Pyridinoline and deoxypyridinoline in the urine

The stability of the collagen matrix is provided by intermolecular irreversible bonds formed between some amino acids entering the polypeptide chain of collagen. Due to the presence of the pyridine ring, the cross bonds are called pyridinoline (Pid) and deoxypyridinoline (Dpid). Pyridine linkages are present only in extracellular collagen fibrils and are characteristic of a differentiated matrix of strong types of connective tissue - bone, cartilage, dentin. They are not included in the collagen of the skin, soft tissues, so their study is more specific for assessing bone resorption.

Pyridine cross connections are specific components of mature collagen. They consist of 2 N- and 2 C-propeptides (telopeptides) of type I collagen. Bone tissue is the main source of pyridinoline biological body fluids. This type of connection is also present in the cartilaginous tissue, tendons. In view of the more active metabolism of bone tissue than in other types of connective tissue, it is believed that the pyridinoline detected in the urine basically reflects destructive processes of a physiological or pathological nature in the bones.

The reference values (norm) of the concentration of pyridinoline and deoxypyridinoline in the urine

Age	PID, nmol / mmol creatinine	Dip, nmol / mmol creatinine
2-10 years	160-440	31-110
11-14 years old	105-400	17-100
15-17 years old	42-200	<59
Adults:
Men	20-61	4-19
Women	22-89	4-21

Dipid is found almost exclusively in bone collagen, in which the ratio PID / DYD corresponds to 4: 1, this ratio persists in urine, where deoxypyridinoline accounts for 20-22% of the total excretion level of pyridine bonds. With diseases of joints of different genesis, the ratio of PID / DID in the urine increases, in contrast to diseases that occur with the destruction of bone tissue.

For the study of pyridinoline and deoxypyridinoline, a second morning urine sample is recommended (from 7 to 11 hours).

The study of pyridinoline and deoxypyridinoline in urine is shown not only to monitor the activity of resorptive processes in bone tissue, but also to evaluate the effectiveness of the treatment. Treatment is considered effective if excretion of pyridinoline and especially deoxypyridinoline is reduced by 25% within 3-6 months of therapy.

The content of pyridinoline and deoxypyridinoline in urine increases significantly with primary hyperparathyroidism and normalizes after surgical removal of parathyroid gland adenoma; the excretion of hydroxyproline during this period remains somewhat elevated.

During menopause, the content of pyridinoline and deoxypyridinoline in urine increases by 50-100% and decreases to normal values after administration of estrogens. In patients with osteoporosis of the spine, the concentration of pyridine cross links in the urine, especially deoxypyridinoline, correlates with bone turnover.

With hypercalcemia in patients with malignant tumors, the release of pyridinoline and deoxypyridinoline in urine increases by an average of 2-3 times, and under the influence of bisphosphonate therapy, the level of pyridine bonds decreases to a lesser extent and more slowly than calcium excretion.

Excretion of pyridinoline and deoxypyridinoline in the urine is increased in osteomalacia, in patients with hypothyroidism, so these indicators can be used as a sensitive marker of normalization of bone metabolism in the treatment of hypothyroidism with levothyroxine sodium.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]