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| {{Syndrome of inappropriate antidiuretic hormone}}
| | [[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Syndrome_of_inappropriate_antidiuretic_hormone]] |
| {{CMG}}; {{AE}} {{Vbe}} | | {{CMG}}; {{AE}}{{Vbe}} |
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| ==Overview== | | ==Overview== |
| [[Syndrome of inappropriate antidiuretic hormone secretion (SIADH)]] was initially described by Leaf and Mamby. SIADH consists of[[ hyponatremia]], inappropriately elevated urine osmolality, excessive urine sodium and decreased serum osmolality in a euvolemic patient without edema. These findings should occur in the absence of diuretic treatment with normal [[cardiac, renal]], [[adrenal]], hepatic and [[thyroid]] function. Hyponatremia occurs in about 30% of hospitalized patients and SIADH is the most frequent cause of hyponatremia. Differentiating hyponatremia due to SIADH from other causes of hyponatremia becomes essential to evaluate the treatment plan. [[Syndrome of inappropriate antidiuretic hormone]] must be differentiated from [[cerebral salt wasting]] , [[adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]],[[psychogenic polydipsia]]
| | Syndrome of inappropriate antidiuretic hormone (SIADH) must be differentiated from other causes of [[hyponatremia]], such as [[cerebral salt wasting syndrome]], [[adrenal insufficiency]], [[hypopituitarism]], and [[psychogenic polydipsia]]. |
| | | ==Differentiating Syndrome of Inappropriate Antidiuretic Hormone from other Diseases== |
| ==Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases== | | [[SIADH]] must be differentiated from cerebral salt wasting, [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], and [[psychogenic polydipsia]].<ref name="pmid27936532">{{cite journal |vauthors=Heidelbaugh JJ |title=Endocrinology Update: Hypopituitarism |journal=FP Essent |volume=451 |issue= |pages=25–30 |year=2016 |pmid=27936532 |doi= |url=}}</ref><ref name="pmid15241506">{{cite journal |vauthors=Hammer F, Arlt W |title=[Hypopituitarism] |language=German |journal=Internist (Berl) |volume=45 |issue=7 |pages=795–811; quiz 812–3 |year=2004 |pmid=15241506 |doi=10.1007/s00108-004-1216-5 |url=}}</ref><ref name="pmid25712898">{{cite journal |vauthors=de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E |title=The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia |journal=Endocr Connect |volume=4 |issue=2 |pages=86–91 |year=2015 |pmid=25712898 |pmc=4401105 |doi=10.1530/EC-14-0113 |url=}}</ref> |
| SIADH must be differentiated from [[cerebral salt wasting]], [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], [[psychogenic polydipsia]]<ref name="pmid27936532">{{cite journal |vauthors=Heidelbaugh JJ |title=Endocrinology Update: Hypopituitarism |journal=FP Essent |volume=451 |issue= |pages=25–30 |year=2016 |pmid=27936532 |doi= |url=}}</ref><ref name="pmid15241506">{{cite journal |vauthors=Hammer F, Arlt W |title=[Hypopituitarism] |language=German |journal=Internist (Berl) |volume=45 |issue=7 |pages=795–811; quiz 812–3 |year=2004 |pmid=15241506 |doi=10.1007/s00108-004-1216-5 |url=}}</ref><ref name="pmid25712898">{{cite journal |vauthors=de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E |title=The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia |journal=Endocr Connect |volume=4 |issue=2 |pages=86–91 |year=2015 |pmid=25712898 |pmc=4401105 |doi=10.1530/EC-14-0113 |url=}}</ref> | |
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| Disease
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| !Causes
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| !Symptoms
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| !Diagnosis and treatment
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| |- Diagnostic criteria of SIADH include:
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| |SIADH
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| |SIADH is a syndrome characterized by excessive release of [[Vasopressin|antidiuretic hormone]] (ADH or vasopressin) from the [[posterior pituitary]] gland or another source. The result is [[hyponatremia]], and sometimes fluid overload.
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| |Symptoms are variable. Ranging from [[nausea/vomiting]],[[cramps]],[[depressed mood]],[[irritability]],[[confusion]] and[[ hallucinations]]. In severe cases [[seizures]] ,[[stupor]] or [[coma ]]may result.
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| |[[Hyponatremia ]] <135 mmol/l
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| [[Decreased effective serum osmolalit]]y<275mosm
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| [[Urine sodium concentration]]>40mmol/litre
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| [[Plasma uric acid]] <200;FeUrate>12%
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| Absence of edematous disease like[[ cardiac failure]], [[liver cirrhosis]],[[ nephrotic syndrome]].
