Differentiating Diabetes insipidus from other diseases: Difference between revisions
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** [[Hypothyroidism]] | ** [[Hypothyroidism]] | ||
** [[Adrenal failure]] | ** [[Adrenal failure]] | ||
** [[Diabetes insipidus]] ( | ** [[Diabetes insipidus]] (e.g., excessive fluid intake and urination) | ||
** Growth failure and [[delayed puberty]] | ** Growth failure and [[delayed puberty]] | ||
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* [[Urine osmolality]] <100 mmol/ | * [[Urine osmolality]] <100 mmol/ | ||
* [[Arginine vasopressin]] level >4.6 pmol/ | * [[Arginine vasopressin]] level >4.6 pmol/ | ||
* | * Little or no response to administration of exogenous [[arginine vasopressin]] | ||
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|[[Hypercalcemia]] | |[[Hypercalcemia]] | ||
Revision as of 14:09, 27 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Omodamola Aje B.Sc, M.D. [2]
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 urine 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, intra-hypothalamic 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
- Congenital malformations
- Acquired
- Nephrogenic diabetes insipidus
- Acquired
- Drug-induced (demeclocycline, lithium, cisplatin, methoxyflurane, etc.)
- Hypercalcemia, hypokalemia
- Infiltrating lesions (sarcoidosis, amyloidosis, multiple myeloma, Sjogren's disease)
- Vascular (sickle cell disease)
- Congenital
- X-linked recessive (OMIM 304800): AVP V2 receptor gene mutations
- Autosomal recessive: AQP2 water channel gene mutations
- Acquired
- Primary polydipsia
- Psychogenic
- Dipsogenic (downward resetting of thirst threshold)
- Gestational diabetes insipidus
- Diabetes mellitus
| Type of DI | Subclass | Disease | Defining signs and symptoms | Lab/Imaging findings |
|---|---|---|---|---|
| Central | Acquired | Histiocytosis |
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| Craniopharyngioma |
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| Sarcoidosis |
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| Congenital | Hydrocephalus |
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Dilated ventricles on CT and MRI | |
| Wolfram Syndrome (DIDMOAD) |
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| Nephrogenic | Acquired | Drug-induced (demeclocycline, lithium) |
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| Hypercalcemia |
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| Hypokalemia |
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| Multiple myeloma |
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| Sickle cell disease |
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| Primary polydipsia | Psychogenic |
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| Gestational diabetes insipidus |
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| Diabetes mellitus |
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References
- ↑ 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.
- ↑ 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.
- ↑ Barrett TG, Bundey SE (1997). "Wolfram (DIDMOAD) syndrome". J Med Genet. 34 (10): 838–41. PMC 1051091. PMID 9350817.
- ↑ Ghosh KN, Bhattacharya A (1992). "Gonotrophic nature of Phlebotomus argentipes (Diptera: Psychodidae) in the laboratory". Rev Inst Med Trop Sao Paulo. 34 (2): 181–2. PMID 1340034.