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Diabetes Insipidus Cortisol Deficiency

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking Of Diabetes Insipidus With Steroid Treatment

Unmasking of diabetes insipidus with steroid treatment Adeel Ghaffar, Barbara McGowan, George Tharakan, Nehal Narayan, Rebecca Cox, Emma Hatfield & Karim Meeran Endocrine Unit, Department of Investigative Medicine, Imperial College Healthcare trust, 6th floor, Commonwealth Building, Hammersmith Hospital, London, UK. A 36-year-old man was referred to the neurologists for leg weakness and pain, fatigue and lethargy for 2 years. Sarcoidosis was diagnosed 6 years previously, on the basis of uveitis, lower motor neurone facial palsy, hilar lymphadenopathy and transbronchial biopsy. Prednisolone had been discontinued 3 years prior to his current presentation. His blood pressure was 99/71. Examination was otherwise unremarkable. His ACE was 109 U/l (1070). His TSH was 1.29 mU/l., with a free T4 of 5.9 pmol/l. Cortisol was 56 nmol/l. Prolactin was 818 mU/l (75375 mU/l). LH and FSH were undetectable. Testosterone was very low at 0.3 nmol/l. GH was 0.5 U/l. IGF-1 was 9 nmol/l (1364). Other bloods, and an LP were unremarkable. MRI of brain and spine showed thickening and contrast enhancement around the pituitary infundibulum and hypothalamus. Peak cortisol on SST was 450 nmol/l. He was commenced on hydrocortisone 10 mg, 5 mg, 5 mg, and thyroxine 50 mcg. He was given 1 g methylprednisolone daily for 3 days. He complained of polyuria and polydipsia. His serum osmolality was 302 mOsmol/kg. Concurrent urinary osmolality was 119 mOsmol/kg. A formal water deprivation test was performed. Continue reading >>

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-independent Mechanism Of Impaired Water Excretion In A Patient With Sarcoidosis Complicated By Central Diabetes Insipidus And Glucocorticoid Deficiency

Arginine Vasopressin-Independent Mechanism of Impaired Water Excretion in a Patient with Sarcoidosis Complicated by Central Diabetes Insipidus and Glucocorticoid Deficiency 1Department of Internal Medicine, Osaka City Sumiyoshi Hospital, 1-2-16, Higashikagaya, Suminoeku, Osaka City, Osaka 559-0012, Japan 2Department of Internal Medicine, Osaka City Juso Hospital, Osaka 532-0034, Japan 3Department of Endocrinology and Metabolism, Osaka City General Hospital, Osaka 534-0021, Japan 4Department of Pathology, Osaka City General Hospital, Osaka 534-0021, Japan Received 13 February 2011; Accepted 7 June 2011 Copyright 2011 Katsunobu Yoshioka et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 28-year-old man was admitted to our hospital because of reduced livido and increased fatigability. Four months before admission, he noticed polyuria, which was gradually relieved by admission. Magnetic resonance imaging revealed enhancing lesion centrally in the pituitary stalk. Biopsy from the skin revealed noncaseating granuloma composed of epithelioid cells, and a diagnosis of sarcoidosis was made. Although plasma arginine vasopressin (AVP) was undetectable after administration of hypertonic saline, urinary output was within normal range (1.5 to 2.2 L/day). The urine osmolality became above plasma levels during the hypertonic saline test. Hormonal provocative tests revealed partial glucocorticoid deficiency. Soon after the glucocorticoid therapy was begun, moderate polyuria (from 3.54.0 liters daily) occurred. At this time, plasma AVP was undetectable, and urine osmolality was consistently below plasma levels durin Continue reading >>

Central Adrenal Insufficiency And Diabetes Insipidus Misdiagnosed As Severe Depression

Central Adrenal Insufficiency And Diabetes Insipidus Misdiagnosed As Severe Depression

Central Adrenal Insufficiency and Diabetes Insipidus Misdiagnosed as Severe Depression 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan 1 Department of Diabetes and Endocrinology, Saiseikai Yokohamashi-Tobu Hospital, Yokohama, Kanagawa, Japan 2 Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine (Omori), Faculty of Medicine, Toho University, Tokyo, Japan Corresponding author email: [email protected] Author information Copyright and License information Disclaimer Copyright 2010 the author(s), publisher and licensee Libertas Academica Ltd. This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited. This article has been cited by other articles in PMC. A 68 year-old Japanese man, who had been suffering from immobilization and disuse syndrome, was admitted to our hospital for evaluation of polyuria with polyposia, hyponatremia and low blood pressure. His plasma osmolality was greater than that of his urine. His endocrinological examinatio Continue reading >>

