Differentiating Diabetes insipidus from other diseases: Difference between revisions

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**Acquired  
**Acquired  
***Trauma (surgery, deceleration injury)  
***Trauma (surgery, deceleration injury)  
***Vascular (cerebral hemorrhage, infarctionanterior communicating artery aneurysm or ligation, intrahypothalamic hemorrhage)  
***Vascular (cerebral hemorrhage, infarction, anterior communicating artery aneurysm or ligation, intrahypothalamic hemorrhage)  
***Neoplastic (craniopharyngioma, meningioma, germinoma, pituitary tumor or metastases)  
***Neoplastic (craniopharyngioma, meningioma, germinoma, pituitary tumor or metastases)  
***Granulomatous (histiocytosis, sarcoidosis)  
***Granulomatous (histiocytosis, sarcoidosis)  
Line 37: Line 37:
**Psychogenic  
**Psychogenic  
**Dipsogenic (downward resetting of thirst threshold)  
**Dipsogenic (downward resetting of thirst threshold)  
*'''Pregnancy'''  
*'''Gestational Diabetes insipidus'''  
*'''Diabetes meliitus'''  
*'''Diabetes meliitus'''  
*'''Sickle cell disease'''
{| class="wikitable"
!Type of DI
!Subclass
!Disease
!Defining signs and symptoms
!Lab findings
!Treatment
|-
|Central
|Acquired
|Histiocytosis
|
* Bone lysis and fracture
* Purulent otitis media
* Diabetes insipidus and delayed puberty
* Maxillary, mandibular, and gingival disease
* Rash and maculoerythematous skin lesions
* Scaly, erythematous scalp patches
* Lung involvement
* GI bleeding
* Lymph node enlargement
|
|
|-
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|
|Pituitary tumor
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|
|-
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|Sarcoidosis
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|-
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|Hydrocephalus
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|-
|
|Congenital
|AVP-neurophysin gene mutations
|
|
|
|-
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|
|Wolfram Syndrome (DIDMOAD)
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|
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|-
|Nephrogenic
|Acquired
|Drug-induced (demeclocycline, lithium)
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|-
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|Hypercalcemia
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|-
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|Hypokalemia
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|-
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|Amyloidosis
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|-
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|Multiple myeloma
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|-
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|Sickle cell disease
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|-
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|Congenital
|AVP V2 receptor gene mutations
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|-
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|AQP2 water channel gene mutations
|
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|-
|Primary polydipsia
|
|Psychogenic
|
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|-
|Pregnancy
|
|Gestational diabetes insipidus
|
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|-
|Diabetes mellitus
|
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|-
|
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|}


==References==
==References==

Revision as of 13:58, 12 July 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Diabetes insipidus must be differentiated from other diseases that cause polyuria which is defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children, increased frequency or nocturia and polydipsia. It is important to know that levels of hypo or hypernatremia is not sufficient to describe the underlying cause of diabetes insipidus.

Differentiating Diabetes insipidus from other Diseases

Differentiating diabetes insipidus based on the type of diabetes insipidus caused

  • Central diabetes insipidus
    • Acquired
      • Trauma (surgery, deceleration injury)
      • Vascular (cerebral hemorrhage, infarction, anterior communicating artery aneurysm or ligation, intrahypothalamic hemorrhage)
      • Neoplastic (craniopharyngioma, meningioma, germinoma, pituitary tumor or metastases)
      • Granulomatous (histiocytosis, sarcoidosis)
      • Infectious (meningitis, encephalitis)
      • Inflammatory/autoimmune (lymphocytic infundibuloneurohypophysitis)
      • Drug/toxin-induced (ethanol, diphenylhydantoin, snake venom)
      • Other disorders (hydrocephalus, ventricular/suprasellar cyst, trauma, degenerative diseases)
      • Idiopathic
    • Congenital
      • Congenital malformations
        • Autosomal dominant: AVP-neurophysin gene mutations
        • Autosomal recessive [1][2]: Wolfram Syndrome (DIDMOAD) [3]
        • X-linked recessive
      • Idiopathic
  • Nephrogenic diabetes insipidus
    • Acquired
      • Drug-induced (demeclocycline, lithium, cisplatin, methoxyflurane, etc.)
      • Hypercalcemia, hypokalemia
      • Infiltrating lesions (sarcoidosis, amyloidosis, multiple myeloma, Sjoergen's disease)
      • Vascular (sickle cell disease)
    • Congenital
      • X-linked recessive (OMIM 304800): AVP V2 receptor gene mutations
      • Autosomal recessive: AQP2 water channel gene mutations
  • Primary polydipsia
    • Psychogenic
    • Dipsogenic (downward resetting of thirst threshold)
  • Gestational Diabetes insipidus
  • Diabetes meliitus
Type of DI Subclass Disease Defining signs and symptoms Lab findings Treatment
Central Acquired Histiocytosis
  • Bone lysis and fracture
  • Purulent otitis media
  • Diabetes insipidus and delayed puberty
  • Maxillary, mandibular, and gingival disease
  • Rash and maculoerythematous skin lesions
  • Scaly, erythematous scalp patches
  • Lung involvement
  • GI bleeding
  • Lymph node enlargement
Pituitary tumor
Sarcoidosis
Hydrocephalus
Congenital AVP-neurophysin gene mutations
Wolfram Syndrome (DIDMOAD)
Nephrogenic Acquired Drug-induced (demeclocycline, lithium)
Hypercalcemia
Hypokalemia
Amyloidosis
Multiple myeloma
Sickle cell disease
Congenital AVP V2 receptor gene mutations
AQP2 water channel gene mutations
Primary polydipsia Psychogenic
Pregnancy Gestational diabetes insipidus
Diabetes mellitus

References

  1. ↑ Willcutts MD, Felner E, White PC (1999). "Autosomal recessive familial neurohypophyseal diabetes insipidus with continued secretion of mutant weakly active vasopressin". Hum Mol Genet. 8 (7): 1303–7. PMID 10369876.
  2. ↑ Abu Libdeh A, Levy-Khademi F, Abdulhadi-Atwan M, Bosin E, Korner M, White PC; et al. (2010). "Autosomal recessive familial neurohypophyseal diabetes insipidus: onset in early infancy". Eur J Endocrinol. 162 (2): 221–6. doi:10.1530/EJE-09-0772. PMID 19897608.
  3. ↑ Barrett TG, Bundey SE (1997). "Wolfram (DIDMOAD) syndrome". J Med Genet. 34 (10): 838–41. PMC 1051091. PMID 9350817.

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