Pyridinoline and deoxypyridinoline in urine

The stability of the collagen matrix is ensured by intermolecular irreversible bonds formed between some amino acids included in the polypeptide chain of collagen. Due to the presence of a pyridine ring, the cross-links are called pyridinoline (Pid) and deoxypyridinoline (Dpid). Pyridine bonds are present only in extracellular collagen fibrils and are characteristic of the 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-links 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 in biological fluids of the body. This type of link is also present in cartilage tissue and tendons. Taking into account the more active metabolism of bone tissue compared to other types of connective tissue, it is believed that pyridinoline determined in urine mainly reflects destructive processes of a physiological or pathological nature in bones.

Reference values (norm) of pyridinoline and deoxypyridinoline concentration in urine

Age	Pid, nmol/mmol creatinine	Dpid, 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

Dpid is found almost exclusively in bone tissue collagen, in which the Pid/Dpid ratio is 4:1, this ratio is also preserved in urine, where deoxypyridinoline accounts for 20-22% of the total excretion of pyridine bonds. In joint diseases of various genesis, the Pid/Dpid ratio in urine increases, in contrast to diseases that occur with bone tissue destruction.

To study pyridinoline and deoxypyridinoline, it is recommended to study the second morning portion of urine (from 7 to 11 am).

The study of pyridinoline and deoxypyridinoline in urine is indicated not only for monitoring the activity of resorptive processes in bone tissue, but also for assessing the effectiveness of the treatment. Treatment is considered effective if the excretion of pyridinoline and especially deoxypyridinoline decreases by 25% within 3-6 months of therapy.

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

During menopause, urinary pyridinoline and deoxypyridinoline levels increase by 50-100% and decrease to normal levels after estrogen administration. In patients with spinal osteoporosis, urinary pyridine crosslinks, especially deoxypyridinoline, correlate with bone turnover.

In hypercalcemia in patients with malignant tumors, the excretion of pyridinoline and deoxypyridinoline in the 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 the excretion of calcium.

Urinary excretion of pyridinoline and deoxypyridinoline is increased in osteomalacia and 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 sodium levothyroxine.

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