upright aldosterone, tumor size. No differences between the two groups were observed as to zona fasciculata-like (84 +/- 3% vs 71 +/- 9%, P NS) and non-zona fasciculata-like cells percentage in adenoma tissues. No inverse correlation was found in either group between the percentage change from supine to upright aldosterone and the percentage of zona fasciculata-like cells. Aldosterone and cortisol responses to ACTH testing were similar in the two groups. Our results indicate that the two subtypes of primary aldosteronism based on different postural responses of aldosterone are not due to a different prevalence of zona fasciculata-like histotype in APA.

Adenoma↗
PubMed1998

Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates.

Hormonal and morphological data were investigated in 202 consecutive patients with adrenal incidentalomas (171 unilateral and 31 bilateral) in an attempt to assess subclinical hyperfunction or malignancy. In addition to the classical evaluation, scintiscan was carried out in a large number of these patients. In unilateral incidentalomas, 83% showed normal hormonal function, whereas 17% had biochemical signs of adrenal overactivity (hyperaldosteronism in 3, hypercortisolism in 17, medullary hyperfunction in 9). [75Se]Methylnorcholesterol scintigraphy depicted malignant, space-occupying lesions as decreased or absent radiotracer uptake by the mass, and cortical adenomas as increased or normal uptake. In cortical adenomas a relationship between radiocholesterol uptake and degree of functional autonomy was demonstrated. [123I]Metaiodobenzilguanidine scintiscan visualized 7 of 8 pheochromocytomas. In bilateral incidentalomas, abnormal adrenal function was more frequent, accounting for 29% of cases (hyperaldosteronism in 3, hypercortisolism in 3, adrenal insufficiency in 2, and congenital adrenal hyperplasia in 1). Malignant lesions were not scintigraphically visualized. [75Se]Methylnorcholesterol scan also provided functional information in the case of a cortisol-secreting adenoma and an aldosteronoma with a concomitant contralateral nonhypersecreting adenoma, showing the greatest uptake in the hyperfunctioning adenomas. In both unilateral and bilateral lesions, endocrine testing failed to differentiate benign from malignant tumors. Although hormonal assessment is mandatory to clarify the functional patterns, only morphofunctional examination by scintiscan seems to provide more data about the likelihood of malignancy.

17-alpha-Hydroxyprogesterone↗