For routine monitoring of established hypoparathyroidism (hypopara) there is no role for checking parathyroid hormone (PTH.) You obviously would check PTHs at least periodically in the early stages postop to assess for recovery, which is not unusual. And in that phase of the disorder you have to be sure a low PTH is due to real deficiency, not appropriate suppression of PTH in the face of aggressive calcium (Ca++) and vitamin D supplementation. That is, if there is suspicion or evidence of residual PTH production, running the supplements at low doses might be illustrative (that is if the PTH rises and prevents hypocalcemia [low Ca++; hypoCa++] then hypopara is not in fact present).
In straight-forward postsurgical hypopara, I treat with around a 2000-mg total daily dose of Ca++ plus however much calcitriol (this is a form of vitamin D; typically the dose is 0.25 to 0.5 mcg daily, but sometimes more) is needed to adjust the total serum Ca++ to levels in the lower half of the normal range or perhaps even slightly low. Mid-normal or higher Ca++ levels in hypopara patients over the long run can bring on renal failure due to Ca++ collecting in the kidneys and can cause kidney stones (without PTH, Ca++ floods through the kidneys and out in the urine).
Labs I check are Ca++ and phosphorus (phos), period. We don't care what the 25D (storage form of vitamin D) level is because it can't be used in the absence of PTH and we don't care what the 1,25D (active form of vitamin D) level is because the Ca++ tells us all we need to know—provided a decent dose of Ca++ is being taken, a Ca++ lower than the goals discussed above means the 1,25D is too low, and Ca++ higher than goal means the 1,25D is too high.
Ideally phos should be normal of course and with us running the Ca++'s relatively low (thus mitigating the 1,25D effect of raising phos) I don't see a lot of hyperphosphatemia (high phos, or hyperphos). When we do have hyperphos, provided the Ca++/phos product (Ca++ level multiplied by the phos level) is below 55 to 70 there should be no problem. I don't check magnesium or urine Ca++ (remember, keeping the blood Ca++ low normal or low, just enough to prevent symptoms, handles the urinary excretion concerns).
(AT THIS POINT SHE ASKED ABOUT COMBINING OVER-THE-COUNTER VITAMIN D SUPPLEMENTS [D2 OR D3, WHICH ARE FORMS OF 25D] AND PRESCRIPTION-ONLY 1,25D PRODUCTS LIKE CALCITRIOL)
If well monitored, there is probably no harm in combining the two forms of vitamin D, and there might be some value, but it wouldn't typically be necessary. I've never deliberately combined them, and there would be greater risk of vitamin D toxicity (that is, dangerously high Ca++, or hyperCa++). Vitamin D2 and D3, have very long half lives, meaning they take a long time to go away if overdosed, but relatively safe because the body has to activate them, which the kidneys won't do in the face of if the Ca++ is too high. On the other hand, calcitriol is riskier because it's more potent—it can directly raise Ca++ levels whether that would be a good thing for the body or not—the regulatory step of converting 25D to 1,25D in bypassed. But it's in the end relatively safe because its half-life is short—it goes away fast. These "safety features" of each would be maintained in a combination, but there is no way the risk, at least short term, for hyperCa++ would not be greater, so I don't see the benefit outweighing the risk. I'd avoid the combo.
Phosphate binders are mostly used in chronic renal failure--I don't, and have not much heard of them being used in hypopara. And remember, renal failure patients typically have low Ca++'s and their PTHs are typically appropriately high in response to the low Ca++, so that is really a totally different situation from hypopara.
Yes, avoid excess dietary phos, give Ca++ at about 2000mg per day as described, and lower the vitamin D supplement to get the Ca++ low or low normal. That should fix the phos level, and again, if the Ca++ times the phos product is ok, I wouldn't worry about it. Really, I haven't had much problem with hyperphos.
I assume by vitamin D analogues you are referring to the brand name drugs Hectorol and Zemplar. These as well as calcitriol (brand name Rocaltrol) all mimic the effects of 1,25D, the active form of vitamin D in the body. All these drugs lower PTH and raise Ca++ and phos. There may be some differences as to the degree of the effects on calcium and phos, which I can't really give any authoritative information about. I always use calcitriol and haven't used the others, which are more commonly used by nephrologists (kidney specialists). They deal with a different group of patients than I do, mostly renal failure patients who have enormously high PTH levels that need to be brought down.
