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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary adrenocortical insufficiency is described in 3 dogs. Clinical signs included marked depression, vomiting, diarrhoea, weakness and bradycardia. Diagnosis was based on clinical signs and biochemical findings of hyperkalaemia, hyponatraemia and a lowered plasma Na+ : K+ ratio. Treatment during the acute illness consisted of intravenous fluids and hydrocortisone sodium succinate. Fludrocortisone acetate has maintained all dogs in good health. One dog was on treatment for 4 years.
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PMID:Adrenocortical insufficiency in the dog. 68 64

A female patient born in 1941, who suffers from affective psychosis and Addison's disease, first received lithium carbonate in 1983 during a severe, therapy-resistent depression. With lithium treatment she showed a considerable improvement. In the following months, with a daily dosage of 24.4 mmol, the blood lithium levels were between 0.8 and 0.9 mmol/l. One year later she suffered a severe lithium intoxication after a virus infection. Shortly afterwards, she had a manic and then a depressive phase. She was now put on a regimen of with 12.2 mmol lithium carbonate per day, which produced blood levels between 0.3 and 0.4 mmol/l. In the following years, values of about 0.9 mmol/l were observed several times, therapy and clinical condition remaining unchanged. These spontaneous fluctuations of the blood lithium level, a hitherto unreported phenomenon are discussed as a possible cause of the lithium intoxication. The consequences for clinical practice are outlined.
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PMID:Lithium treatment of a patient with Addison's disease and affective psychosis. 271 62

The discovery of specific behavioral effects of several neuropeptides and the expanded appreciation of a wide range of endocrine disturbances in depressive illness have recently renewed interest in the nature of the relationship between mood and endocrine changes. Major depressive disorders are a major and life-threatening complication of Cushing's syndrome, Addison's disease, hyperthyroidism, hypothyroidism and hyperprolactinemic amenorrhea. A treatment primarily directed to the physical condition may be more effective than antidepressant drugs in such organic affective syndromes. The influence of hormonal disturbances in the development of depression in Conn's disease, pheochromocytoma, parathyroid disturbances, SIADH, acromegaly, hirsutism and other endocrine diseases should be individually evaluated. Antidepressant drugs remain the most specific and readily available treatment of major depressive disorders in the setting of endocrine illness.
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PMID:Major depression associated with endocrine disease. 332 99

Corticotropin releasing factor (CRF) is a 41 amino acid peptide first isolated from sheep hypothalami and thought to be a principal modulator of the hypothalamic-pituitary-adrenal cortical (HPA) axis. We report herein a series of clinical studies with CRF in healthy volunteers and in patients with abnormalities in HPA function, including depression, Cushing's disease, Cushing's syndrome, and Addison's disease. Our data indicate that CRF can be a diagnostic aid in distinguishing various disorders of the HPA axis from one another, including Cushing's disease from depression and secondary from tertiary adrenal insufficiency. Moreover, the hormone responses to CRF help clarify the pathophysiology of the HPA abnormalities in several disorders. For instance, our data indicate that hypercortisolism in Cushing's disease results principally from a defect at the level of the pituitary; in contrast, in depression the defect seems to be hypothalamic, possibly involving hypersecretion of endogenous CRF. This latter possibility is of particular interest in light of clinical observations that depression often can be precipitated by stress. Moreover, data from experimental animals show that CRF may influence several processes known to be altered in the overall symptom complex of depression, including not only pituitary-adrenal function, but also motor activity, appetite regulation and sexual behavior.
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PMID:Clinical studies with corticotropin releasing factor: implications for the diagnosis and pathophysiology of depression, Cushing's disease, and adrenal insufficiency. 387 72

Hyperactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis in depression has received considerable attention, particularly in the now numerous studies utilizing the dexamethasone suppression test. The possibility of HPA axis hypoactivity in this population however has not been similarly explored. To examine this latter possibility, the metyrapone test, a well-established neuro-endocrine assay for determining pituitary reserve, was administered to ten endogenously depressed males and ten matched controls. Consistent with the findings of an earlier study on ten female depressives, one of the depressed males but none of the controls showed clear evidence of HPA axis hypoactivity. This suggests that HPA axis dysfunction in depressives may be more complex than originally anticipated. This finding also has implications for the psychiatric symptomatology classically associated with such illnesses as Addison's disease.
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PMID:The metyrapone test in depressed males. 400 33

