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The problems associated with hyperandrogenism are not uncommon in primary care settings. In fact, polycystic ovary syndrome, a common cause of androgen excess, exists in 5% to 10% of women during their reproductive years, with onset typically in adolescence. The subject of this column is the AACE's Hyperandrogenism Guidelines, which review the evaluation and treatment of the disorders causing androgenic excess.
Blood neutrophil/lymphocyte ratio and plasma cortisol levels were measured before and after (1) the injection of adrenocorticotrophic hormone (ACTH1-24) in 8 Thoroughbreds and (2) exercise in 5 Thoroughbreds in training. Plasma cortisol levels were significantly (P less than 0.01) increased within 60 mins of injection of ACTH1-24 and immediately after exercise. The mean neutrophil/lymphocyte ratio altered significantly (P less than 0.01) at 240 mins after ACTH1-24 administration and at 180 mins after a training gallop. A transient lymphocytosis occurred following exercise.
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Adrenal responsiveness to angiotensin II (AII) and the diastolic blood pressure responses to saralasin were studied in 19 patients with high renin essential hypertension (HREH) on a 10-meq Na(+)/100 meq K(+) diet. The increment in plasma renin activity (PRA) between supine and upright positions was used as an estimate of the acute stimulation of the adrenal gland by endogenous AII; the normal increment in plasma aldosterone divided by the increment in PRA was >3.8. 7 of 19 had abnormal upright posture responses with significantly greater mean PRA increments (24+/-6 ng/ml per h) and significantly smaller plasma aldosterone increments 47 +/- 16 ng/dl) (P < 0.036) compared to the increments observed in HREH patients with normal adrenal responsiveness (PRA = 15 +/- 1 ng/ml per h; plasma aldosterone = 87 +/- 17 ng/dl). When AII was infused at doses of 0.1-3 ng/kg per min, only patients with normal posture responses had normal plasma aldosterone increments; plasma aldosterone levels failed to significantly increase even at the highest infusion rate in the patients with the abnormal upright posture responses. The AII competitive inhibitor, saralasin (0.3-30 mug/kg per min) was then infused to study the occurrence of angiotensinogenic hypertension in both HREH subgroups. The mean decline in diastolic blood pressure to saralasin in the subnormal adrenal responsive patients (-15 +/- 3 mm Hg) was significantly greater than in the normal adrenal responsive group (-3 +/- 2 mm Hg) (P < 0.02).It is concluded that patients with HREH are not a homogeneous population; approximately one-third have AII-dependent hypertension. In these patients, the mechanism responsible for the elevated renin and blood pressure could be a compensatory increase secondary to decreased adrenal responsiveness to AII. In the remainder, the high PRA levels have little, if any, causal role in the pathogenesis of the hypertension but could reflect a marker of other pathophysiologic processes.
Steroid use in critically ill, vasopressor-dependant, septic patients has gained increased acceptance in recent years with the publication of encouraging data. However, with renewed interest and/or attention comes increased debate and analysis. As a result, it is not surprising to find that there is still significant controversy with regards to the role of steroids in many patients. In this article, two expert groups debate the role of steroid use in a septic shock patient with arguably no clear evidence of adrenal insufficiency.
Etomidate is a potent suppressant of adrenal steroidogenesis,effectively inducing reversible pharmacological adrenalectomy. Recent evidence suggests that for every five patients with septic shock given etomidate without corticosteroid supplementation, one patient will die as a consequence. Other critically ill patients are also at possible risk, and this risk requires further exploration. Etomidate will also confound investigations into the effects of disease states on adrenal function, and should therefore be avoided. A moratorium on the use of etomidate in critically ill patients outside clinical trials may be prudent until its safety is established.
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The metabolic mechanism for increased circulating free fatty acids in post-menopausal women with metastatic breast cancer was investigated. Hormone and metabolic response to glucose and growth hormone were compared to cancer patients and control subjects; thyroid, adrenal and pituitary function were evaluated. The results of these studies indicated that breast cancer patients had glucose intolerance and delayed and prolonged insulin secretion, increased basal growth hormone levels and insensitivity of adipose tissue to growth hormone. Cortisol and protein-bound iodine levels were normal and there was no lipolytic factor in the sera of breast cancer patients. The changes observed in breast cancer patients were not attributable to age, obesity, inanition or stress. These metabolic abnormalities may characterize host susceptibility to breast cancer or be effects of tumor.