Hydrocortisone|the Pituitary Foundation

Hydrocortisone|the Pituitary Foundation

Hydrocortisone (HC) is a steroid hormone produced by the adrenal gland. It plays a complex role in regulating body functions Hydrocortisone is taken as a replacement for the natural hormone where this is deficient, either because there is a failure of hydrocortisone production by the adrenal gland (Addisons disease/primary adrenal insufficiency), or pituitary deficiency (secondary adrenal insufficiency) of ACTH (the hormone that stimulates the production of hydrocortisone by the adrenal gland). Replacement therapy is also required for people who have congenital adrenal hyperplasia, which is a birth defect. Hydrocortisone is available as tablets under the trade name Hydrocortisone, containing 10mg or 20mg. Prednisolone may be prescribed to individual patients instead of hydrocortisone and works in the same way as hydrocortisone. Prednisolone is available as tablets under the trade name Deltacortrilcontaining 2.5mg or 5mg or Prednisolone 1mg or 5mg. Plenadren is a novel, once daily hydrocortisone modified-release tablet, designed to better mimic the bodys natural cortisol production compared to standard treatment. The Plenadren tablet is available in 5 and 20 mg strengths. The immediate release outer coating provides physiological cortisol concentrations within 20 minutes of intake; the extended release core provides a smooth serum cortisol level with reduced exposure in the late afternoon and over the 24-hour period. An injection containing 100mg Hydrocortisone is available foremergency situations for those on hydrocortisone or prednisolone. For children, there are lower dose emergency injections available. The usual dose for hydrocortisone is 15-20mg by mouth, split over twoor three times daily, and depending on your individual endocrinologists recommendations. For exa Continue reading >>

Acute Glucocorticoid Deficiency And Diabetes Insipidus Are Common After Acute Traumatic Brain Injury And Predict Mortality

Acute Glucocorticoid Deficiency And Diabetes Insipidus Are Common After Acute Traumatic Brain Injury And Predict Mortality

Acute Glucocorticoid Deficiency and Diabetes Insipidus Are Common After Acute Traumatic Brain Injury and Predict Mortality Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Address all correspondence and requests for reprints to: Dr Mark J. Hannon or Professor Christopher J. Thompson, Academic Department of Endocrinology, Beaumont Hospital/Royal College of Surgeons in Ireland Medical School, Beaumont Hospital, Dublin 9, Ireland. Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Search for other works by this author on: Search for other works by this author on: Critical Care (R.O'D.), Dublin 9, Ireland Search for other works by this author on: Chemical Pathology (W.T.), Beaumont Hospital/Royal College of Surgeons in Ireland Medical School, Dublin 9, Ireland Search for other works by this author on: Departments of Endocrinology (M.J.H., R.K.C., L.A.B., E.P.O'S., M.M.C.O'B., M.S., C.J.T.), Dublin 9, Ireland Address all correspondence and requests for reprints to: Dr Mark J. Hannon or Professor Christopher J. Thompson, Acad Continue reading >>