Of the various hypothalamic-pituitary-end organ axes, the thyroid and adrenal systems have been implicated most often in affective disorders. Patients with primary thyroid disease have high rates of depression, and patients with Addison's disease or Cushing's syndrome have relatively high rates of affective and anxiety symptoms. However, the major support for these endocrine axes in the pathophysiology of mood disorders comes from studies in which alterations in components of the hypothalamic-pituitary-thyroid (HPT) and the hypothalamic-pituitary-adrenal (HPA) axes have been documented in patients with primary depression. Concerning the HPT axis, depressed patients have been reported to have: (a) alterations in thyroid-stimulating hormone response to thyrotropin-releasing hormone (TRH); (b) an abnormally high rate of antithyroid antibodies; and (c) elevated cerebrospinal fluid (CSF) TRH concentrations. Moreover, tri-iodothyronine has been shown conclusively to augment the efficacy of various antidepressants. Concerning the HPA axis, depressed patients have been reported to exhibit: (a) adrenocorticoid hypersecretion; (b) enlarged pituitary and adrenal gland size; and (c) elevated CSF corticotropin-releasing factor concentrations. All of the HPA axis alterations in depression studied thus far are state-dependent, whereas the HPT axis alterations may be partially trait and partially state markers.
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PMID:Depression and endocrine disorders: focus on the thyroid and adrenal system. 886 58

The clinical correlate of chronic hypercortisolism is Cushing's syndrome (CS). After exclusion of an iatrogenic cause (glucocorticoid administration), two reliable laboratory methods for establishing the diagnosis are (i) measurement of "free" (unmetabolised) cortisol in a 24-hour urine (UFC) sample and (ii) the low-dose (1 or 1.5 mg) dexamethasone (Dex) test. For the latter, Dex is taken orally at midnight, and plasma cortisol is measured at 8 a.m. In normals and in the absence of CS, the morning cortisol (200-650 nmol/L) is suppressed to <80 nmol/L. In endogenous CS of all causes, cortisol suppression by Dex is absent or incomplete. In patients with severe mental depression or stress, suppression may also be incomplete ("false-positives"). However, UFC is normal or only slight increased in the latter group, while it is always markedly increased in clinically apparent CS. In CS, UFC rises proportionally more than plasma cortisol because the cortisol binding plasma protein (transcortin) can bind only about 500 nmol/L cortisol. Protein-bound cortisol is not excreted by the kidney. After establishing the diagnosis CS, the differentiation between its pituitary (ca. 70%), adrenocortical (ca. 20%) or "ectopic" (ACTH production by non-pituitary tumours) (ca. 10%) origin is made by plasma ACTH measurement, a corticotropin releasing hormone injection test (with plasma ACTH/cortisol measurement) and a high-dose Dex (8 mg or more) suppression test. Chronic hypocorticolism can be primary (adrenal disease, Addison's disease) or secondary (pituitary or hypothalamic disorder). UFC measurement is not an established method for confirming hypocortisolism because most analytical methods are too unspecific and insensitive in the subnormal range. Low-normal or subnormal plasma cortisol plus elevated ACTH is the hallmark of Addison's disease. Injection of high doses of ACTH does not lead to a rise in plasma cortisol in these patients. A clearly subnormal cortisol plus low ACTH proves secondary hypocortisolism. Mild forms with low-normal plasma cortisol, however, are more difficult to prove. So-called "dynamic" tests stimulating the whole hypothalamo-pituitary-adrenal axis (insulin hypoglycemia test or metyrapone test) are necessary to confirm the diagnosis. Patients with hypocortisolism, depending on disease severity, must be treated permanently or only in stressful situations with hydrocortisone unless they may die after passing the clinical state of an "adrenal crisis".
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PMID:Clinical diagnosis of hyper- and hypocortisolism. 1268 70

