SSRIs and the Syndrome of Inappropriate Antidiuretic Hormone Secretion

Jan 23, 2009 | Posted by: roboblogger | Full story: Nursing Center

Selective serotonin reuptake inhibitors, which include some of the mostly widely prescribed drugs in the United States, produce fewer adverse effects than other types of antidepressants.

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Since: Aug 08

Houston, TX

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#1
Mar 25, 2009
 

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Charming. Yet another side effect of SSRI/SNRI use. Anyone considering this type of drug should really do their homework.

And if you think the side effects are bad, just wait 'til you decide to try to get OFF the stuff. You might as well have been on heroin, it's that difficult to withdraw.
Rhonda off effexor

United States

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#2
Apr 5, 2009
 
I have been on effexor for about 2 years now and as of lately my insurance will not cover the perscription so i am tring to get off this medication. However, that isn't as easy as told...this has been a nightmare. I am not having an easy time coming off of this medicine. I am at week three and finally down to 37.5mg, and still can't get off of it. Does anybody know what it is about this medicine that makes it so difficult. I spoke with the pharmacy and I was told it is the hardest to come off of. I have a four year old son, so i can't do cold turkey and if i miss a does i literally go crazy. I shiver, feels like my head is on another planet, get sick, feels like i am crawling out of my skin, get emotional, i can hardly stand up. this is a nightmare. If anybody out there has any solution on how to do this and still manage to stay alive and sane, please email me at stardust_rhonda@yahooo.com
thank you and hopefully hear from somebody, as for the rest of you out their, please spread the word that it may fix things at first, but it turns into a nightmare...this medication is the worst out there and i would love to have a word or two with the makers....Rhonda Nichols
Norris Sevigny

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#3
Dec 3, 2011
 

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SSRI does have a network of different side effects. You should really get more information from your doctor before taking this drug. You can also get info at http://www.paxilbirthdefectlaw.com/paxil-fda-... for other need-to-knows about Paxil.
Anthony Stange

Torrance, CA

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#4
Dec 12, 2011
 

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Paxil is one of the leading antidepressants prescribed by doctors. Although the sad truth about it is that it has a lot of side effects. One of them is birth defects. Some babies born form women who took Paxil during the first trimester of pregnancy have developed birth defects. You can also read all about the use of SSRI at this site http://www.paxilbirthdefectlaw.com/paxil-info... .
btd

Bowmanville, Canada

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#5
Dec 12, 2011
 

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Anthony Stange wrote:
Paxil is one of the leading antidepressants prescribed by doctors. Although the sad truth about it is that it has a lot of side effects. One of them is birth defects. Some babies born form women who took Paxil during the first trimester of pregnancy have developed birth defects. You can also read all about the use of SSRI at this site http://www.paxilbirthdefectlaw.com/paxil-info... .
spam!!!@
btd

Bowmanville, Canada

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#6
Jan 20, 2012
 
SIADH, first reported by Bartter and Schwartz in 1967,1 is an osmoregulatory disorder with a number of causes, including drugs (box FB1).2 It is associated with impaired water excretion resulting in dilutional hyponatraemia. Plasma osmolarity is reduced (<280 mOsm/kg), while the urine is inappropriately concentrated (urine osmolarity >100 mOsm/kg). The differential diagnosis includes hyponatraemia caused by excessive sodium loss, such as with diuretic therapy, diarrhoea, vomiting or Addison's disease. Drugs are thought to cause SIADH by direct or indirect stimulation of vasopressin release from the posterior pituitary gland, although the mechanism is not known. Symptoms generally present at plasma sodium concentrations less than 130 mmol/l and include anorexia, nausea and vomiting, headache, diarrhoea, weakness, lethargy, confusion, convulsions and coma. Severity is usually determined by the speed of onset and extent of the fluid and electrolyte disturbances.
http://pmj.bmj.com/content/75/886/509.full

This completely explains why I felt better after drinking pedialite a baby ecletorlite replacement for those who want to know I could not handle the adult version of this. That is why the baby one was used...you could find me leaning on the wall outside the drug store like a wino popping lids of these bottles that look like baby bottles designed to just pop a nipple from a bottle on and feed to the baby... there I was sucking this orange colored drink out of a tiny hole...bottle after bottle.
Ahh the memories. I was so sick.
btd

Bowmanville, Canada

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#7
Jan 20, 2012
 
Demeclocycline is sometimes used to treat chronic SIADH,2but is not usually necessary in drug-induced SIADH since this usually resolves spontaneously once the responsible drug is withdrawn.

