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Purpose The aim of the study was to examine subjective health-related quality of life (HRQoL) in patients undergoing adrenalectomy. Methods The study included patients scheduled for adrenalectomy 2014–2017 after giving informed consent. The SF-36 questionnaire was administrated before operation and 1 year postoperatively. Results were compared with published normative values in Sweden. Results Some 50 patients were included. SF-36 scores for the whole cohort improved significantly after adrenalectomy in all dimensions except for bodily pain. Compared with the general Swedish population, the patients reported a significantly reduced HRQoL before and after adrenalectomy in all domains except for bodily pain postoperatively. Patients with benign functional tumours had lower HRQoL in physical domains before adrenalectomy than patients with benign non-functional tumours; Physical Component Summary (PCS), median 33.1 (range 17.1–62.9) vs. 44.2 (20.0–66.5), p = 0.018. Postoperatively, HRQoL was similar in the two groups of patients. Patients with benign functional tumours reported significantly improved HRQoL in all dimensions after adrenalectomy: PCS 33.1 (17.1–62.9) preoperatively vs. 47.6 (19.8-57.3) postoperatively, p = 0.005; Mental Component Summary (MCS) 33.8 (11.8–62.0) preoperatively vs. 52.7 (16.4–59.8) postoperatively, p = 0.004. These improvements were not seen in patients with benign non-functional or malignant tumours. Patients with malignant tumours reported no difference in SF-36 scores before or after adrenalectomy compared with patients with benign non-functional tumours. Conclusions Adrenalectomy improved HRQoL in patients with benign functional tumours. Adrenalectomy did not improve HRQoL in patients with benign non-functional tumours or in patients with malignant tumours.

Background Evaluating the patient with adrenal disease is challenging due to the lack of precise clinical and biochemical parameters for disease control. Quality of life (QOL) evaluation aims to measure the patient's subjective experience. Objective To describe how QOL is defined and measured in adrenal disease, critically appraise the use of QOL tools in published literature, discuss the implications of these findings and provide direction for further research in this field. Materials and methods We searched the Cochrane library, EMBASE, Google Scholar, PsycINFO, PubMed, Web of Science databases to identify only primary studies where self-reported QOL was measured as a parameter in adults with confirmed adrenal disease, and results presented in English. Key data were independently extracted from each study and adherence to reporting guidelines evaluated. Results A total of 117 studies involving 13 717 subjects were included. The vast majority of studies did not define QOL. The most common approach was to combine generic and domain-specific tools, although disease-specific tools are increasingly being used. Adherence to reporting guidelines was variable. A narrative synthesis of the findings was performed. Conclusion We present the first systematic review of QOL in adrenal disease. Quality of life is reduced in patients with adrenal disease, irrespective of adrenal hyperfunction or hypofunction. Quality of life improved with therapy but was not completely reversed despite biochemical remission. Authors should adhere to consistent reporting practices which are interpretable by clinicians. Further research is required to explain the mechanisms driving impaired QOL and value of QOL evaluations in the clinical context.

