Adipsia

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Adipsia
Other nameshypodipsia
Vasopressin structure.png
Molecular structure of vasopressin. This hormone is related to Type A and Type B adipsia.

Adipsia, also known as hypodipsia, is a symptom of inappropriately decreased or absent feelings of thirst. [1] [2] It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys. This causes the person to retain water and ultimately become unable to feel thirst. Due to its rarity, the disorder has not been the subject of many research studies.

Contents

Adipsia may be seen in conditions such as diabetes insipidus [3] and may result in hypernatremia. [4] It can occur as the result of abnormalities in the hypothalamus, pituitary and corpus callosum, [5] as well as following pituitary/hypothalamic surgery. [6]

It is possible for hypothalamic dysfunction, which may result in adipsia, to be present without physical lesions in the hypothalamus, although there are only four reported cases of this. [7] There are also some cases of patients experiencing adipsia due to a psychiatric disease. In these rare psychogenic cases, the patients have normal levels of urine osmolality as well as typical ADH activity. [8]

Cause

Dopamine

Dopamine, a neurotransmitter, has been linked with feeding behaviors. In an experiment, scientists measured how much food and water mice consumed when they were born without dopamine in their systems. They found that without dopamine, the mice would starve and be dehydrated to the point of death. The scientists then injected the mice without dopamine with its precursor, L-DOPA, and the mice started eating again. But, even though the mice were born without dopamine in their systems, they still had the capacity to control their feeding and drinking behaviors, suggesting that dopamine does not play a role in developing those neural circuits. Instead, dopamine is more closely related to the drive for hunger and thirst. Although the lack of dopamine resulted in adipsia in these rats, low levels of dopamine do not necessarily cause adipsia. [9]

The nigrostriatal pathway (highlighted in blue) is crucial for dopamine production and transmission. Nigrostriatal pathway.png
The nigrostriatal pathway (highlighted in blue) is crucial for dopamine production and transmission.
Location of the hypothalamus in the brain. 1806 The Hypothalamus-Pituitary Complex.jpg
Location of the hypothalamus in the brain.

Other findings in support of the role of dopamine in thirst regulation involved the nigrostriatal pathway. After completely degenerating the pathway, the animal becomes adipsic, aphagic, and loses its interest in exploring. Although dopamine plays a role in adipsia, there is no research involving exclusively the relationship between adipsia and dopamine, as changes in dopamine simultaneously mediate changes in eating and curiosity, in addition to thirst. [10]

Hypothalamus

Adipsia can tend to result from lesions to hypothalamic regions involved in thirst regulation. These lesions can be congenital, acquired, trauma, or even surgery. Lesions or injuries to those hypothalamic regions cause adipsia because the lesions cause defects in the thirst regulating center which can lead to adipsia. Lesions in that region can also cause adipsia because of the extremely close anatomical proximity of the hypothalamus to ADH-related osmoreceptors. [8]

Diagnosis

Symptoms

Diagnosing adipsia can be difficult as there is no set of concrete physical signs that are adipsia specific. Changes in the brain that are indicative of adipsia include those of hyperpnea, muscle weakness, insomnia, lethargy, and convulsions (although uncommon except in extreme cases of incredibly rapid rehydration). Patients with a history of brain tumors, or congenital malformations, may have hypothalamic lesions, which could be indicative of adipsia. [4] Some adults with Type A adipsia are anorexic in addition to the other symptoms. [11]

Testing

Initial testing for adipsia involves electrolyte, blood urea nitrogen (BUN) and creatinine levels, serum and urine osmolality, blood hormone levels, like vasopressin (AVP). In patients who have defects in thirst regulation and vasopressin secretion, serum vasopressin levels are low or absent. [12] Measurements of urine electrolytes and osmolality are critical in determining the central, rather than renal, nature of the defect in water homeostasis. In adipsia, the fractional excretion of sodium is less than 1%, unless a coexisting defect in AVP secretion is present. In salt intoxication, the urine sodium concentrations are very high and fractional excretion of sodium is greater than 1%. Initial test results may be suggestive of diabetes insipidus. The circulating AVP levels tend to be high, which indicate an appropriate response of the pituitary to hyperosmolality. Patients may have mild stable elevations of serum sodium concentrations, along with elevations in both BUN and creatinine levels and in the BUN/creatinine ratio. [4]