The elderly appear to be particularly at risk of developing drug-induced SIADH. In 1994 the CSM/MCA reported on 116 cases of antidepressant-induced hyponatraemia; 88 of these involved selective serotonin re-uptake inhibitors (SSRIs)
btd

Bowmanville, Canada

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#8
Jan 20, 2012
 
http://journals.lww.com/psychopharmacology/Ci...
Effexor induced SIADH yes it is there but I have no money to pay for it so I can't read it. Who wants to pay to read.. if your rich get and lets have a look.

Canadian Pharmacists Journal - Online Publication - Review of ...
www.cpjournal.ca Canadian Pharmacists Journal May 2009by S Zerjav - 2009 - Cited by 2 - Related articles
In addition to duloxetine and venlafaxine, there are 2 other SNRI-like ..... of these drugs to cause hyponatremia may all contribute to SNRI-induced seizures. ooo seizures nice...
btd

Bowmanville, Canada

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#9
Jan 20, 2012
 

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btd wrote:
SIADH, first reported by Bartter and Schwartz in 1967,1 is an osmoregulatory disorder with a number of causes, including drugs (box FB1).2 It is associated with impaired water excretion resulting in dilutional hyponatraemia. Plasma osmolarity is reduced (<280 mOsm/kg), while the urine is inappropriately concentrated (urine osmolarity >100 mOsm/kg). The differential diagnosis includes hyponatraemia caused by excessive sodium loss, such as with diuretic therapy, diarrhoea, vomiting or Addison's disease. Drugs are thought to cause SIADH by direct or indirect stimulation of vasopressin release from the posterior pituitary gland, although the mechanism is not known. Symptoms generally present at plasma sodium concentrations less than 130 mmol/l and include anorexia, nausea and vomiting, headache, diarrhoea, weakness, lethargy, confusion, convulsions and coma. Severity is usually determined by the speed of onset and extent of the fluid and electrolyte disturbances.
http://pmj.bmj.com/content/75/886/509.full
This completely explains why I felt better after drinking pedialite a baby ecletorlite replacement for those who want to know I could not handle the adult version of this. That is why the baby one was used...you could find me leaning on the wall outside the drug store like a wino popping lids of these bottles that look like baby bottles designed to just pop a nipple from a bottle on and feed to the baby... there I was sucking this orange colored drink out of a tiny hole...bottle after bottle.
Ahh the memories. I was so sick.
"Drugs are thought to cause SIADH by direct or indirect stimulation of vasopressin release from the posterior pituitary gland, although the mechanism is not known."
There it is again "thought to" just is not good enough now that I know they used the same "term" with all the ads as they are "thought to" a certain way...
look at the damage they have caused by guessing and even more damage they can't admit too because they kept covering it up..... the jig is up.
btd

Bowmanville, Canada

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#10
Jan 20, 2012
 
Syndrome of inappropriate secretion of antidiuretic hormone due to ...
www.sciencedirect.com/science/article/pii/s01... (06)00216-7by S Romero - 2007 - Cited by 16 - Related articles
Both SSRIs and venlafaxine have been associated with SIADH in numerous case ... of the clinical features associated with SSRI-induced SIADH in the elderly.

Introduction
Selective serotonin reuptake inhibitors (SSRIs) and venlafaxine are often used to treat depression in the elderly due to their low incidence of side effects. All five of the SSRIs currently available and venlafaxine have been associated with hyponatremia.

Case Report
This article describes the case of an 87-year-old man with depression who presented with hyponatremia after starting treatment with citalopram. After excluding other common causes of hyponatremia, a diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was confirmed. Sodium levels returned to the normal range following discontinuation of citalopram. Subsequently, due to the persistence of depression, treatment with venlafaxine was initiated. Three weeks later, hyponatremia associated with SIADH was once again diagnosed and venlafaxine was discontinued. The hyponatremia resolved in 2 weeks.

Discussion
Both SSRIs and venlafaxine have been associated with SIADH in numerous case reports and retrospective studies. Risk factors for developing hyponatremia with these drugs are advanced age and treatment with other medications. To our knowledge, this is the first case report in which SIADH was associated with two different families of antidepressants in the same patient.