Growth is disturbed by adrenal hypersecretion of androgens or cortisol. Androgen excess in virilizing adrenal tumours causes advanced growth and bone age. In 9 girls with virilizing tumours, mean heights at diagnosis and final heights were 1.23 ± 0.42 and 1.3 ± 0.37 SDS respectively. In poorly controlled CAH, excess androgens cause early epiphyseal fusion and adult short stature. Increased growth occurs only after 18 months of age, even in untreated CAH, i.e. hydrocortisone >10 mg/m2/day is not generally required and may suppress infantile growth, affecting childhood and adult height. Growth was studied in 19 patients, aged 6.4–17.8 years, with Cushing’s disease (CD). At diagnosis, mean height SDS was –1.81 (1.2 to –4.17), 53% < –1.8 SDS, height velocity in 6 was 0.9–3.8 cm/year and mean BMI SDS 2.29 (0.7–5.06). From 1983 to 2001, CD was cured in 18 patients (61%) by transsphenoidal surgery (TSS) alone and 39% by TSS plus pituitary irradiation (RT). In 13 patients, growth hormone (GH) was assessed by ITT/glucagons at 1–108 months after cure. Four had severe GH deficiency (30 mU/l) GH status. Subnormal GH was present in 7 subjects >2 years after TSS or RT cure. In 10 subjects, aged 12.9 ± 3.4 years, growth after cure was studied for 9.1 ± 5.0 years. Nine had no catch-up growth in the interval of 0.3–1.1 years after cure (mean HV 5.3 ± 2.4 cm/year). All these had GH deficiency peak GH 0.5–20.9 mU/l, and received hGH 2.7 mg/m2/week, 3 with GnRHa. All 10 showed long-term catch-up growth with mean delta SDS at diagnosis (Ht SDS–target Ht SDS) –1.72 ± 1.26 improving to –0.83 ± 1.08 (p = 0.0005) at latest of final Ht. At diagnosis, virilization was present in 82% of 17 patients with CD. Mean SDS values of serum androstenedione, DHEA-S and testosterone were normal, i.e. 0.72 (–2.9 to 3.0), –0.8 (6.0 to 2.2), 0.7 (–7.9 to 9.5) respectively, whereas SHBG was reduced at –2.1 (–5.3 to 1.2), increasing free androgen levels. Bone age (BA) was delayed (mean 1.46 years) in 14/16 patients, suggesting cortisol excess contributed more then androgen effect to skeletal maturation. In conclusion, most paediatric patients with CD had subnormal linear growth with delayed BA. After cure by TSS or pituitary irradiation, GH deficiency was frequent and persisted for many years. Treatment with hGH induced significant long-term catch-up growth leading to reasonable final height.

Introduction: The traditional approach for adrenalectomy in children has been the transperitoneal technique. In adults, the posterior retroperitoneoscopic (PR) approach has been promoted.1...

OBJECTIVE To determine the clinical outcomes and follow-up imaging characteristics for incidentally discovered adrenal nodules at a large metropolitan health care center, as well as compliance with National Institutes of Health guidelines for the evaluation of these lesions. METHODS Between October 2003 and June 2005, computed tomographic (CT) scanning performed at Harvard Vanguard Medical Associates detected 165 adrenal nodules (incidentalomas) in 129 patients without extra-adrenal malignant lesions or evidence of adrenal hyperfunction. Nodule characteristics, including size at baseline, change in size at follow-up, CT attenuation values, biochemical data, and clinical outcomes, were analyzed. RESULTS Of the 165 adrenal incidentalomas, 96% were smaller than 4 cm. When attenuation values were determined, 65% were low (

Hypotensive drug tolerance and liver monooxygenase activity were investigated in 24 refractory arterial hypertension patients before and after surgical suppression of adrenal hyperfunction. Liver monooxygenase activity was studied using antipyrine test. It was found that hypotensive drug tolerance was decreased after one and two side operations on adrenal glands. In parallels halftime of antipyrine elimination was shown to be prolonged by 88.5% in 3 months - 3 years after suppression of adrenal hyperfunction. Our findings suggest that the hypotensive drug tolerance diminution may be the consequence of liver monooxygenase activity reduction. This assumption is in accordance with well known the hypotensive drug metabolism by microsomal liver monooxygenases

Primary aldosteronism is a relatively common cause of secondary hypertension. It is often important to diagnose this disease accurately, since appropriate surgical therapy may result in cure of the disease. Assessment of the laterality of adrenal hyperfunction is possible using adrenal venous sampling of steroid hormones, but this procedure may not be feasible in patients with allergy to iodinated radiocontrast agents. In this paper, we report a patient with primary aldosteronism who was found to have bilateral adrenal tumors on CT. Because preoperative localization of the hyperfunctioning tumor was important, adrenal venous sampling and venography was performed by a highly-experienced radiologist using the MRI contrast agent gadolinium. After reviewing the data, the patient received a right adrenalectomy. This case report demonstrates that it was possible to perform adrenal venography using gadolinium in this patient, however the safety and efficacy should be re-assessed in individual cases.

A patient with an apparent abnormality of cortisol binding globulin (CBG) is reported. Investigations showed that while the plasma CBG binding capacity (equivalent to the plasma CBG concentration) was normal, the binding affinity was reduced by a factor of four. The significance of this observation is discussed with regard to its possible role in the development of the adrenocortical hyperfunction also seen in this patient.