Characteristic

Type A

Type A (essential hypernatremia syndrome) involves an increase of the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst. This is the most characterized sub-type of adipsia, however there is no known cause for Type A adipsia. There is debate over whether osmoreceptor resetting could lead to the increase in threshold. Other studies have shown that it is the loss of osmoreceptors, not resetting, that cause the change in threshold. [13] Patients with Type A adipsia can be at risk of seizures if they rapidly re-hydrate or quickly add a significant amount of sodium into their bodies. If not treated, Type A adipsia could result in both a decrease in the size of the brain and bleeding in the brain. [11]

Type B

Type B adipsia occurs when vasopressin responses are at decreased levels in the presence of osmotic stimuli. Although minimal, there is still some secretion of AVP. This type may be due to some elimination of osmoreceptors. [13]

Type C

Dopamine pathways in the brain. The production of dopamine is concentrated in the Ventral Tegmental Area and the Substantia Nigra. Dopamine Pathways.png
Dopamine pathways in the brain. The production of dopamine is concentrated in the Ventral Tegmental Area and the Substantia Nigra.

Type C adipsia (type C osmoreceptor dysfunction) involves complete elimination of osmoreceptors, and as a result have no vasopressin release when there normally would be. Type C is generally the adipsia type found in patients with adipsic diabetes insipidus. [13]

Type D

Type D is the least commonly diagnosed and researched type of adipsia. The AVP release in this subtype occurs with normally functioning levels of osmoregulation. [13]

Management

People affected by adipsia lack the ability to feel thirst; thus, they often must be directed to drink. Adipsic persons may undergo training to learn when it is necessary that they drink water. Currently, there is no medicine available to treat adipsia. For people with adipsia because of hypothalamic damage, there is no surgical or medicinal option to fix the damage. In some cases where adipsia was caused by growths on thirst centers in the brain, surgical removal of the growths was successful in treating adipsia. Although adipsic persons must maintain a strict water intake schedule, their diets and participation in physical activities are not limited. People affected by diabetes insipidus have the option of using the intranasal or oral hormone desmopressin acetate (DDAVP), which is molecularly similar enough to vasopressin to perform its function. In this case, desmopressin helps the kidneys to promote reabsorption of water. [4] Some doctors have reported success in treating psychogenic adipsic patients with electroconvulsive therapy, although the results are mixed and the reason for its success is still unknown. [8] Additionally, some patients who do not successfully complete behavioral therapy may require a nasogastric tube in order to maintain healthy levels of fluids. [8]

See also

Related Research Articles

<span class="mw-page-title-main">Diabetes insipidus</span> Condition characterized by large amounts of dilute urine and increased thirst

Diabetes insipidus (DI), alternately called arginine vasopressin deficiency (AVP-D) or arginine vasopressin resistance (AVP-R), is a condition characterized by large amounts of dilute urine and increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of fluid has little effect on the concentration of the urine. Complications may include dehydration or seizures.

<span class="mw-page-title-main">Hypothalamus</span> Area of the brain below the thalamus

The hypothalamus is a small part of the vertebrate brain that contains a number of nuclei with a variety of functions. One of the most important functions is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. It forms the basal part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is about the size of an almond.

Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. Symptoms can be absent, mild or severe. Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance. Severe symptoms include confusion, seizures, and coma; death can ensue.

<span class="mw-page-title-main">Vasopressin</span> Mammalian hormone released from the pituitary gland

Human vasopressin, also called antidiuretic hormone (ADH), arginine vasopressin (AVP) or argipressin, is a hormone synthesized from the AVP gene as a peptide prohormone in neurons in the hypothalamus, and is converted to AVP. It then travels down the axon terminating in the posterior pituitary, and is released from vesicles into the circulation in response to extracellular fluid hypertonicity (hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into the circulation from the filtrate in the kidney tubules of the nephrons. Second, AVP constricts arterioles, which increases peripheral vascular resistance and raises arterial blood pressure.

<span class="mw-page-title-main">Posterior pituitary</span> Posterior lobe of the pituitary gland

The posterior pituitary is the posterior lobe of the pituitary gland which is part of the endocrine system. The posterior pituitary is not glandular as is the anterior pituitary. Instead, it is largely a collection of axonal projections from the hypothalamus that terminate behind the anterior pituitary, and serve as a site for the secretion of neurohypophysial hormones directly into the blood. The hypothalamic–neurohypophyseal system is composed of the hypothalamus, posterior pituitary, and these axonal projections.

<span class="mw-page-title-main">Renal physiology</span> Study of the physiology of the kidney

Renal physiology is the study of the physiology of the kidney. This encompasses all functions of the kidney, including maintenance of acid-base balance; regulation of fluid balance; regulation of sodium, potassium, and other electrolytes; clearance of toxins; absorption of glucose, amino acids, and other small molecules; regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D.

