I will write out what I think about the case now, but recognize that I'm just a med student and this is a real patient, so my thoughts aren't necessarily the correct ones.
As far as why she was managed the way she was managed, I can only give you the thought process of the physicians who managed her according to their notes. They thought that she did not have hyper-PTH because her PTH levels were normal. Measuring intact PTH levels is usually pretty sensitive and specific for PT adenomas. Therefore, once hyper-PTH was thought to have been ruled out, the physicians thought that it would be appropriate to start her on Hctz, which would treat the hypercalciuria, which they believed was the sole etiology of her stone formation.
Nephrolithiasis is most commonly secondary to calcium oxalate crystals, which are most commonly secondary to hypercalciuria. Absortpive hypercalciuria is the most common cause of hypercalciuria; other causes include resorptive hypercalciuria (which our patient actually had, secondary to hyperparathyroidism) and renal hypercalciuria (renal tubule dysfunction). For hypercalciuria secondary to abosrptive hypercalciuria or renal hypercalciuria, thiazide therapy is an appropriate choice of therapy. Thiazides will decrease calcium secretion from the kidneys, causing the potential side effect of hyper-calcinemia. That's why it's important to rule out hyper-PTH, because otherwise, you will worsen the patient's hypercalcinemia. I believe that's what happened in our patient. Her chief complaint causing her to d/c the hctz was b/l pain in the thighs, which I thought might have been secondary to hypokalemia (a known adverse effect of hctz, as a diuretic), but she informed me that her potassium levels were normal at this time. So, I added the stuff with fatigue and constipation to give her a more typical presentation of hypercalcinemia (using my artistic liscense as case writer)
. Remember that hypercalcinemia's mneumonic is bones, stones, abdominal groans, and psychic overtones. 90% of cases of hypercalcinemia are secondary to either hyperPTH or metastatic/malignant disease effecting the bones. Other potential causes can be remmebered by the mneumonic CHIMPANZEES (calcium supplementation, hyper pth, iatrogenic (hctz)/immobility, milk alkali syndrome, paget's disease, adison's disease/acromegaly, neoplasms, zollinger ellison syndrome (MEN I), exces vit A, excess vit D, and sarcoidosis (through vit D synthesis of granuloma). Treatment of hypercalcinemia is with IV hydration and furosemide diuresis to secrete out the excess calcium. Other potential methods include the bisphosphanates, dialysis, calcitonin, and steroids. I failed to mention that our patient actually had a few high normal calcium levels along with a few slightly above normal levels in the interim because I didn't want to confuse the case, and her ca never rose to be all that high, so that, combined with the "normal" pth mislead the physicians responsible for her care to believe that she did not have hyper pth.
Their work-up of the patient was somewhat appropriate. I agree with the 24 hr urinary calcium and oxalate in order to w/u the cause. I would have also drawn uric acid levesl as high uric acid levels can cause calcium nephrolithiasis in addition to the uric acid nephrolithiasis; and I would have measured urinary citrate levels because citrate inhibits calcium stone formation and would be treated differently. Given the size of her stones and the amount of pain she was in at the time (not very much), I agree with their decision to attempt spontaneous passage of the stone. Had that failed, or if the stones had been greater then 6 mm, causing ureter obstruction, or had she been experiencing more intractable pain; extracorpeal shock wave lithotrsy or ureteroscopic stone extraction would have been appropriate. Follow up films would have been appropriate as well. We had not done this yet when the patient came to visit us last week. The patient was also placed on a low calcium diet, which is also appropriate until further w/u is completed, but it's important to recognize that most urinary calcium stones are actually associated with high dietary sodium and not high dietary calcium. Non-medical management of all sotnes includes encouraging the patient to keep over-hydrated (drinking water every second that he or she can, even during the night). Most patients cannnot follow through with such a regimen. Other reccomendations include diet restriction in sodium and protein (which is made into uric acid). Only one specific type of calcium nephrolithiasis patient (type II aborptive hypercalciuria) will benefit from decreasing calcium in their diet.
The user who explained why the patient had hyper-PTH was correct. Given hypercalcinemia, if the PTH gland was functioninge normally, PTH levels would be low normal. PTH is very sensitive to calcium levels. Having a high normal in tact PTH level ruled out the possibility of this being secondary to a paraneoplatic process secreting PTH-rP, which we did not check levels for because it wasn't necessary given the in tact PTH level.
Regarding the Techemetium-99 Sestamibi scan, one was eventuall ordered (in 1/04) and it was read as normal. This does not mean that she does not have a hyper-PTH adenoma though, the sensitivity of this scan is 90% in single adenomas (as is the case 80-90% of the time), but it's sensitivity drops to ~50% in multi-glandular adenomas. I was told by an endocrinologist that we informally consulted that many ENT doc's don't bother with scan for that reason; apparently, there is some nifty way of measuring PTH levels inside the OR which tells them which gland(s) are effected. Surgery is not always indicated for hyper-PTH. Hyper-PTH is a growing diagnosis in the elderly population as we are routinely checking more calcium levels, and since PT adenomas are almost always benign, it's not always worthwhile to go into the OR to offer the definitive treatment. Surgical removal of the PT gland is also associated with bad complications such as persistent hypoPTH, in which case our only therapy is calcium and calcitrol supplementation which doesn't work all that well. Indications for surgery include fractures, pruitis, calciphlaxis, and nephrolithiasis, particularly in our relatively young patient. Bisphosphanates can be used to treat patients medically who you do not want to take to the OR. Bone density studies were done on our patient, examining the hips and lumbar spine. They were read as normal. I suppose that the bone density studies can help you decide what therapy you want the patient to undergo. We did order vitamin D levels, but these levels (except for the one hydroxylated by the kidney, forget which one) should be normal if we are correct about our hyper-PTH dx.
MEN 1 is an excellent thought that I failed to consider. MEN-1 most commonly presents with hyper-PTH with hyperplasia of all four glands (consistent with our scan). A gastrinoma may even account for her "IBS" dx. Most women typicall present in their 30's, but I don't think that her being 51 is too far of a stretch. I will ask the attending whether or not he wants to work her up for this if she comes back while I am still in clinic. We sent our patient to a different endocrinogist and an endocrine surgeon, so hopefully, one of them will think of the diagnosis. Thanks for pointing it out, that's one of the reasons why I like posting interesting cases in here; I always learn something new too.
Anyways, thanks again for participating in my case guys. Keep the comments coming!