Serum corticosterone concentrations were measured to see if there was any correlation between adrenal activity and reproductive inhibition. Males and females from two growing and one stable (asymptotic) population had significantly smaller reproductive organs (seminal vesicles, testes, uteri, ovaries) than controls. The weights of the adrenal glands of population mice were smaller, often significantly so, than those of controls, but the mean serum corticosterone concentrations were higher than those of control mice for the two growing populations and significantly higher for the asymptotic population. These data suggest that adrenal function may be associated with the reproductively inhibited condition, but not in a direct or dose-response fashion and that adrenal hyperfunction in this species may not be reflected by adrenal hypertrophy.

A 6-year-old girl with lymphosarcoma developed Cushing's syndrome. Suppression-stimulation studies verified adrenal hyperfunction secondary to bilateral adrenocortical hyperplasia, and the course suggested the possibility of "ectopic ACTH" production by the neoplasm as the etiology.

Monosodium glutamate (MSG) has been shown to alter several neuroendocrine functions in neonatally treated rats. To evaluate for possible alterations in the hypothalamic-pituitary-adrenal axis, we injected rats during the neonatal period with MSG or saline (controls). An increase in basal plasma corticosterone levels associated with a blunted circadian variation was observed. Ether exposure produced a significant elevation in plasma corticosterone concentration in both groups of animals. However, while the increase in controls was 181.3% for male and 193.9% for female rats, in the MSG-treated rats it was only 60.7 and 31.6%, respectively. The intraperitoneal administration of high dexamethasone doses blocked corticosterone secretion in both groups. However, whereas the lowest dose (0.10 microgram/kg) suppressed corticosterone secretion in control animals, it was ineffective in MSG-treated rats. The morphological study of adrenals revealed signs of a hyperfunctional state in MSG-treated rats. These data suggest that the central lesions produced by MSG treatment disrupt the regulation of the hypothalamic-pituitary-adrenal axis.

An eighteen year old girl had clinical and laboratory evidence of hyperaldosteronism without an adrenal tumor or obvious adrenal hyperplasia. It is suggested this represents a distinctive form of congenital adrenal hyperfunction. The administration of ACTH led to increased aldosterone excretion and simultaneous sodium retention. Subtotal adrenalectomy after preoperative preparation with potassium resulted in correction of the abnormalities.

With the use of 6 male rabbits weighing from 2, 500 to 3, 000 grams that were subjected daily for 2 hours to an inhalation of sulfur dioxide of 100 ppm a 6-month tracing of variations in the amounts of chlorine, sodium, potassium and calcium in their sera was made and the following results were obtained. 1) Conspicuous changes were observed in the amounts of serum sodium and potassium, while such changes were not noted in the amounts of chlorine and calcium. Sodium displayed a remarkable reduction on the 7th day of the inhalation of sulfur dioxide showing 84.7% of the preinhalation value. Then, an increase was seen with a maximal value on the 21st day, reaching 139.4% of the preinhalation value. Thereafter, comparatively high values were shown until the 90th day with a subsequent decline, though the value was not lower than that of the preinhalation period. Potassium decreased down to 74.7% of the preinhalation value on the 7th day and the value remained between 59.5 and 75.3% of the preinhalation value throughout the subsequent course. 2) Variations in the amounts of chlorine, sodium, potassium, and calcium in the sera of rabbits exposed daily to sulfur dioxide of low concentrations showed almost the same tendency as in the case of refiners in Matsuo Mine described in Part I, bearing probable effects due to variations in adrenal hyperfunction.

For an analysis of the effect of the tumor metabolites upon the organism of the tumor-bearing animal, correlation and kinetics of unspecific changes in some organs, such as thymus, adrenals, and liver

Dr. Findley reviewed his previous studies in which salt hyperexcretion in hypertension followed the pattern seen in adrenal hyperfunction and reemphasized the evidence for an unusual cellular change in the anterior pituitary gland in renal and renoprival hypertension. He reviewed work in progress in which he is attempting to reproduce Skelton's type of adrenal regeneration hypertension in dogs and puppies. Dr. Tobian reviewed the current status of his studies on electrolyte changes in the tissues in animals made hypertensive by various technics.