Conclusion
Physicians should be aware of the risk of hyponatremia when prescribing SSRIs and venlafaxine in elderly patients with multiple drug therapies. Sodium levels should be monitored during treatment.

I was 46 tho I never did get a doc to dx it at the 4 different emergency rooms I went to. I do not think 46 is elderly. Especially now days with Madonna still doing videos at 50.
btd

Bowmanville, Canada

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#11
Jan 20, 2012
 
Pathophysiology
Serum sodium concentration is regulated by stimulation of thirst, secretion of ADH, feedback mechanisms of the renin-angiotensin-aldosterone system, and variations in renal handling of filtered sodium. Increases in serum osmolarity above the normal range (280-300 mOsm/kg) stimulate hypothalamic osmoreceptors, which, in turn, cause an increase in thirst and in circulating levels of ADH. ADH increases free water reabsorption from the urine, yielding urine of low volume and relatively high osmolarity and, as a result, returning serum osmolarity to normal. ADH is also secreted in response to hypovolemia, pain, fear, nausea, and hypoxia.

Aldosterone, synthesized by the adrenal cortex, is regulated primarily by serum potassium but also is released in response to hypovolemia through the renin-angiotensin-aldosterone axis. Aldosterone causes absorption of sodium at the distal renal tubule. Sodium retention obligates free water retention, helping to correct the hypovolemic state. The healthy kidney regulates sodium balance independently of ADH or aldosterone by varying the degree of sodium absorption at the distal tubule. Hypovolemic states, such as hemorrhage or dehydration, prompt increases in sodium absorption in the proximal tubule. Increases in vascular volume suppress tubular sodium reabsorption, resulting in natriuresis and helping to restore normal vascular volume. Generally, disorders of sodium balance can be traced to a disturbance in thirst or water acquisition, ADH, aldosterone, or renal sodium transport.

Hyponatremia is physiologically significant when it indicates a state of extracellular hyposmolarity and a tendency for free water to shift from the vascular space to the intracellular space. Although cellular edema is well tolerated by most tissues, it is not well tolerated within the rigid confines of the bony calvarium. Therefore, clinical manifestations of hyponatremia are related primarily to cerebral edema. The rate of development of hyponatremia plays a critical role in its pathophysiology and subsequent treatment. When serum sodium concentration falls slowly, over a period of several days or weeks, the brain is capable of compensating by extrusion of solutes and fluid to the extracellular space. Compensatory extrusion of solutes reduces the flow of free water into the intracellular space, and symptoms are much milder for a given degree of hyponatremia.

When serum sodium concentration falls rapidly, over a period of 24-48 hours, this compensatory mechanism is overwhelmed and severe cerebral edema may ensue, resulting in brainstem herniation and death.
btd

Bowmanville, Canada

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#12
Jan 20, 2012
 
Epidemiology
Frequency
United States
Hyponatremia is the most common electrolyte disorder, with a marked increase among hospitalized and nursing home patients. A 1985 prospective study of inpatients in a US acute care hospital found an overall incidence of approximately 1% and a prevalence of approximately 2.5%. On the surgical ward, approximately 4.4% of postoperative patients developed hyponatremia within 1 week of surgery. Hyponatremia has also been observed in approximately 30% of patients treated in the intensive care unit.[1]

International
Though clearly not indicative of the overall prevalence internationally, hyponatremia has been observed in as high as 42.6% of patients in a large acute care hospital in Singapore and in 30% of patients hospitalized in an acute care setting in Rotterdam.[2, 3]

Mortality/Morbidity
Pathophysiologic differences between patients with acute and chronic hyponatremia engender important differences in their morbidity and mortality.

Patients with acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema for a given serum sodium level. The primary cause of morbidity and death is brainstem herniation and mechanical compression of vital midbrain structures. Rapid identification and correction of serum sodium level is necessary in patients with severe acute hyponatremia to avert brainstem herniation and death.

Patients with chronic hyponatremia (developing over more than 48 h) experience milder degrees of cerebral edema for a given serum sodium level. Brainstem herniation has not been observed in patients with chronic hyponatremia. The principal direct causes of morbidity and death are status epilepticus (when chronic hyponatremia reaches levels of 110 mEq/L or less) and cerebral pontine myelinolysis (an unusual demyelination syndrome that occurs in association with chronic hyponatremia).

