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Suprarenal haematoma versus neuroblastoma complicated by haemorrhage. A diagnostic dilemma in the newborn.

Concomitant neonatal suprarenal haemorrhage and neuroblastoma is rare. The clinical and radiologic manifestations recorded in 11 patients with this entity are compared with the findings in 32 cases with simple adrenal haemorrhage. Because of the many similarities in presentation the combined lesion must always be considered when a neonate is found to have a retroperitoneal, extra-renal mass. Our present approach to the investigation includes conventional chest and abdominal radiography aimed to demonstrate possible paravertebral widening. Serial ultrasonographies are easy to carry out and indispensable. The low specificity of urography makes us refrain from this modality as a routine. Scintigraphy, in infants and children considered useful in demonstrating extent and spread of neuroblastoma, has hardly been employed in neonates. The true value of the modality in this particular age group remains to be settled. CT scanning does not seem to provide essential information additional to that of sonography and may therefore be excluded from the protocol. Determination of urinary excretion of catecholamine metabolites is of crucial significance and a compulsory part of the investigation.

Adrenal Gland Diseases↗
PubMed1995

Incidentally discovered adrenal masses.

Independently, endocrinology, radiology, and nuclear medicine can not optimally differentiate the etiology of the incidental adrenal mass. Rather, the insight necessary for this task must be contributed by all three disciplines. Incidentally discovered adrenal masses are being detected at an increasing rate. This trend is expected to continue based on the incidence of adrenal masses in autopsy series and the increasing use of high resolution abdominal imaging techniques. CT and MRI are able to definitely characterize only a minority of these lesions (simple cyst, myelolipoma, obvious local malignant invasion). Biochemical screening for hormone excess is essential regardless of a nonsuggestive complete history and physical examination. An argument may be made for not further pursuing nonhypersecreting lesions with the typical features of a benign adenoma on CT scan and an attenuation value of 0 HU or less. Adrenocortical scintigraphy is recommended in all patients with normal biochemical screening tests, especially those with CT attenuation values greater than 0 HU. In this setting, we believe that the functional and anatomical information provided by NP-59 and [75Se]selenomethylnorcholesterol scintigraphy allows one to noninvasively, accurately, and less expensively (Table 9) categorize adrenal masses as benign nonhypersecretory adenomas (the vast majority) vs. a possibly malignant lesion (the minority). In the presence of normal biochemistry, a concordant NP-59 imaging pattern is diagnostic of a nonhypersecretory benign adrenal adenoma and requires no immediate therapeutic intervention. Conversely, patients with discordant patterns of NP-59 scintigraphy have lesions that carry a significant risk for malignancy, and the pursuit of a tissue diagnosis is indicated, usually by means of FNA. Normal adrenocortical tissue on cytological studies in this setting may represent inadvertent sampling of adjacent normal adrenocortical tissues or the presence of a well differentiated adrenocortical carcinoma. In patients with lesions larger than 2 cm in whom NP-59 scintigraphy is nonlateralizing, the possibility of a periadrenal or pseudoadrenal mass is likely and should prompt review, or perhaps even repeat, of high resolution adrenal imaging (occasionally angiography may be helpful). In lesions shown to be 2 cm or less in size with a nonlateralizing NP-59-scan, there is a possibility of a periadrenal or pseudoadrenal mass; however, once this is excluded it must be recognized that benign and malignant lesions, because of the limitations of scintigraphy, cannot always be clearly distinguished by this method when masses are small.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Gland Diseases↗
PubMed2005

Development, maintenance, and function of the adrenal gland in early postnatal proopiomelanocortin-null mutant mice.