Ruder syndrome is an unusual varient of adrenal hyperfunction characterized clinically by debilitating osteopenia, and pathologically by bilateral micronodular adrenal hyperplasia. A unique case resembling Ruder syndrome is described in which the dominant pathologic feature was unilateral adrenal adenomatosis.

Hyperfunctioning non-neoplastic adrenal glands may be associated with Cushing's syndrome, congenital adrenal hyperplasia, and aldosteronism. The problems in radiographic diagnosis may be resolved by correlation of the angiogram with the clinical and laboratory findings.

A patient with active Cushing's disease who became pregnant following treatment with cyproheptadine is described. Despite stopping the cyproheptadine treatment at 3 mth gestation, the previous amelioration of the clinical and biochemical features of the adrenal hyperfunction was maintained and the pregnancy progressed satisfactorily. Moreover, serial evaluation of maternal glucose tolerance proved to be normal and it is suggested that this matabolic aspect is an important determinant in the outcome of pregnancies occurring in patients with Cushing's syndrome.

The plasma-hydrocortisone response following the administration of synthetic lysine-8-vasopressin (L.V.P.) was measured in 5 patients with Cushing's syndrome. By this means a pituitary origin of this condition could be differentiated from other causes of adrenal hyperfunction.

The purposes of surgery of the human adrenal glands are to remove neoplasms of these structures or to abolish functional activities which are deleterious to the organism; both conditions may be coeval. The principle of abolition of dangerous physiological functions of the adrenals, of course, is the opposite to stimulation of these glands by a corticotrophic agent, for example, corticotrophin (ACTH). There are several clear indications for the removal of nonneoplastic adrenals at present; no doubt more will be found, and the subject will assume greater importance. Frequently disease conditions caused by adrenal hyperfunction or those mediated through normal activity of these glands can be cured or alleviated by surgical procedures, with impressive results. Adrenal surgery is now in a fast-moving evolutionary stage. Recently there have been four major developments in this area. These are (a) methods of maintenance of life in the absence of the adrenal glands or in

Six women with atypical forms of adrenal cortical hyperfunction were studied by means of urinary excretion of 17-ketosteroids and 17-hydroxycorticoids and their response to ACTH stimulation and corticosteroid suppression. Unusual responses were observed, particularly with respect to the independence of 17-KS and 17-OHCS excretion. The adrenals of 3 patients were anatomically normal whereas the others showed hyperplasia. Minced adrenal tissue was incubated with 4-14C progesterone and the metabolites isolated and definitively identified. The pattern of biosynthesized corticosteroids showed great variation, and in some instances clarified certain clinical features. The pattern of certain C19-metabolites could not be studied adequately because of the use of a Δ4 rather than a Δ5 substrate.

The variation in both the clinical and biochemical response to administered adrenal steroids or corticotropin suggests that naturally occurring adrenal hypercorticism might not always be manifested as fully developed Cushing's syndrome. Until recently, the diagnosis of adrenal hyperfunction depended for the most part on typical clinical findings, since analytical methods for the corticosteroids were not quantitatively reliable. Within the past few years newer methods of steroid analysis have been developed which permit a more accurate measure of cortical function. One of these procedures (1, 2) has been used extensively in the course of evaluating many patients with one or more of the features of Cushing's syndrome. Among these were patients with obesity, hirsutism, diabetes, osteoporosis or hypertension. The 2 patients who are the subject of this report were found to have cortical hyperfunction. Their appearance so belied Cushing's syndrome that the correct diagnosis had not been made by many competent o...

CLINICAL differentiation of active from inactive acromegaly is often difficult. At the present time a diagnosis of active disease is often based on the tenuous correlation of certain signs and symptoms and several inconsistent chemical indexes of growth-hormone excess. Of the latter, hyperphosphatemia is extremely variable, and often absent,1 and plasma growth-hormone assays have not shown consistent elevations in active cases.2 In a recent publication Hamwi et al.3 reported that adrenal function was normal in acromegaly. This conclusion was based on measurement of basal steroid excretion and the glucocorticoid response to ACTH. These workers, however, did not describe or comment . . .