Ankylosing Spondylitis Diary and Diet Research

"ASp is characterized by significantly reduced elimination of hydraxyproline, higher metabolic pool of calcium, lower elimination of calcium in urine and faeces and lower accretion to bone."
[Calcium, phosphorus, hydroxyproline and nitrogen in inflammatory joint diseases], Z Rheumatol. 1977 Jan-Feb;36(1-2):60-72

"Corrected calcemia was also normal in ankylosing spondylitis, but it was significantly higher in polymyalgia rheumatica. Phosphoremia was shown to be normal but alkaline phosphatases were higher than normal in the three groups."
[Changes in blood calcium, phosphorus and alkaline phosphatase levels in rheumatoid polyarthritis and other types of inflammatory rheumatism], Rev Rhum Mal Osteoartic. 1979 Jun;46(6):389-95.

An attempt was made to determine whether a relationship exists between ankylosing spondylitis (AS) and hyperparathyroidism (HP). Twenty patients with definite AS, studied for biochemical evidence of HP, did not show consistent abnormalities in serum calcium, phosphorus, alkalinephosphatase, or parathyroid hormone levels or in bone-density measurements. Reviewing roentgenograms of 39 patients with HP showed one patient with sacroiliitis, and one of the 28 hyperparathyroid patients tissue-typed as HLA B27-positive. Both AS and HP are independent entities that have no causative or pathological relationship to each other.
Ankylosing spondylitis and hyperparathyroidism, JAMA, August 25, 1978

[Ed: An old study with too few patients. Must have been a poorly executed study as it says there were no consistant abnormalities in alkalinephosphatase. It is however well known now that alkalinephosphatase tends to be raised in A.S.]

"Vitamin D deficiency in adults causes secondary hyperparathyroidism that can precipitate and exacerbate osteoporosis (2, 9, 11). The secondary hyperparathyroidism associated with vitamin D deficiency often maintains the serum calcium concentration within the normal range, but it causes a loss of phosphorus in the urine. This loss results in inadequate serum calcium x phosphorus to promote mineralization of the osteoid in the bone, which in turn results in osteomalacia, ie, nonmineralization of the collagen matrix."

"The parathyroid glands secrete parathyroid hormone (PTH), a substance that helps maintain the correct balance of calcium and phosphorous in the body. PTH regulates release of the calcium from bone, absorption of calcium in the intestine, and excretion of calcium in the urine.

"When the amount of calcium in the blood falls too low, the parathyroid glands secrete just enough PTH to restore the balance. [..]

"If the glands secrete too much hormone, as in hyperparathyroidism, the balance is disrupted: blood calcium rises. This condition of excessive calcium in the blood, called hypercalcemia, is what usually signals the doctor that something may be wrong with the parathyroid glands.[..]

"This excess PTH triggers the release of too much calcium into the bloodstream. The bones may lose calcium, and too much calcium may be absorbed from food. The levels of calcium may increase in the urine, causing kidney stones. PTH also acts to lower blood phosphorous levels by increasing excretion of phosphorus in the urine.[..]

"When symptoms do appear, they are often mild and nonspecific, such as a feeling of weakness and fatigue, depression, or aches and pains. With more severe disease, a person may have a loss of appetite, nausea, vomiting, constipation, confusion or impaired thinking and memory, and increased thirst and urination. Patients may have thinning of the bones without symptoms, but with risk of fractures. Increased calcium and phosphorous excretion in the urine may cause kidney stones. Patients with hyperparathyroidism may be more likely to develop peptic ulcers, high blood pressure, and pancreatitis."