Adult mouse mutants homozygous for an engineered proopiomelanocortin (POMC)-null allele lack macroscopically distinct adrenal glands and circulating adrenal hormones. To understand the basis for this adrenal defect, we compared the development of adrenal primordia in POMC-null mice and littermate controls. POMC-null mutant mice are born with adrenal glands that are morphologically indistinguishable from those of their wild-type littermates. However, in mutants adrenal cells fail to proliferate postnatally and adrenals atrophy until they have disappeared macroscopically in the adult. While present, mutant adrenals are differentiated as evidenced by the presence of enzymes for the final steps in the synthesis of corticosterone, aldosterone, and catecholamines. However, in contrast to adrenals of wild-type littermates, adrenals of POMC-null mutants do not produce corticosterone, not even in response to acute stimulation with exogenous ACTH. They do produce aldosterone; however, it is produced at reduced levels correlating with adrenal size. Transplantation of POMC-null mutant adrenals to adrenalectomized wild-type littermates results in adrenals with normal morphology and production of both corticosterone and aldosterone. These findings demonstrate that POMC peptides are not required for prenatal adrenal development and that POMC peptides in addition to ACTH are required for postnatal proliferation and maintenance of adrenal structures capable of producing both glucocorticoids and mineralocorticoids.

Adrenal Gland Diseases↗
PubMed1985

Sympathetic adrenal denervation decreases adrenal blood flow without altering the cortisol response to hemorrhage.

To test whether or not adrenal sympathetic innervation is required for the adrenocortical response to small hemorrhage, awake dogs were studied after unilateral adrenal sympathetic denervation. Bilateral adrenal vein cannulas were placed chronically to permit measurement of cortisol, epinephrine, and norepinephrine secretion rates and adrenal blood flow simultaneously from the intact and the denervated adrenal. Plasma ACTH concentration was measured and the presentation rate of ACTH was calculated as the product of plasma ACTH concentration and adrenal plasma flow. Unilateral isolation of the sympathetic chain from the spinal cord at thoracic levels 9-12 (T9-12) had no effect on adrenal blood flow, on the presentation rate of ACTH, or on cortisol secretion after 10 mg/kg hemorrhage. However, thoracic levels 9-12 denervation prevented the secretory response of catecholamines to hemorrhage without lowering basal catecholamine secretion. Unilateral splanchnicotomy, the sectioning of the thoracic and upper lumbar splanchnic nerves, reduced adrenal blood flow and the presentation rate of ACTH, suppressed basal catecholamine secretion, and prevented the catecholamine response to hemorrhage. However, there was no reduction in the secretory response of cortisol to 10% or 20% hemorrhage. These findings suggest that in the absence of sympathetic innervation to the adrenal, increases in adrenal sensitivity to ACTH occur to offset decreased ACTH presentation rate resulting in a normal cortisol response to hemorrhage. However, adrenal sensitivity to exogenous ACTH was not increased in non-hemorrhaged dogs after unilateral splanchnicotomy. Thus, hemorrhage must activate a non-ACTH mechanism that is independent of sympathetic adrenal innervation to augment adrenal sensitivity to ACTH. Sympathetic innervation to the adrenal has profound effects on catecholamine secretion and on adrenal blood flow but is not required for the secretory response of cortisol to small hemorrhage.

Adrenal Gland Diseases↗
PubMed2002

Eutopic overexpression of vasopressin v1a receptor in adrenocorticotropin-independent macronodular adrenal hyperplasia.

Arginine vasopressin (AVP) stimulates cortisol secretion through its vascular type V(1a) receptor in the adrenal glands, in addition to stimulating ACTH secretion through pituitary V(3) receptor. Because hyper-response of plasma cortisol to vasopressin is documented in some patients with Cushing's syndrome due to adrenal adenoma (CS) or ACTH-independent macronodular adrenocortical hyperplasia (AIMAH), we analyzed the expression of V(1a), V(2), V(3) receptor and AVP mRNA in human adrenal tissues by quantitative competitive RT-PCR or real-time PCRs. V(1a) receptor mRNA levels (ratio against glyceraldehyde 3-phosphate dehydrogenase) were 0.378 +/- 0.143 (mean +/- SE) in preclinical CS (n = 5) and 0.630 +/- 0.072 in AIMAH (n = 4), which were significantly higher than those (0.046 +/- 0.012; n = 9) in control adrenals, whereas those in overt CS (0.143 +/- 0.048; n = 10) or aldosterone-producing adenomas (0.069 +/- 0.018; n = 12) were similar to control adrenals. Although ectopic expression of V(2) or V(3) receptor was detected in half of AIMAH cases, the absolute levels were low. Furthermore, V(1a) receptor mRNA levels in the adjacent adrenal glands (0.190 +/- 0.039, n = 9) of aldosterone-producing adenomas were higher than those in control adrenals and in the corresponding tumor portions (0.079 +/- 0.024). In contrast, there were no significant differences in AVP mRNA levels among these groups. These results suggest that eutopic V(1a) receptor overexpression is involved in the etiology of AIMAH and a subset of adrenal adenomas causing overt or preclinical Cushing's syndrome. Our results imply a possible association of V(1a) receptor expression with adrenal hyperplasia.