The distinction between acute hyponatremia and chronic hyponatremia has critical implications in terms of morbidity and mortality and in terms of proper corrective therapy.

A 2009 study of 98,411 hospitalized patients found that even mild degrees of hyponatremia were associated with increased in-hospital, 1-year and 5-year mortality rates. Mortality was particularly increased in those with cardiovascular disease, metastatic cancer, and those undergoing orthopedic procedures.[4]

A 2009 study in Copenhagen concluded that hyponatremia in the range of 130-137 mEq/L is also associated with increased mortality rates in the general population.[5]

Sex
Overall incidence of hyponatremia is approximately equal in males and females, though postoperative hyponatremia appears to be more common in menstruant females.

Age
Hyponatremia is most common in the extremes of age; these groups are less able to experience and express thirst and less able to regulate fluid intake autonomously. Specific settings that have been known to pose particular risk include the following:

Infants fed tap water in an effort to treat symptoms of gastroenteritis
Infants fed dilute formula in attempt to ration
Elderly patients with diminished sense of thirst, especially when physical infirmity limits independent access to food and drink
btd

Bowmanville, Canada

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#13
Jan 20, 2012
 
History
The number and severity of symptoms increase with the degree of hyponatremia and the rapidity with which it develops. When the serum sodium level falls gradually, over a period of several days or weeks, sodium levels as low as 110 mEq/L may be reached with minimal symptomatology. In contrast, an equivalent fall in serum sodium level over 24-48 hours may overwhelm compensatory mechanisms, leading to severe cerebral edema, coma, or brainstem herniation.

Symptoms range from mild anorexia, headache, and muscle cramps, to significant alteration in mental status including confusion, obtundation, coma, or status epilepticus.

Hyponatremia is often seen in association with pulmonary/mediastinal disease or CNS disorders. Hyponatremia must be considered in patients with pneumonia, active tuberculosis, pulmonary abscess, neoplasm, or asthma, as well as in patients with CNS infection, trauma, or neoplasm. Patients with carcinoma of the nasopharynx, duodenum, stomach, pancreas, ureter, prostate, or uterus also have an increased risk.

Hyponatremia is associated with numerous medications. The patient's medication list should be examined for drugs known to cause hyponatremia.

Hyponatremia has been noted in patients with poor dietary intake who consume large amounts of beer (called beer potomania) and after use of the recreational drug N- methyl-3,4-methylenedioxyamphe tamine (ie, MDMA or ecstasy). MDMA-induced hyponatremia occurs via multiple mechanisms; these include the induction of syndrome of inappropriate antidiuretic hormone secretion (SIADH), the encouragement to drink large amounts of water to prevent unpleasant side effects of the drug, and the tendency among those intoxicated to be involved in vigorous physical activity that results in heavy sweating.

A history of hypothyroidism or adrenal insufficiency should be sought because each is associated with hyposmolar hyponatremia.

Patients with clinically significant hyponatremia present with nonspecific symptoms attributable to cerebral edema. These symptoms, especially when coupled with a recent history of altered fluid balance, should suggest the possibility of hyponatremia.

Anorexia
Nausea and vomiting
Difficulty concentrating
Confusion
Lethargy
Agitation
Headache
Seizures
btd

Bowmanville, Canada

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#14
Jan 20, 2012
 
Physical
Physical findings are highly variable and dependent on the degree and the chronicity of hyponatremia. Patients with acutely developing hyponatremia are typically symptomatic at a level of approximately 120 mEq/L. Those patients with chronic hyponatremia tolerate much lower levels.

Most abnormal findings on physical examination are characteristically neurologic in origin.

Level of alertness ranging from alert to comatose
Variable degrees of cognitive impairment (eg, difficulty with short-term recall; loss of orientation to person, place, or time; frank confusion or depression)
Focal or generalized seizure activity
In those patients with acute severe hyponatremia, signs of brainstem herniation, including coma; fixed, unilateral, dilated pupil; decorticate or decerebrate posturing; sudden severe hypertension and respiratory arrest
In addition to neurologic findings, patients may exhibit signs of hypovolemia or hypervolemia. Determining the hydration status of the patient may help establish the etiology of the hyponatremia and direct subsequent treatment.