A 38-yr-old male presented with severe symptomatic osteopenia secondary to adrenal hyperfunction without any clinical expression of Cushing's syndrome. The predominantly axial distribution of his osteopenia and the presence of rib fractures healing with abundant callus formation, despite insignificant elevations in serum alkaline phosphatase, were characteristic of glucocorticoid excess syndromes. The histological features of the pretreatment bone biopsy were typical of those associated with excess glucocorticoids, namely decreased quantities of nonmineralized bone matrix, reflecting sites of bone formation, and an increase in the number of osteoclasts, indicating enhanced bone resorption. Six weeks after adrenalectomy, repeat bone biopsy revealed a marked increase in bone matrix synthesis and a significant decrease in bone resorption. These observations suggest that stimulators of skeletal turnover, like sodium fluoride, may be inappropriate in the initial treatment of steroid-induced osteopenia after surgical cure and that vitamin D and calcium therapy offers a more rational approach. Furthermore, the importance of the routine evaluation of adrenal function in any patient presenting with osteopenia is stressed, as well as the fact that relatively isolated skeletal involvement, classically described in micronodular adrenal disease, is not necessarily peculiar to a specific subset of the syndrome but may potentially attend any cause of glucocorticoid excess.
The alpha ACTH-(1-24) threshold dose and the response slope were determined for cortisol (F), delta 4-androstenedione (A), and dehydroepiandrosterone (DHEA) in 10 normal and 16 obese eumenorrheic nonhirsute women matched for age. Each woman received 1 mg dexamethasone at 2300 h and again at 0700 h the next morning. At 0700 h, a continuous alpha ACTH-(1-24) infusion was begun at an initial dose of 30 ng/1.5 m2 body surface area X hr. The ACTH infusion rate was doubled every hour for 5 consecutive h to a maximum dose of 480 ng/1.5 m2 X h. Blood samples were collected for steroid assays before the infusion and at the end of each hour. The ACTH threshold dose was defined as the dose that produced a steroid response significantly above the basal level. The ACTH threshold dose for serum F and DHEA stimulation was not different between the groups, but the threshold dose for A was significantly lower in the obese women. Basal and stimulated serum DHEA to F ratios were significantly higher in the obese women. In both groups, the mean F response slope was significantly higher than that for DHEA, which in turn, was significantly higher than that for A. The mean DHEA response slope was significantly greater in the obese women. The F and A response slopes were not different between the groups. We conclude that the relative responsivity of the steroids to ACTH was the same in both groups: F greater than DHEA greater than A; in the obese women, the ACTH threshold dose for F stimulation was lower (greater sensitivity) than for DHEA or A stimulation; and in the obese women, the ACTH threshold dose for A was significantly lower (increased sensitivity) and the slope of the DHEA response to ACTH was steeper (greater responsivity) than in normal women.
Adrenal, gonadal, and thyroid function were assessed in 40 asymptomatic subjects in whom infection with the human immunodeficiency virus (HIV) had recently been documented. None of the patients had historical or clinical evidence of endocrine dysfunction. Their mean serum hormone levels were also within the expected ranges, but several differences were noted compared to those of seronegative controls. Basal cortisol, basal aldosterone, and ACTH-stimulated cortisol were significantly lower in the HIV group. One subject (2.5%) had a subnormal cortisol response, and two (5%) had abnormal aldosterone responses to ACTH. PRA tended to be higher, and serum angiotensin-converting enzyme levels somewhat lower in the HIV group. Serum free testosterone was markedly elevated in the HIV patients and was associated with an exaggerated LH response to GnRH, but PRL, estradiol, and basal and peak GnRH-stimulated FSH did not differ between groups. Three subjects (8%) had subclinical hypothyroidism. Serum thyroid hormone levels were normal, but basal T3 was lower in the HIV group compared to control values. While of little immediate clinical importance, many subtle endocrine aberrations are evident very early in the course of HIV infection. These findings obtained in HIV-seropositive subjects without infections or tumors and who were not receiving medical therapy suggest an effect of HIV on each of the endocrine systems examined.