Adrenal Gland Diseases↗
PubMed2003

Overexpression of serotonin4 receptors in cisapride-responsive adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia causing Cushing's syndrome.

The serotonin4 (5-HT4) receptor agonists cisapride and/or metoclopramide have been shown to stimulate cortisol secretion in some patients with ACTH-independent bilateral macronodular adrenal hyperplasias (AIMAH) causing Cushing's syndrome. In the present study, we have investigated quantitatively and qualitatively the expression of the 5-HT4 receptor in both normal adrenal cortex and tissues removed from six patients (P1-P6) with cisapride-responsive AIMAH and Cushing's syndrome. Real-time quantitative PCR assay revealed that the 5-HT4 receptor was overexpressed in four of the six hyperplasias studied when compared with normal adrenal cortex. In these tissues, 5-HT4 receptor mRNA expression was 3 to 16 times higher than in normal glands, likely explaining the abnormal in vivo cortisol response to cisapride. Characterization of 5-HT4 receptor splice variants by RT-PCR in both hyperplastic and normal adrenals showed that the variants present in the two hyperplasias that did not overexpress the 5-HT4 receptor, i.e. P2 and P5, could also be detected in the normal adrenal tissue. In addition, sequencing of the full-length cDNAs encoding 5-HT4 receptors in hyperplasias P2 and P5 did not reveal any mutation. Taken together, our results show an overexpression of the 5-HT4 receptor in cisapride-responsive AIMAH. However, in two cases, the level of expression of the receptor in the hyperplastic adrenal cortex was similar to that of normal adrenal gland. The enhanced sensitivity of these two tissues to 5-HT4 receptor agonists was not due to ectopic expression of 5-HT4 receptor isoforms or to the occurrence of somatic gain-of-function mutation of the receptor.

Adrenal Gland Diseases↗
PubMed2003

Virilization in bilateral macronodular adrenal hyperplasia controlled by luteinizing hormone.

We report a case of a virilized 59-yr-old woman with elevated serum testosterone levels and bilateral macronodular adrenal hyperplasia. The patient underwent laparoscopic right adrenalectomy, after which the elevated testosterone level transiently normalized. The immediate postoperative depression of the testosterone level suggested that the process was driven by gonadotropins that were suppressed by the stress of surgery. The excised right adrenal mass contained testosterone by immunohistochemistry and LH receptor mRNA by in situ hybridization. The recurrence of hyperandrogenemia suggested that the enlarged left adrenal was also secreting testosterone. The serum testosterone level increased in response to im injection of human chorionic gonadotropin, suggesting control by aberrant LH receptors. Injection of leuprolide acetate (7.5 mg im) to suppress LH levels resulted in normalization of the testosterone level 12 d later that persisted for several weeks. Ectopic receptors mediating Cushing's syndrome have been described in several cases of bilateral adrenal hyperplasia and adrenal adenoma. This is the first case to our knowledge in which pure androgen overproduction in adrenal hyperplasia has been shown to be controlled by LH receptors. In our patient, the control of androgen secretion by LH may explain the postmenopausal onset of virilization and the transient postoperative normalization of the serum testosterone level.

Adrenal Gland Diseases↗