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

2016 Endocrine Society Guidelines: Central Adrenal Insufficiency

We suggest measuring serum cortisol levels at 89 am as the first-line test for diagnosing central adrenal insufficiency. We recommend against using a random cortisol level to diagnose AI. We suggest that a cortisol level <3 g/dL is indicative of adrenal insufficiency and a cortisol level >15 g/dL likely excludes an AI diagnosis. We suggest performing a corticotropin stimulation test when morning cortisol values are between 3-15 g/dL to diagnose AI. Peak cortisol levels <18.1 g/dL at 30 or 60 minutes indicate AI. We suggest that clinicians perform biochemical testing for the hypothalamic-pituitary-adrenal (HPA) axis at least 1824 hours after the last hydrocortisone (HC) dose or longer for synthetic glucocorticoids (GC). We recommend using hydrocortisone, usually 1520 mg total daily dose in single or divided doses. Patients using divided doses should take the highest dose in the morning at awakening and the second in the afternoon (two-dose regime) or the second and third at lunch and late afternoon, respectively (three-dose regime). We suggest using longer-acting glucocorticoids in selected cases (eg, non-availability, poor compliance, convenience). We recommend that clinicians teach all patients with adrenal insufficiency regarding stress-dose and emergency GC administration and instruct them to obtain an emergency card/bracelet/necklace regarding AI and an emergency kit containing injectable high-dose GC. We recommend against using fludrocortisone in patients with central adrenal insufficiency. We recommend that clinicians treat patients with suspected adrenal crisis (AC) due to secondary AI with an immediate parenteral injection of 50100 mg hydrocortisone. We suggest evaluating central hypothyroid patients for adrenal insufficiency before starting LT4 therapy. If thi Continue reading >>

Diabetes Insipidus

Diabetes Insipidus

Diabetes insipidus (DI) is a condition characterized by large amounts of dilute urine and increased thirst.[1] The amount of urine produced can be nearly 20 liters per day.[1] Reduction of fluid has little effect on the concentration of the urine.[1] Complications may include dehydration or seizures.[1] There are four types of DI, each with a different set of causes.[1] Central DI (CDI) is due to a lack of the hormone vasopressin (antidiuretic hormone).[1] This can be due to damage to the hypothalamus or pituitary gland or genetics.[1] Nephrogenic diabetes insipidus (NDI) occurs when the kidneys do not respond properly to vasopressin.[1] Dipsogenic DI is due to abnormal thirst mechanisms in the hypothalamus while gestational DI occurs only during pregnancy.[1] Diagnosis is often based on urine tests, blood tests, and the fluid deprivation test.[1] Diabetes mellitus is a separate condition with an unrelated mechanism, though both can result in the production of large amounts of urine.[1] Treatment involves drinking sufficient fluids to prevent dehydration.[1] Other treatments depend on the type.[1] In central and gestational disease treated is with desmopressin.[1] Nephrogenic disease may be treated by addressing the underlying cause or the use of a thiazide, aspirin, or ibuprofen.[1] The number of new cases of diabetes insipidus each year is 3 in 100,000.[4] Central DI usually starts between the ages of 10 and 20 and occurs in males and females equally.[2] Nephrogenic DI can begin at any age.[3] The term "diabetes" is derived from the Greek word meaning siphon.[5] Signs and symptoms[edit] Excessive urination and extreme thirst and increased fluid intake (especially for cold water and sometimes ice or ice water) are typical for DI.[6] The symptoms of excessive urination Continue reading >>

Unmasking Of Central Diabetes Insipidus In A Patient After Steroid Treatment

Unmasking Of Central Diabetes Insipidus In A Patient After Steroid Treatment

SESSION TYPE: Critical Care Student/Resident Case Report Posters IPRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PMINTRODUCTION: Central diabetes insipidus is a condition characterized by excretion of large volumes of dilute urine secondary to either a deficiency in the production or release of arginine vasopressin. Glucocorticoids are necessary for the kidneys to excrete salt free water. Symptoms of central diabetes insipidus may be masked by concomitant ACTH deficiency. Polyuria may appear when corticosteroid replacement is instituted. We present a case of a woman who developed shock and was given dexamethasone for secondary adrenal insufficiency subsequently unmasking diabetes insipidus.CASE PRESENTATION: A 40-year-old Caucasian female with a remote history of pituitary surgery, presented with a 2-month history of recurrent vomiting, diarrhea and generalized weakness. Physical examination demonstrated drowsiness, tachycardia and hypotension. Initial labs revealed hyponatremia of 130 mmol/dl, hypokalemia 3.1mmol/dl, urine specific gravity of 1.030 and normal renal function. She was started on normal saline boluses but subsequently required vasopressors for refractory shock. Her work up included a serum cortisol which was found to be very low at 0.9 mcg/dl (normal cortisol level 5-25 mcg/dl). Cosyntropin stimulation test was positive for secondary adrenal insufficiency, and dexamethasone was initiated. The patient's symptoms resolved, however she subsequently developed polyuria. Further workup now revealed a low urine osmolality of 209 mOsmol/kg, plasma osmolality of 307 mOsmol/kg and hypernatremia of 149 mmol/dl. She was started on desmopressin for a new diagnosis of central diabetes insipidus. The patient improved and was discharged home on dexamethason Continue reading >>

