Diabetes insipidus natural history, complications and prognosis: Difference between revisions
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==Natural History== | ==Natural History== | ||
Diabetes insipidus if left untreated results in polyuria, nocturia, and polydipsia. This leads to an elevation in serum sodium and osmolality. The hyperosmolarity seen in this patients may also present with neurologic symptoms such as confusion, altered mental status, seizures, coma and death. | |||
The serum sodium concentration in untreated CDI is often in the high to normal range. This is required in order to provide the sensation of thirst in a patient and stimulate drinking in order to replace the water lost in the urine. However in patients that have some form of central nervous disorders, moderate to severe hypernatremia can develop as thirst is impaired or cannot be expressed. This can also occur in infants and young children who cannot independently access free water, and in the postoperative period in patients with unrecognized diabetes insipidus (DI). | |||
Patients with CDI may develop decreased bone mineral density at the lumbar spine and femoral neck, even in those treated with desmopressin (dDAVP).<ref name="pmid9661594">{{cite journal |vauthors=Pivonello R, Colao A, Di Somma C, Facciolli G, Klain M, Faggiano A, Salvatore M, Lombardi G |title=Impairment of bone status in patients with central diabetes insipidus |journal=J. Clin. Endocrinol. Metab. |volume=83 |issue=7 |pages=2275–80 |year=1998 |pmid=9661594 |doi=10.1210/jcem.83.7.4987 |url=}}</ref> It is unclear how the deficiency of ADH results in bone loss, particularly since treatment fails to prevent bone disease. However, since ADH acts upon both V1 and V2 receptors and desmopressin principally upon V2 receptors, one possible mechanism is that activation of V1 receptors stimulates bone formation. | |||
==Complications== | ==Complications== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Natural History
Diabetes insipidus if left untreated results in polyuria, nocturia, and polydipsia. This leads to an elevation in serum sodium and osmolality. The hyperosmolarity seen in this patients may also present with neurologic symptoms such as confusion, altered mental status, seizures, coma and death.
The serum sodium concentration in untreated CDI is often in the high to normal range. This is required in order to provide the sensation of thirst in a patient and stimulate drinking in order to replace the water lost in the urine. However in patients that have some form of central nervous disorders, moderate to severe hypernatremia can develop as thirst is impaired or cannot be expressed. This can also occur in infants and young children who cannot independently access free water, and in the postoperative period in patients with unrecognized diabetes insipidus (DI).
Patients with CDI may develop decreased bone mineral density at the lumbar spine and femoral neck, even in those treated with desmopressin (dDAVP).[1] It is unclear how the deficiency of ADH results in bone loss, particularly since treatment fails to prevent bone disease. However, since ADH acts upon both V1 and V2 receptors and desmopressin principally upon V2 receptors, one possible mechanism is that activation of V1 receptors stimulates bone formation.
Complications
Prognosis
References
- ↑ Pivonello R, Colao A, Di Somma C, Facciolli G, Klain M, Faggiano A, Salvatore M, Lombardi G (1998). "Impairment of bone status in patients with central diabetes insipidus". J. Clin. Endocrinol. Metab. 83 (7): 2275–80. doi:10.1210/jcem.83.7.4987. PMID 9661594.