My use of agents that stimulate the 1,25D receptor, like calcitriol, mostly
involves hypopara (low, rather than high PTH). These people need 1,25D replacement because they lack PTH, which is needed to trigger 25D to 1,25D conversion in the kidneys (storage form to active form). No PTH, no 1,25D, and Ca++ drops dangerously low because of a lack of vitamin D effect on the kidneys and intestine, and lack of PTH effect on kidneys and bone. Phos already may be high owing to the PTH lack (PTH lowers phos) and we have to monitor to be sure the 1,25D doesn't dangerously elevate phos at the same time as it's raising Ca++.
The other commonly used vitamin D supplements (D2 and D3) are forms of 25VitD, the storage form, and have to be converted to 1,25D, which most people with normal parathyroid and kidney function do just fine. D2 and D3, in very large doses, in hypopara, might raise Ca++ and phos a little, but not very efficiently.
In people with intact parathyroid glands and intact kidneys (no renal failure),
who have elevated PTH levels for whatever reason, all these vitamin D forms would
be expected to lower PTH.
(AT THIS POINT SHE ASKS ABOUT MODIFYING TREATMENT TO HELP PTH PRODUCTION RECOVER, IN THE CASE OF SOMEONE WITH SOME RESIDUAL PARATHYROID FUNCTION)
The primary driver of PTH release is CA++. So, if CA++ IS low (8.1 and 8.5 in your case, with a lower limit of 8.6), then PTH has to be deficient—it matters not that you have residual function—most do—what matters is PTH is deficient relative to your needs. PTH will always be produced at maximal levels in the face of low Ca++, regardless of calcitriol doses. So if your Ca++ is low, you are deficient, period, and after 4 years recovery is unlikely--not impossible, but very unlikely.
Now, you may be subtly better off for having that residual function—easier to control, more stable—owing to your body perhaps being able to do some fine-tuning to make up for some deficit in your replacement regimen, but in overall terms of how we manage this it doesn't matter.
You might be right that, given residual PTH function, your body might be able to somewhat utilize D3, but to what end? If the object is to lower the calcitriol dose and lessen some perceived adverse effect of calcitriol—remember, D3 works through its conversion to 1,25D, which is the same thing as calcitriol, with the same potential side effects. So why bother? Just take one drug, the more effective one—calcitriol.
I doubt there would be any benefit to lowering your replacement doses to promote PTH recovery. If it was going to recover, those low calciums would have done it already. And there are risks to making your hypoCa++ worse, including seizures, so why take the chance? (below I'm going to talk about weaning calcitriol for the purpose of seeing what your minimum effective treatment regimen is, but not for the purpose of promoting PTH recovery, see?)
On the other hand, if there is some remote chance of recovery, getting you to that minimum effective level of treatment would mean our treatment would interference with that hypothetical recover to the lowest possible degree, while still “taking care of business.”
With respect to your management, based upon data provided—first, it's not clear to me anything has to be changed—the most important parameter to watch is Ca++. It needs to be high enough to prevent symptoms—and you say you don't have symptoms—and it needs to be low enough not to cause kidney stones or renal damage. That is, they should range from mildly low to somewhere in the lower half of the normal range. You're there! Now, if I were going to change anything, I would do the following:
1) Up the Ca++ to 2000 mg from 1200 mg—you don't want to be depending on your dietary Ca++ intake in this situation—it's too variable—taking 2000 mg per day masks fluctuations in day-to-day intake.
2) Take Ca++ with food in at least 2 divided doses, at least 2 hours after your thyroid hormone.
3) Once the Ca++ is at 2000/day, then fine tune the serum Ca++ level using calcitriol. And here's an advantage of taking more calcium—there's no harm in more calcium—it's not that well absorbed anyway—but you've expressed concern about calcitriol side effects (hyperphos for instance). On 2000/day of Ca++, you might be able to back down on the calcitriol.