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| normal [[adrenal]] and thyroid function
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| | {| style="border: 0px; font-size: 90%; margin: 3px; width: 1000px" align="center" |
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| | ! style="background: #4479BA; width: 200px;" | {{fontcolor|#FFF|Differential Diagnosis}} |
| | ! style="background: #4479BA; width: 300px;" | {{fontcolor|#FFF|Similar Features}} |
| | ! style="background: #4479BA; width: 300px;" | {{fontcolor|#FFF|Differentiating Features}} |
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| |Cerebral salt wasting | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[SIADH]] |
| | Cerebral salt wasting is defined as the renal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume. | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| |polyuria,polydipsia,lightheadedness, muscle cramps,[[orthostatic hypotension]],[[headaches]]
| | *Excessive release of [[Vasopressin|antidiuretic hormone (ADH or vasopressin)]] from the [[posterior pituitary]] gland or another source. |
| |The patient is[[ hypovolemic]] and [[hyponatremic]]. | | *[[Hyponatremia]] |
| Treatment is with adequate [[hydration]] and [[sodium]] replacement.
| | *[[Fluid]] overload |
| | *[[Hyponatremia]] <135 mmol/l |
| | *Effective serum [[osmolality]] < 275 mOsm |
| | *Urine [[sodium]] concentration > 40 mMol/l |
| | *Plasma [[uric acid]] < 200 |
| | *Absence of [[edema]]-inducing diseases, such as [[heart failure]], [[liver cirrhosis]], and [[nephrotic syndrome]] |
| | *Normal [[adrenal]] and [[thyroid]] function |
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| | * [[Weight loss]] (in case of [[malignancy]]) |
| | * History of head [[trauma]] |
| | * History of medication intake |
| | * Positive [[family history]] |
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| |[[Adrenal insufficiency]] | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Cerebral salt wasting syndrome]] |
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| | *[[Hyponatremia]] |
| | *Urine [[sodium]] concentration > 40 mMol/l |
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| |[[Adrenal insufficiency]] ranges from mild nonspecific symptoms to life-threatening [[shock]] like condition. | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| An important distinction in these patients is the presence of[[ mineralocorticoid deficiency]]. Those with [[secondary]] or [[tertiary adrenal insufficiency]] will typically have preserved[[ mineralocorticoid]] function due to the separate feedback systems.
| | *[[Hypovolemia]] |
| Adrenal insufficiency can be [[primary]], [[secondary]] or[[ tertiary]].
| | *Intracranial [[diseases]], such as: |
| | | **[[Tumor]] |
| Common causes of primary adrenal insufficiency:
| | **[[Trauma]] |
| *[[Autoimmune]] | | **[[Hematoma]] |
| *[[Iatrogenic]] | |
| *[[Drugs]] | |
| *Others- [[adrenal hemorrhage]], [[cancer]],[[ infection]]. | |
| *[[congenital]]. | |
| Secondary adrenal insufficiency refers to decreased [[adrenocorticotropic hormone]] (ACTH) stimulation of the [[adrenal cortex]] and therefore does not affect [[aldosterone levels]]. [[Traumatic brain injury (TBI) ]]and [[panhypopituitarism]] are common causes.
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| Tertiary adrenal insufficiency refers to decreased hypothalamic stimulation of the pituitary to secrete ACTH.
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| Exogenous steroid administration is the most common cause of tertiary adrenal insufficiency.
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| * fatigue
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| * muscle weakness
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| * loss of appetite
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| * weight loss
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| * abdominal pain
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| *diarrhea
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| *Vomiting
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| Chronic disease is characterized by weight loss,sparse axillary hair,hyperpigmentation of the skin,orthostatic hypotension.
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| Acute addisonian crisis is characterized by fever and hypotension. A low sodium with a high potassium level and mild acidosis are also present.
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| |The diagnosis of Addison disease is made through rapid ACTH administration and measurement of cortisol.Lab findings include white blood cell count with moderate neutropenia,lymphocytosis,and eosinophilia;elevated serum potassium and urea nitrogen;low sodium;low blood glucose;and morning low plasma cortisol.
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| The definitive diagnosis is the cosyntropin or ACTH stimulation test. A cortisol level is obtained before and after administering ACTH. A normal person should show a brisk rise in cortisol level after ACTH administration.
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| Management: The management of Addison disease involves:
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| *Gluocorticoid
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| *Mineralocorticoid
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| *Sodium chloride replacement.
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| Adrenal crisis:
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| *In adrenal crisis,get a cortisol level,then rapidly administer fluids and hydrocortisone.( Adrenal crisis may occur in previously undiagnosed patient with adrenal insufficiency who has
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| *Undergone surgery
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| *Serious infection
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| *Any major stressful conditions.