Dry mucous membranes, tachycardia, diminished skin turgor, and orthostasis suggest hypovolemic hyponatremia due to excessive loss of body fluids and replacement with inappropriately dilute fluids.
Pulmonary rales, S3 gallop, jugular venous distention, peripheral edema, or ascites suggest hypervolemic hyponatremia due to excess retention of sodium and free water (ie, cirrhosis, nephrotic syndrome, congestive heart failure).
Patients who lack findings of hypovolemia or hypervolemia are considered to have euvolemic hyponatremia, which is consistent with such etiologies as exogenous free water load, hypothyroidism, cortisol deficiency, or SIADH.
Other nonspecific signs include muscle weakness and cramping. Rhabdomyolysis is an occasional consequence of hyponatremia and should be considered in patients with muscle pain or tenderness.
This one I know "Rhabdomyolysis" look for urine that is the color of blood.
btd

Bowmanville, Canada

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#15
Jan 20, 2012
 
A list of drugs that cause it, if you are taking them be aware and if you are taking more than one you may want to talk to your doctor about that or do more research yourself..

Uncorrected hypothyroidism or cortisol deficiency (adrenal insufficiency, hypopituitarism)
Consumption of large quantities of beer or use of the recreational drug MDMA (ecstasy)
Hyponatremia can be caused by many medications. Known offenders include acetazolamide, amiloride, amphotericin, aripiprazole, atovaquone, thiazide diuretics, amiodarone, basiliximab, angiotensin II receptor blockers, angiotensin-converting enzyme inhibitors, bromocriptine, carbamazepine, carboplatin, carvedilol, celecoxib, cyclophosphamide, clofibrate, desmopressin, donepezil, duloxetine, eplerenone, gabapentin, haloperidol, heparin, hydroxyurea, indapamide, indomethacin, ketorolac, levetiracetam, loop diuretics, lorcainide, mirtazapine, mitoxantrone, nimodipine, oxcarbazepine, opiates, oxytocin, pimozide, propafenone, proton pump inhibitors, quetiapine, sirolimus, ticlopidine, tolterodine, vincristine, selective serotonin reuptake inhibitors, sulfonylureas, trazodone, tolbutamide, venlafaxine, zalcitabine, and zonisamide.

Previous
btd

Bowmanville, Canada

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#16
Jan 20, 2012
 
I personally was taking venlafaxine proton pump inhibitors and celecoxib
of course the venlafaxine was first then came the celecoxib and last the proton pump inhibitor... I think each new drug treats the side effects of the previous drug. me again I am like that always saying the darndest things.
btd

Bowmanville, Canada

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#17
Jan 20, 2012
 
Differentials (other things it could be)
Adrenal Insufficiency and Adrenal Crisis
Cirrhosis
Congestive Heart Failure and Pulmonary Edema
Gastroenteritis
Hypothyroidism and Myxedema Coma
Nephrotic Syndrome
Renal Failure, Acute
Renal Failure, Chronic and Dialysis Complications
Syndrome of Inappropriate Antidiuretic Hormone Secretion
Rob Smith

Chicago, IL

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#18
Jan 26, 2012
 
There are indeed many side effects that a person would encounter when using antidepressants. A person may react differently to a given medication and this article has given one of the most distressing side effects to the drug. If you want to know more about SSRIs, feel free to visit this site http://www.zoloftsertralinebirthdefects.com/s... .
Mr Sensible

Prestonpans, UK

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#19
Jan 26, 2012
 
btd, just glancing thru what youve posted and a new side effect thats appeared with me since I returned to being awake all night 3 wks ago is quite a powerful thirst if I go to bed and try and sleep. Never bothered last night, its 10.30pm and Ive been awake since 9pm last night I just end up going to bed and sleeping for bout 14 hrs when I do this then back to same pattern, but I did have a good day today, good run up the hill behind my house this morning suprised how quick I was given my delayed sleep phase, apparently the correct term getting the right amount of sleep but not at the right time
btd

Bowmanville, Canada

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#20
Jan 26, 2012
 
Rob Smith wrote:
There are indeed many side effects that a person would encounter when using antidepressants. A person may react differently to a given medication and this article has given one of the most distressing side effects to the drug. If you want to know more about SSRIs, feel free to visit this site http://www.zoloftsertralinebirthdefects.com/s... .
What we want to know Rob is when are you ambulance chasers going to do the decent thing and start taking withdrawal and drug damaged human being cases... figure out a way! It is the right thing to do and you know it.
Till then get lost.

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