4) You're already on a very low calcitriol dose—I dose most people daily—if you do go down further, to say twice weekly, it should be for one of two reasons—either your calcium is too high (which it isn’t), or to see if you can wean off it. Some hypopara patients get by with Ca++ only. If on twice weekly calcitriol your Ca++ is above 8 and you have no symptoms, try stopping it (not sure once a week would be a worthwhile step). On the other hand, if Ca++ is below 8, especially if there are symptoms (cramping, spasms), just go back to 3 per week and stay there.
5) If off calcitriol for a week or two, and Ca++ is still above 8 with no symptoms, I probably would then add D3 1000-2000 units/d, which is probably good for most normal people, you certainly would want to do at least that.
6) From that point on—if you get there—monitor Ca++ and 25D and maybe an occasional phos, but if that's normal initially I'd drop it.
Now, assuming you do just stay on Ca++ and some dose of calcitriol—I would monitor Ca++ and phos, period. We covered what the Ca++ goal should be. The phos should be normal, but a slightly high level may be a necessary evil and I wouldn't worry about it. Just make sure the Ca++ level times the phos level is not over 55.
I'm going to end with some constructive criticism. I think you're trying to micromanage this too much. This is very complex—too complex for any of us to fine tune every little link in the chain. My advice is to pay attention to the key end results: symptoms and Ca++ levels. If they're okay, don't worry about PTHs and vitamin D’s (and phos usually isn't an issue either as we've said). Obviously working with an endocrinologist with a lot of experience in this area should be helpful.
A last bit of wisdom:
This is a difficult problem to manage under the best of conditions. It is a complication of surgery best avoided rather than to have to be treated. An experimental human recombinant PTH product may help things in the future, but we aren't there yet. Thus, prevention is key: only do thyroid and parathyroid surgery when it’s absolutely needed, and make sure the best surgeon (that is, a lot of experience in the neck, and proven low complication rates) you have access to is doing the case. (With any luck, the physician referring you for the surgery will be able to tell you who that is.) A couple of years ago one of my patients needed thyroid surgery and I recommended a local community general surgeon I've worked closely with for 16 years and from whom I have rarely if ever seen a Ca++-related surgical complication. She flouted my advice and went instead to a surgeon somebody recommended at a world-class university medical center in the next county, and now I'm managing her permanent postsurgical hypopara, just as you are dealing with.
(THE EMAILER THEN CAME BACK WITH A CONCERN ABOUT RAISING THE CA++ DOSE TO 2000MG/DAY, CITING HER URINE CA++’S ALWAYS RUNNING HIGH.)
This is precisely what I mean by micromanaging. I don't believe that in 25 years I have ever checked a 24-hour urine Ca++ in a hypopara patient. I've checked them in hyperpara, and in osteoporosis, but not hypopara. I suppose if you've had multiple kidney stones, or renal insufficiency, you might have reason to be concerned—if not, don't check it. And if you were having kidney stones you could take a thiazide diuretic to lower the urine Ca++. You're forgetting that my protocol mitigates renal Ca++ exposure by setting the serum Ca++ goal low. And I don't believe that in 25 years I've had a hypopara patient have kidney stones either, that I recall anyway.
Say you do as I advise and your urine Ca++ is still high? (which you're telling me is, in fact, the case). In the absence of a clinical problem like renal failure or kidney stones, doesn't matter. Fugggedaboutit!
In focusing on, and worse, acting on the urine Ca++ and serum phos you are making the common error of equating biochemical testing, falling outside the lab's reference range, with a disease that needs to be treated. The two aren't the same thing. I make this point very strongly in The Thyroid Paradox. A lab abnormality is a signal that deserves investigation, it is not a disease; it is not, necessarily, a demand for action. I ignore numerous minor lab abnormalities everyday, every physician does. The job of a quality healthcare practitioner is to evaluate a patient with a history and an exam and--labs!--and perhaps radiology or even tissue pathology studies, and put all that together and decide what is going on, and what if anything to do. The answer might be nothing. Reading a lab report comes no where close to the work that needs to be done.
Hope that helps!