Polydipsia is excessive thirst or excess drinking. The word derives from the Greek πολυδίψιος (poludípsios) "very thirsty", which is derived from πολύς + δίψα. Polydipsia is a nonspecific symptom in various medical disorders. It also occurs as an abnormal behaviour in some non-human animals, such as in birds.

<span class="mw-page-title-main">Hypopituitarism</span> Medical condition

Hypopituitarism is the decreased (hypo) secretion of one or more of the eight hormones normally produced by the pituitary gland at the base of the brain. If there is decreased secretion of one specific pituitary hormone, the condition is known as selective hypopituitarism. If there is decreased secretion of most or all pituitary hormones, the term panhypopituitarism is used.

<span class="mw-page-title-main">Desmopressin</span> Medication

Desmopressin, sold under the trade name DDAVP among others, is a medication used to treat diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease, and high blood urea levels. In hemophilia A and von Willebrand disease, it should only be used for mild to moderate cases. It may be given in the nose, by injection into a vein, by mouth, or under the tongue.

Hypernatremia, also spelled hypernatraemia, is a high concentration of sodium in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain. Normal serum sodium levels are 135–145 mmol/L. Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. Severe symptoms typically only occur when levels are above 160 mmol/L.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia.

<span class="mw-page-title-main">Conivaptan</span> Chemical compound

Conivaptan, sold under the brand name Vaprisol, is a non-peptide inhibitor of the receptor for anti-diuretic hormone, also called vasopressin. It was approved in 2004 for hyponatremia. The compound was discovered by Astellas and marked in 2006. The drug is now marketed by Cumberland Pharmaceuticals, Inc.

An osmoreceptor is a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure. Osmoreceptors can be found in several structures, including two of the circumventricular organs – the vascular organ of the lamina terminalis, and the subfornical organ. They contribute to osmoregulation, controlling fluid balance in the body. Osmoreceptors are also found in the kidneys where they also modulate osmolality.

Nephrogenic diabetes insipidus, recently renamed arginine vasopressin resistance (AVP-R) and previously known as renal diabetes insipidus, is a form of diabetes insipidus primarily due to pathology of the kidney. This is in contrast to central or neurogenic diabetes insipidus, which is caused by insufficient levels of vasopressin. Nephrogenic diabetes insipidus is caused by an improper response of the kidney to vasopressin, leading to a decrease in the ability of the kidney to concentrate the urine by removing free water.

<span class="mw-page-title-main">Primary polydipsia</span> Medical condition

Primary polydipsia and psychogenic polydipsia are forms of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. Psychogenic polydipsia caused by psychiatric disorders—oftentimes schizophrenia—is frequently accompanied by the sensation of dry mouth. Some conditions with polydipsia as a symptom are explicitly non-psychogenic. Primary polydipsia is a diagnosis of exclusion.

<span class="mw-page-title-main">Fluid deprivation test</span>

A fluid or water deprivation test is a medical test which can be used to determine whether the patient has diabetes insipidus as opposed to other causes of polydipsia. The patient is required, for a prolonged period, to forgo intake of water completely, to determine the cause of the thirst.

<span class="mw-page-title-main">Neurophysin II</span> Cleavage product of the arginine vasopressin gene

Neurophysin II is a carrier protein with a size of 19,687.3 Da and is made up of a dimer of two virtually identical chains of amino acids. Neurophysin II is a cleavage product of the AVP gene. It is a neurohypophysial hormone that is transported in vesicles with vasopressin, the other cleavage product, along axons, from magnocellular neurons of the hypothalamus to the posterior lobe of the pituitary. Although it is stored in neurosecretory granules with vasopressin and released with vasopressin into the bloodstream, its biological action is unclear. Neurophysin II is also known as a stimulator of prolactin secretion.

Central diabetes insipidus, recently renamed arginine vasopressin deficiency (AVP-D), is a form of diabetes insipidus that is due to a lack of vasopressin (ADH) production in the brain. Vasopressin acts to increase the volume of blood (intravascularly), and decrease the volume of urine produced. Therefore, a lack of it causes increased urine production and volume depletion.

Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, genetic disorders, radiation, surgery, head trauma, lesion, tumour or other physical injury to the hypothalamus. The hypothalamus is the control center for several endocrine functions. Endocrine systems controlled by the hypothalamus are regulated by antidiuretic hormone (ADH), corticotropin-releasing hormone, gonadotropin-releasing hormone, growth hormone-releasing hormone, oxytocin, all of which are secreted by the hypothalamus. Damage to the hypothalamus may impact any of these hormones and the related endocrine systems. Many of these hypothalamic hormones act on the pituitary gland. Hypothalamic disease therefore affects the functioning of the pituitary and the target organs controlled by the pituitary, including the adrenal glands, ovaries and testes, and the thyroid gland.