Endocrine Smorgasbord! Adrenal Insufficiency, Hypercalcemia, Diabetes Insipidus

Endocrine Smorgasbord! Adrenal Insufficiency, Hypercalcemia, Diabetes Insipidus

UCSF Internal Medicine Chief Resident Hub Today in report, we spoke about primary vs secondary adrenal insufficiency, workup and treatment of hypercalcemia, and diabetes insipidus.I thought wed touch on a few fun facts of each endocrinopathy apologies for the length! Take Home Points: Adrenal Insufficiency, Hypercalcemia, DI Adrenal Insufficiency Symptoms of Primary vs Secondary/Tertiary Primary AI adrenal gland failure of cortisol production Acute adrenal crisis: hypotension/shock (90%),abdominal/flank/back pain (86%), lethargy, fever (66%), anorexia, n/v (47%), confusion or disorientation (42%), abdominal tenderness or rebound tenderness (22%) Chronic adrenal insufficiency: hyperpigmentation (POMC is the ACTH precursor that cleaves into ACTH and melanocyte stimulating hormone, so hyper-secretion of ACTH means higher levels of MSH), GI symptoms, weight loss In both, will see electrolyte abnormalities due to mineralocorticoid loss: hyponatremia, hyperkalemia. Hypoglycemia less common in primary AI unless patients are also infected or fasting. Secondary (pituitary failure of ACTH production) and Tertiary AI (hypothalamic failure of CRH production)Similar symptoms to primary AI with the exception of: Hyperpigmentation not present, since ACTH is not hyper-secreted Mineralocorticoid function is preserved so: Hyponatremia may be present, but due to increased vasopressin secretion from low cortisol (ie more water, not less salt) Hypovolemia and hyperkalemia are not seen Hypoglycemia is more common in secondary AI May see loss of other anterior pituitary hormones in some causes of secondary AI (FSH,LH,TSH,Prolactin, GH) Hypercalcemia Common Causes and the Mechanisms Behind Them Primary hyperparathyroidism most often due to an adenoma Mechanisms increased bone resorption, incr Continue reading >>

Pituitary Disorders-diabetes Insipidus And Cushing's Syndrome

Pituitary Disorders-diabetes Insipidus And Cushing's Syndrome

Pituitary disorders-Diabetes Insipidus and Cushing's Syndrome Diabetes insipidus is a clinical disorder characterized by the excretion of large quantities of diluted urine and caused either by failure of ADH release (hypothalamic diabetes insipidus) or by lack of response of the tubules to normal quantities of circulating ADH (nephrogenic diabetes insipidus). Criteria for the diagnosis of hypothalamic diabetes insipidus include: (1) insufficient ADH release despite serum hyperosmolalityand (2) an increase in urine osmolality in response to exogenous ADH. Causes of hypothalamic diabetes insipidus: 1.Surgery: section of the supraopticohypophyseal tract above the median em inence. Disruption of the tract at the level of the pituitary stalk leads 10 transient diabetes insipidus which disappears in 1 to 2 weeks. 2.Trauma to the hypothalamus or the median eminence. Most commonly, dia betes insipidus resulting from trauma is transient, but it may be permanent. 3.Tumors that destroy the site of production and release of ADH are either primary, such as craniopharyngioma or metastatic, the most common being carcinoma of the breast. 4.Infiltration of the hypothalamus by leukemic cells, granuloma (sarcoidosis, tuberculosis), histiocytes (Hand-Schuller-Christian disease), or infections. All these are rare causes of diabetes insipidus. Diabetes insipidus can be masked by a concomitant deficiency of the anterior pituitary hormones. In the absence of cortisol, there may be enhanced release of ADH as well as increased sensitivity of the tubules to ADH, both of which lead to an impairment in water excretion. In addition, growth hormone, cortisol, and thyroxin increase the glomerular filtration rate. In patients with panhypopituitarisrn, diabetes insipidus becomes clinically manifest whe Continue reading >>

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency

Neurosarcoidosis-associated Central Diabetes Insipidus Masked By Adrenal Insufficiency