Adrenal dysfunction has been reported in patients infected with the human immunodeficiency virus (HIV). To evaluate the prevalence and degree of adrenal dysfunction in HIV-infected patients, we performed a longitudinal study in 53 ambulatory HIV patients. The plasma cortisol, aldosterone, and dehydroepiandrosterone (DHEA) responses to cosyntropin (250 micrograms, i.v.) were evaluated at 6-month intervals for 24 months and compared to those of normal subjects. The basal and peak cortisol responses to cosyntropin were normal in all HIV patients during the study. There was no difference in the mean basal or stimulated cortisol measurements between Center for Disease Control (CDC) class II-III and CDC class IV patients. Although the mean peak aldosterone response to cosyntropin in HIV patients did not differ from that in normal subjects during the study, the aldosterone secretory capacity was significantly less in CDC class IV than CDC class II-III patients at 6- and 18-month intervals. In addition, there was an impaired aldosterone response to cosyntropin in 31-53% of CDC class IV patients and in only 0-26% of CDC class II-III patients. The mean peak DHEA response to cosyntropin in HIV patients was significantly less than that in normal subjects during the entire study. Basal plasma aldosterone, PRA, cortisol, and DHEA levels did not change in 25 HIV patients who were followed for the entire 24-month period. However, plasma ACTH in these 25 patients was significantly increased at 24 months (9.7 +/- 0.9 pmol/L) compared to that at study entry (7.0 +/- 0.7 pmol/L). Of these 25 patients, 8 had plasma ACTH concentrations that exceeded the normal range at 24 months. The subnormal aldosterone and DHEA secretion with normal cortisol production in these HIV patients is similar to the alterations in adrenal function reported in seriously ill patients without HIV infection. Although we found that clinically significant adrenal insufficiency is uncommon, the elevations in plasma ACTH in several patients at the end of our 2-yr study suggest that adrenocortical capacity may become compromised.
The pharmacokinetics, responses of plasma ACTH and cortisol, urinary excretion of steroid hormones, and safety of MCI-028, a synthetic human corticotropin-releasing hormone (hCRH), were examined in eight healthy adult male volunteers after intravenous administration of 33, 100 and 200 micrograms of the drug. The disappearance of MCI-028 from plasma could be fitted to a biexponential decay curve, the plasma half-lives (T1/2) were 0.12 to 0.15 h for alpha phase, and 0.57 to 0.67 h for beta phase. Plasma ACTH and cortisol concentrations and the urinary excretion of steroid hormones (particularly free cortisol) increased significantly in relation to the MCI-028 dose administrated. Although hot flushing and an increase in the heart rate were observed at higher doses, they were mild and transient. It is also considered that the urinary excretion of free cortisol after the administration of MCI-028 can be an index reflecting the functioning of this system.
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In the present study we determined the efficacy of the measurement of fecal cortisol and androgen metabolite concentrations to monitor adrenal and testicular activity in the jaguar (Panthera onca). Three captive male jaguars were chemically restrained and electroejaculated once or twice within a period of two months. Fecal samples were collected daily for 5 days before and 5 days after the procedure and stored at -20 degrees C until extraction. Variations in the concentrations of cortisol and androgen metabolites before and after the procedure were determined by solid phase cortisol and testosterone radioimmunoassay and feces dry weight was determined by drying at 37 degrees C for 24 h under vacuum. On four occasions, fecal cortisol metabolite levels were elevated above baseline (307.8 +/- 17.5 ng/g dry feces) in the first fecal sample collected after the procedure (100 to 350% above baseline). On one occasion, we did not detect any variation. Mean (+/- SEM) fecal androgen concentration did not change after chemical restraint and electroejaculation (before: 131.1 +/- 26.7, after: 213.7 +/- 43.6 ng/g dry feces). These data show that determination of fecal cortisol and androgen metabolites can be very useful for a noninvasive assessment of animal well-being and as a complement to behavioral, physiological, and pathological studies. It can also be useful for the study of the relationship between adrenal activity and reproductive performance in the jaguar.
The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dogs was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.
A patient with hypopituitarism which is believed to have developed immediately after birth had been treated with thyroid hormones alone for a prolonged year of seven years until the time of the initial examination by the author. The subject has severe emaciation and lack of secondary sexual characteristics, but no past history of adrenocortical crisis was present, and, in fact, she manifested hyperthyroidism. It is questionable whether the preceding administration of thyroid hormones on the case with hypopituitarism should have been contraindicated. The two major complaints were improved through proper supplementary hormone treatment.