Copeptin is a 39-amino acid-long peptide derived from the C-terminus of pre-pro-hormone of arginine vasopressin, neurophysin II and copeptin. Arginine vasopressin (AVP), also known as the antidiuretic hormone (ADH), is encoded by the AVP gene and is involved in multiple cardiovascular and renal pathways and abnormal level of AVP are associated with various diseases. Hence measurement of AVP would be useful, but is not commonly carried out in clinical practice because of its very short half-life making it difficult to quantify. In contrast, copeptin can be immunologically tested with ease and therefore can be used as a vasopressin surrogate marker.

References

  1. ↑ "adipsia | pathology". Encyclopædia Britannica. Retrieved 2016-04-26.
  2. ↑ Lin, M; Liu, SJ; Lim, IT (August 2005). "Disorders of water imbalance". Emergency Medicine Clinics of North America. 23 (3): 749–70, ix. doi:10.1016/j.emc.2005.03.001. PMID   15982544.
  3. ↑ Crowley, R. K.; Sherlock, M.; Agha, A.; Smith, D.; Thompson, C. J. (2007). "Clinical insights into adipsic diabetes insipidus: a large case series". Clinical Endocrinology. 66 (4): 475–82. doi:10.1111/j.1365-2265.2007.02754.x. PMID   17371462. S2CID   28845882.
  4. 1 2 3 4 Dharnidharka, V.R.; Langman, C.B. (2014). "Adipsia treatment and management". EMedicine.
  5. ↑ Kim, Boo Gyoung; Kim, Ka Young; Park, Youn Jeong; Yang, Keun Suk; Kim, Ji Hee; Jung, Hee Chan; Nam, Hee Chul; Kim, Young Ok; Yun, Yu Seon (2012). "A Case of Adipsic Hypernatremia Associated with Anomalous Corpus Callosum in Adult with Mental Retardation". Endocrinology and Metabolism. 27 (3): 232–6. doi: 10.3803/EnM.2012.27.3.232 .
  6. ↑ Sherlock, M.; Agha, A.; Crowley, R.; Smith, D.; Thompson, C. J. (2006). "Adipsic diabetes insipidus following pituitary surgery for a macroprolactinoma". Pituitary. 9 (1): 59–64. doi:10.1007/s11102-006-8280-x. PMID   16703410. S2CID   8678093.
  7. ↑ Hayek, A; Peake, GT (1982). "Hypothalamic adipsia without demonstrable structural lesion". Pediatrics. 70 (2): 275–8. doi:10.1542/peds.70.2.275. PMID   6808452. S2CID   32259354.
  8. 1 2 3 4 Harrington, C.; Grossman, J.; Richman, K. (2014). "Psychogenic adipsia presenting as acute kidney injury: case report and review of disorders of sodium and water metabolism in psychiatric illness". Psychosomatics. 55 (3): 289–295. doi: 10.1016/j.psym.2013.06.013 . PMID   24012289.
  9. ↑ Zhou, Q.Y.; Palmiter, R.D. (1995). "Dopamine-deficient mice are severely hypoactive, adipsic, and aphagic". Cell. 83 (7): 1197–1209. doi: 10.1016/0092-8674(95)90145-0 . PMID   8548806.
  10. ↑ Ungerstedt, U. (2014). "Adipsia and Aphagia after 6-Hydroxydopamine induced degeneration of the nigro-striatal dopamine system". Acta Physiologica. 82(S367): 95–122. doi:10.1111/j.1365-201X.1971.tb11001.x. PMID   4332694.
  11. 1 2 Braun, Michael; Barstow, Craig; Pyzocha, Natasha (May 1, 2015). "Diagnosis and management of sodium disorders: Hyponatremia and hypernatremia". American Family Physician. 91 (5): 299–307. PMID   25822386 . Retrieved April 26, 2016.
  12. ↑ "Adipsia Workup: Laboratory Studies, Imaging Studies, Other Tests". emedicine.medscape.com. Retrieved 2016-04-10.
  13. 1 2 3 4 Holley, A.D.; Green, S.; Davoren, P. (2007). "Extreme hypernatraemia: a case report and brief review" (PDF). Critical Care and Resuscitation. 9 (1): 55–8. PMID   17352668.
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