Central diabetes insipidus (CDI) is an infrequent complication of neurosarcoidosis (NS). Its presentation may be masked by adrenal insufficiency (AI) and uncovered by subsequent steroid replacement. A 45-year-old woman with a history of NS presented 2 weeks after abrupt cessation of prednisone with nausea, vomiting, decreased oral intake and confusion. She was diagnosed with secondary AI and intravenous hydrocortisone was promptly begun. Over the next few days, however, the patient developed severe thirst and polyuria exceeding 6 L of urine per day, accompanied by hypernatraemia and hypo-osmolar urine. She was presumed to have CDI due to NS, and intranasal desmopressin was administered. This eventually normalised her urine output and serum sodium. The patient was discharged improved on intranasal desmopressin and oral prednisone. AI may mask the manifestation of CDI because low serum cortisol impairs renal-free water clearance. Steroid replacement reverses this process and unmasks an underlying CDI. The full text of all Editor's Choice articles and summaries of every article are free without registration The full text of Images in ... articles are free to registered users Only fellows can access the full text of case reports (apart from Editor's Choice) - become a fellow today, or encourage your institution to, so that together we can grow and develop this resource Don't forget to sign up for content alerts so you keep up to date with all the case reports as they are published, and let us know what you think by commenting on the Editor's blog Continue reading >>

Unmasking Of Partial Diabetes Insipidus During Stress But Not Maintenance Dosing Of Glucocorticoids In An Infant With Septo-optic Dysplasia

Unmasking Of Partial Diabetes Insipidus During Stress But Not Maintenance Dosing Of Glucocorticoids In An Infant With Septo-optic Dysplasia

International Journal of Pediatric Endocrinology Unmasking of Partial Diabetes Insipidus during Stress but Not Maintenance Dosing of Glucocorticoids in an Infant with Septo-Optic Dysplasia Background. It is well acknowledged that glucocorticoid (GC) replacement can unmask diabetes insipidus (DI) in subjects with hypopituitarism. Objective. To increase the awareness and monitoring for transient and symptomatic DI in children with partial hypopituitarism during periods in which increased GC needs are required. Methods/Case. A 2-month-old female infant with septo-optic dysplasia (SOD; on thyroid and maintenance GC replacement therapy at 8 mg/m2/day) developed transient DI during 2 separate episodes of stress (one hypothermia, one febrile) when stress dosing of GC (25 mg/m2/day) was instituted. Conclusion. Children not diagnosed with DI during initial evaluation for hypopituitarism may benefit from rescreening of serum sodium levels during acute periods of stress that demand "stress" GC dosing. This will permit treatment and/or increased vigilance for ensuing permanent DI. Diabetes InsipidusHypopituitarismCorticotropin Release HormoneSerum Sodium LevelStress Dose Septo-optic dysplasia (SOD) is a malformation syndrome in which at least 50% of children have associated hypopituitarism [ 1 , 2 ]. This condition includes agenesis of the septum pellucidum, hypoplasia, or aplasia of the optic nerves and chiasm that results in various degrees of visual impairment and abnormality of the hypothalamus causing secondary hypopituitarism [ 3 ]. Diabetes insipidus (DI) is a condition characterized by excretion of large volumes of dilute urine secondary to either a deficiency in the production/release of the hormone arginine vasopressin (AVP) that is synthesized in the hypothalamus and tr Continue reading >>

