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Can Veltam Cause SIADH?
Question: Can Veltam cause SIADH? Is there a benchmark protocol to trace cause of SIADH? What are the side effects of Tolvaptan? Can common salt capsules do the needful?
Hi.
Thanks for asking in Healthcare Magic.
Syndrome of inappropriate ADH secretion (SIADH) is due to improper water excretion and the resultant hyponatremia. (decreased sodium level ). This is due to inappropriate ADH (anti diuretic hormone) secretion, can be a non physiologic release of vasopressin (ADH) or due to ectopic source.
The clinical manifestations are lethargy, nausea, vomiting and muscle cramps. There is no clear cut cause and the causes may be many. It can occur due to lung diseases, neuro psychiatric diseases, malignant tumors and major surgery (post operative pain), infections, trauma and some drugs. Clinical symptoms and plasma sodium level are useful in the diagnosis.
None of the drugs that you are taking (Atenolol, Clopidogrel, Finasteride, Tamsulosin) is reported to cause SIADH. The most common drugs causing SIADH are anti psychotic drugs like SSRI, tricyclic anti depressants, phenothiazines, anti cancer drugs like Cyclophosphamide and vinca alkaloids, Clonidine, Enalapril, Methyldopa and so on.
Tolvaptin is a vasopressin antagonist. Too rapid correction of hyponatremia with Tolvaptan can cause problems. It can cause GIT symptoms, increase in blood sugar level and fever. Less common are deep vein thrombosis (clopidogrel will reduce this),ischemic colitis, pulmonary embolism and increase in prothrombin time.
Salt capsules are secondary lines of treatment and used only in those with persistent hyponatremia.
I hope this is useful. Please address to me if you have any further concerns.
Regards.
Thanks for asking in Healthcare Magic.
Syndrome of inappropriate ADH secretion (SIADH) is due to improper water excretion and the resultant hyponatremia. (decreased sodium level ). This is due to inappropriate ADH (anti diuretic hormone) secretion, can be a non physiologic release of vasopressin (ADH) or due to ectopic source.
The clinical manifestations are lethargy, nausea, vomiting and muscle cramps. There is no clear cut cause and the causes may be many. It can occur due to lung diseases, neuro psychiatric diseases, malignant tumors and major surgery (post operative pain), infections, trauma and some drugs. Clinical symptoms and plasma sodium level are useful in the diagnosis.
None of the drugs that you are taking (Atenolol, Clopidogrel, Finasteride, Tamsulosin) is reported to cause SIADH. The most common drugs causing SIADH are anti psychotic drugs like SSRI, tricyclic anti depressants, phenothiazines, anti cancer drugs like Cyclophosphamide and vinca alkaloids, Clonidine, Enalapril, Methyldopa and so on.
Tolvaptin is a vasopressin antagonist. Too rapid correction of hyponatremia with Tolvaptan can cause problems. It can cause GIT symptoms, increase in blood sugar level and fever. Less common are deep vein thrombosis (clopidogrel will reduce this),ischemic colitis, pulmonary embolism and increase in prothrombin time.
Salt capsules are secondary lines of treatment and used only in those with persistent hyponatremia.
I hope this is useful. Please address to me if you have any further concerns.
Regards.
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Was taken to emergency upon a seizure. A CT scan of the brain was done which which was normal. Sodium level was 93. They started on very slow Hypertonic Saline 3% Sodium Chloride infusion brought sodium level to 135 in a week. But again the sodium level fell to 120 in 10 days. N S infusion was done, now sodium level is 138. Free water has been stopped. Cap of one litre of water per day has been put. Told that output (urine) has to be more than input (liquids) in the ratio 1.5::1.0; this is very difficult to do. What should be the regime to maintain correct sodium level? Tolvaptin has not been started yet.
The moment sodium level begins to fall there is disorientation. Body pain is continuous. Cannot read or write properly. A PET SCAN and a MRI of the brain has been asked for. The Neurologist says the nuero problem may be drug induced?.
Please advice.
The moment sodium level begins to fall there is disorientation. Body pain is continuous. Cannot read or write properly. A PET SCAN and a MRI of the brain has been asked for. The Neurologist says the nuero problem may be drug induced?.
Please advice.
Hi.
Welcome back.
As I wrote earlier, SIADH could be caused by many factors. In normal person elevation of vasopressin results in decreased water intake as thirst will be suppressed in them as a compensatory measure. So the chances of hyponatremia (low sodium level) is less . But in excessive vasopressin secretion, there will be intense thirst (although initially, the thirst and aldosterone secretion will be minimal) resulting in hyponatremia. The cause for excessive vasopressin needs to be identified and treated as this will offer a permanent measure.
3% hypertonic saline is given only when there is severe hyponatremia (Na < 115 mEq/L) or when mental changes like confusion or seizure are present. Usually it is a slow correction to prevent rapid fluid shifts. As you have mentioned, fluid intake is restricted to less than the urine output and loss due to sweating and other reasons, although strict monitoring is needed for this. The level of hyponatremia indirectly indicates the severity of the condition. The regimen will be decided by the treating Dr as it depends upon the severity and the level of plasma sodium.
Drugs like Tolvaptan or Conivaptan are vasopressin antagonists. They are also called as 'aquaretics' as they increase water excretion with little or no change in electrolyte excretion. Tolvaptan has a more specific action. Both are approved by FDA for the treatment of both euvolemic (normal volume) and hypervolemic (more volume) hyponatremic (low sodium) SIADH and I feel those are the first line drugs for you. Demeclocycline is an other alternative.
Please consult your Neurologist about the suitability of these drugs for you as they are the best judges in deciding your treatment.
I hope I have succeeded in providing the information you are looking for.
Best Wishes.
Welcome back.
As I wrote earlier, SIADH could be caused by many factors. In normal person elevation of vasopressin results in decreased water intake as thirst will be suppressed in them as a compensatory measure. So the chances of hyponatremia (low sodium level) is less . But in excessive vasopressin secretion, there will be intense thirst (although initially, the thirst and aldosterone secretion will be minimal) resulting in hyponatremia. The cause for excessive vasopressin needs to be identified and treated as this will offer a permanent measure.
3% hypertonic saline is given only when there is severe hyponatremia (Na < 115 mEq/L) or when mental changes like confusion or seizure are present. Usually it is a slow correction to prevent rapid fluid shifts. As you have mentioned, fluid intake is restricted to less than the urine output and loss due to sweating and other reasons, although strict monitoring is needed for this. The level of hyponatremia indirectly indicates the severity of the condition. The regimen will be decided by the treating Dr as it depends upon the severity and the level of plasma sodium.
Drugs like Tolvaptan or Conivaptan are vasopressin antagonists. They are also called as 'aquaretics' as they increase water excretion with little or no change in electrolyte excretion. Tolvaptan has a more specific action. Both are approved by FDA for the treatment of both euvolemic (normal volume) and hypervolemic (more volume) hyponatremic (low sodium) SIADH and I feel those are the first line drugs for you. Demeclocycline is an other alternative.
Please consult your Neurologist about the suitability of these drugs for you as they are the best judges in deciding your treatment.
I hope I have succeeded in providing the information you are looking for.
Best Wishes.
Note: For more detailed guidance, please consult an Internal Medicine Specialist, with your latest reports. Click here..
Above answer was peer-reviewed by :
Dr. Chakravarthy Mazumdar
Answered by
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