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| *Bilateral adrenal infarction or hemorrhage
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| *Patient who is abruptly withdrawn from chronic glucocorticoid therapy
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| |Hypopituitarism: | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Adrenal insufficiency]] |
| |Hypopituitarism is defined as the partial or complete loss of anterior pituitary function that can result from acquired or congenital causes. | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| Etiology is as follows:
| | *[[Hyponatremia]] |
| *Pituitary tumors | |
| *Sellar tumors
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| *Head trauma
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| *Infection
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| *empty sella
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| *infiltration
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| *Idiopathic
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| *congenital
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| Signs and symptoms of hypopituitarism vary, depending on the deficient
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| hormone and severity of the disorder,some of the symptoms may be as follows:
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| * Fatigue | | *[[Weight loss]] |
| * Weight loss
| | *Sparse [[axillary]] hair |
| * Decreased libido | | *[[Hyperpigmentation]] |
| * Decreased appetite | | *[[Orthostatic hypotension]] |
| * Facial puffiness | | *[[Fever]] |
| * Anemia | | *[[Hypotension]] |
| * Infertility | | *[[Eosinophilia]] |
| * Cold insensitivity. | | *[[Hyperkalemia]] |
| * amenorrha,inability to lactate in breast feeding women | | *[[Hypoglycemia]] |
| * Decreased facial or body hair in men | | *Morning low plasma [[cortisol]] |
| * Short stature in children | |
| |The diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitary hormone deficiency. The clinical manifestations of hypopituitarism result from the degree of the specific hormone deficiency. A thorough and longitudinal history and physical examination, including visual field testing, are important.
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| Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary (in order of frequency: growth hormone deficiency>secondary hypogonadism>secondary hypothyroidism>secondary adrenal failure).The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones (hydrocortisone, DHEA, thyroxine, testosterone or oestradiol, growth hormone. surgery, and/or radiotherapy to restore normal endocrine function and quality of life. Patients with hypopituitarism require lifelong monitoring of serum hormone levels and symptoms of hormone deficiency or excess. Long-term care and monitoring of patients with hypopituitarism requires a experienced endocrinologist.
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| |Hypothyroidism | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Hypopituitarism]] |
| |Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to autoimmune causes described below: | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Congenital | | *[[Hyponatremia]] |
| *Autoimmune
| | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Drugs | | * [[Fatigue]] |
| *Post surgery | | * [[Weight loss]] |
| *post radiation | | * Decreased [[libido]] |
| *Infiltrative e.g., amyloid | | * Decreased [[appetite]] |
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| | * Facial [[puffiness]] |
| * Fatigue
| | * [[Anemia]] |
| * Constipation | | * [[Infertility]] |
| * Dry skin | | * [[Cold intolerance]] |
| * Weight gain | | * [[Amenorrhea]] |
| * Cold intolerance | | * Inability to lactate in [[breast feeding]] women |
| * Puffy face | | * Decreased [[facial]] or [[body hair]] in men |
| * Hoarseness | | * [[Short stature]] in children |
| * Muscle weakness
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| * Elevated blood cholesterol level
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| * Bradycardia
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| * Myopathy
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| * Depression | |
| * Impaired memory | |
| | Diagnosis of hypothyroidism is based on blood tests,T3(triiodothyronine),T4(Thyroxine) and TSH (thyroid stimulating hormone). Signs and symptoms are neither sensitive nor specific for the diagnosis. TSH is the most sensitive tool for screening,diagnosis and treatment follow up, when pituitary is normal. The drug of choice for treatment is Levothyroxine.
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| |Psychogenic polydipsia | | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Psychogenic polydipsia]] |
| | Also called as primary polydipsia is characterized by polyuria and polydipsia. Causes could be: | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| * Defect in the hypothalamus | | *[[Fluid]] overload |
| *Adverse effect of a medication | | *[[Hyponatremia]] |
| *Traumatic brain injury | | | style="padding: 5px 5px; background: #F5F5F5;" | |
| *Psychiatric disorders such as schizophrenia | | *Defect in the [[hypothalamus]] |
| |polyuria,polydipsia,confusion,lethargy,psychosis,seizures and sometimes, even death.
| | *[[Polyuria]] |
| |Evaluation of psychiatric patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria, hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy in psychiatric patients should include fluid restriction and behavioral and pharmacologic modalities. The water deprivation test is the gold standard test to differentiate central or nephrogenic diabetes insipidus (DI) from primary polydipsia (PP) in patients with polyuria and polydipsia. n healthy subjects, water deprivation causes the plasma osmolality to rise above 280–290 mOsmol/kg, which leads to the release of AVP into the circulation. In the collecting ducts of the kidney, AVP binds to the vasopressin type 2 receptor and this is followed by expression of aquaporin 2 channels. This results in increased water retention with a rise in urine osmolality to a maximum of 1000–1200 mOsmol/kg and restoration of plasma osmolality toward the reference range.
| | *[[Polydipsia]] |
| | *[[Confusion]] |
| | *[[Lethargy]] |
| | *[[Psychosis]] |
| | *[[Seizures]] |
| |} | | |} |
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| ==References== | | ==References== |
| {{Reflist|2}} | | {{Reflist|2}} |
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| [[Category:Needs content]] | | [[Category:Medicine]] |
| [[Category:Endocrinology]] | | [[Category:Endocrinology]] |
| | [[Category:Nephrology]] |
| [[Category:Neurology]] | | [[Category:Neurology]] |
| [[Category:Nephrology]] | | [[Category:Up-To-Date]] |
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