Cortisol Deficiency

Cortisol Deficiency

- granulomatous disease (eg sarcoid, TB, eosinophilic granuloma, Wegener's) necrosis or bleeding into pituitary macroadenoma surgery for lesions in region of hypothalamus, pituitary or midbrain Cortisol deficiency due to hypothalamic or midbrain lesions is more likely tobe asociated with diabetes insipidus than cortisol deficiency due to pituitarylesions. Only features which distinguish primary from secondary form are associated features of failure of pituitary function other than ACTH in the secondary type and endocrine pigmentation and features of associated diseases in the primary type. Addisonian pigmentation useful when present but often absent in auto-immune cases - characteristically seen in palmar creases , other skin creases, exposed areas, scars and buccal mucosa . May be associated vitiligo Weight loss - cmst symptom of cortisol insufficiency Non-specific abdo pain, often severe and colicky Shock and hypotension (Addisonian crisis - may be ppt. by intercurrent disease or infection) Acute cortisol deficiency results in muscle cramps, myalgia with unexplained fever, shock and hypotension. Secondary hypoadrenalism results in reproductive failure, +/- skin thickening, accentuation of tendency to hypoglycaemia (GH deficiency). Secondary hypothyroidism is a late feature. - consider diagnosis in presence of unexplained catecholamine-resistanthypotension, especially if the patient has hyperpigmentation, vitiligo, pallor,scanty axillary and pubic hair, hyponatraemia, or hyperkalaemia - possibility of spontaneous adrenal insufficiency due to adrenal haemorrhage oradrenal vein thrombosis must be considered in patients with upper abdominal orloin pain, abdominal rigidity, vomiting, confusion, and arterial hypotension - raised urea - most consistent biochemical abnormali Continue reading >>

Panhypopituitarism Clinical Presentation: History, Physical, Causes

Panhypopituitarism Clinical Presentation: History, Physical, Causes

Author: Robert P Hoffman, MD; Chief Editor: Sasigarn A Bowden, MD more... Suspect hypopituitarism in children with midline defects or optic atrophy (suggestive of septo-optic dysplasia) [ 6 , 7 ] and in boys with micropenis (suggestive of gonadotropin deficiency). [ 8 , 9 ] Evaluate hypopituitarism prior to the development of overt problems due to hormonal deficiencies. Infants with hypopituitarism without such abnormalities present in various ways. For example, children with severe growth hormone (GH) deficiency and adrenocorticotropic hormone (ACTH) deficiency may develop hypoglycemia, which leads to the diagnosis. Another presentation is hypernatremic dehydration due to diabetes insipidus. Accompanying cortisol deficiency may obscure diabetes insipidus because cortisol is necessary to excrete a free water load. [ 10 ] Some infants come to medical attention because of low thyroid hormone concentrations discovered on neonatal thyroid screen. Children with milder defects present with poor growth at varying ages. The symptoms include fatigue, dry skin, and constipation due to thyroid-stimulating hormone (TSH) deficiency and concomitant hypothyroidism and/or nausea, vomiting, and malaise due to ACTH and cortisol deficiency. Similar to children with congenital hypopituitarism, many children with acquired hypopituitarism are identified before symptoms are observed. Pituitary function should be routinely evaluated before and after treatment in children with craniopharyngiomas or other hypothalamic or pituitary tumors. The same is true for children who have received cranial irradiation (eg, before bone marrow transplant or for cranial tumors). Children without a known hypothalamic or pituitary insult with hypopituitarism frequently present with growth failure because of GH d Continue reading >>

Hypopituitarism

Hypopituitarism

Hypopituitarism is a general term that refers to any under function of the pituitary gland. This is a clinical definition used by endocrinologists and is interpreted to mean that one or more functions of the pituitary are deficient. The term may refer to both anterior and posterior pituitary gland failure. Causes of hypopituitarism Deficient pituitary gland function can result from damage to either the pituitary or the area just above the pituitary, the hypothalamus. The hypothalamus contains releasing and inhibitory hormones which control the pituitary. Since these hormones are necessary for normal pituitary function, damage to the hypothalamus can also result in deficient pituitary gland function. Injury to the pituitary can occur from a variety of insults, including damage from an enlarging pituitary tumor, irradiation to the pituitary, pituitary apoplexy, trauma and abnormal iron storage (hemochromatosis). With increasing damage there is a progressive decrease in function. There appears to be a predictable loss of hormonal function with increasing damage. The progression from most vulnerable to least vulnerable is usually as follows: first is growth hormone (GH), next the gonadotropins (LH and FSH which control sexual/reproductive function), followed by TSH (which control thyroid hormone release) and finally the last to be lost is typically ACTH (which controls adrenal function). Sheehan's Syndrome Sheehan's syndrome is a condition that may occur in a woman who has a severe uterine hemorrhage during childbirth. The resulting severe blood loss causes tissue death in her pituitary gland and leads to hypopituitarism following the birth. For more on this Sheehan's syndrome, please visit MedlinePlus on Sheehan's Syndrome. Deficiency of ACTH and cortisol Deficiency of ACT Continue reading >>

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