Adrenal necrosis has been described in golden hamsters where it occurs during the course of infection with Besnoilia jellisoni. This necrosis results directly from the active intracellular proliferation by this obligate intracellular protozoan organism. After infection, adrenal necrosis is rarely observed in hypophysectomized hamsters. In unoperated animals adrenal necrosis is suppressed to varying degrees by cortisone (E), hydrocortisone (F), corticosterone (B), 11-dehydrocorticosterone (A), and possibly by 11-desoxycorticosterone (DOCA). Besnoitia organisms proliferate in otherwise "immune" hamsters around the subcutaneous deposits of the acetates of cortisone (E), hydrocortisone (F), and 11-dehydrocorticosterone (A); a marked depression of general immunity follows the administration of pharmacologic doses of the former two hormones. Organisms do not proliferate around the sites of corticosterone acetate (B) and 11desoxycorticosterone acetate (DOCA) injection, nor next to deposits of testosterone propionate, 11-desoxy-17-hydroxycorticosterone acetate (Reichstein's compound S) and epinephrine in oil. It is postulated that certain glucocorticoids can so modify immunity mechanisms locally, that general immunity becomes ineffective; this occurs in the adrenal glands owing to endogenous corticoid production, at the sites of exogenous corticoid injection, and proximal to that in the lungs. A comparison is made with the pathogenesis of tuberculosis and histoplasmosis of the adrenal gland which results in Addison's disease in man, and it is concluded that a similar pathogenetic mechanism is operative. The use of glucocorticoids for replacement therapy is discussed in reference to their relative resistance-depressing activities in pharmacologic doses. These undesirable side effects would appear to be less pronounced, if not absent, if corticosterone (B) rather than cortisone (E) and hydrocortisone (F) therapy were used. Porcine adrenocorticotrophic hormone (ACTH) appearsto depress the incidence of adrenal necrosis in unoperated hamsters, and supports proliferation of organisms in the adrenal cortex with subsequent necrosis in only a small proportion of hypophysectomized hamsters. The possibility is discussed that ACTH from a different species (hog) might lead to a change in the secretory activity of the hamster adrenal gland.
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PMID:Effects of hormones on the adrenal necrosis produced by Besnoitia jellisoni in golden hamsters. 1329 93

This report describes a 52-year-old male patient with idiopathic Addison's disease presenting depression as a first symptom. His psychomotor inhibition, depressive mood, sleep disturbances, general fatigue, muscular pain, and arthralgia were considered to be due to intense work in a stressful environment. Neither his physician nor his orthopedist found any physical disease. Therefore, he was diagnosed with endogenous depression by a psychiatric clinic, and antidepressants were prescribed. Antidepressants were not sufficient for improving his symptoms, and he was admitted to our hospital. Endocrine blood examination revealed primary adrenocortical insufficiency. Treatment with glucocorticoid induced rapid improvement in both the psychiatric and physical symptoms. It is well known that psychiatric symptoms occur in the progressive stage of Addison's disease. At present, however, the occurrence of psychiatric symptoms is very rare, mainly because of a decrease in the incidence of this disease or an increase in mild cases. In addition, Addison's disease presenting with psychiatric features in the early stage has the tendency to be overlooked and misdiagnosed. Thus, we suggest the necessity of blood work for ACTH and cortisol in the field of psychiatry.
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PMID:[A case of Addison's disease presented with depression as a first symptom]. 1558 Aug 69

Addisonian crisis represents a state of acute adrenocortical insufficiency and occurs in patient with Addison's disease who are exposed to stress of infection, surgery, trauma, vomiting and diarrhea. We present a case with a 39-year-old female patient who admitted to the hospital with Addisonian crisis and, interestingly, her electrocardiograph showed ST depression and inverted T waves on inferior and V4-V6 leads. She did not have a history of angina pectoris and coronary artery disease, and her cardiac enzymes were normal. Exercise stress testing and echocardiographic assessment revealed normal findings. When faced with such a patient who has hypotension and ischemic ECG changes without having underlying angina, Addisonian crisis should be considered in differential diagnosis.
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PMID:Inverted T waves in patient with Addisonian crisis. 1633 1


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