Sunlight and vitamin D: both good for cardiovascular health.

Fahrleitner et al.1 report that patients with severe peripheral artery disease (PAD) had a high prevalence of vitamin D deficiency. The authors should be congratulated for realizing that many of the non-specific symptoms associated with PAD and immobility, i.e., muscle pain and weakness, bone aches and pains, and fatigue are also indicative for vitamin D deficiency. They found that 71% of patients with severe PAD had serum 25-hydroxyvitamin D [25(OH)D] levels that were below 9 ng/mL. Remarkably, 13% had serum calciums below the normal range and 40% had overt secondary hyperparathyroidism. The serum calcium levels are usually normal, but can be low in severe, chronic vitamin D deficiency. The hallmark for vitamin D deficiency is the measurement of a low or undetectable level of 25(OH)D in the blood.2 Although the lower limit of the normal range was 9 ng/mL, as noted by the authors, there is strong evidence that blood levels of less than 20 ng/mL lead to secondary hyperparathyroidism.2,3 Thus, if the authors had used 20 ng/mL as their cutoff, it is likely that essentially 100% of their patients were vitamin D insufficient or deficient. The clinical signs and symptoms of vitamin D deficiency are extremely subtle or nonspecific. Vitamin D deficiency causes a decrease in the efficiency of intestinal calcium absorption, which in turn, leads to an increase in the production of parathyroid hormone (PTH). PTH stimulates the kidney to produce 1,25-dihydroxyvitamin D [1,25(OH)2D], which increases the intestinal calcium absorption and with PTH stimulates osteoclast precursors to become mature osteoclasts, which in turn mobilize calcium stores from the skeleton. The increase in osteoclastic activity can precipitate and exacerbate osteoporosis. The more subtle effect, however, is that PTH also causes phosphaturia and hypophosphatemia. As a result, the calcium x-phosphate product in the blood is inadequate for normal mineralization of the bone collagen matrix resulting in osteomalacia. In adults, it is not possible to distinguish osteoporosis and osteomalacia, either by x-ray examination or by bone densitometry. Osteoporosis, i.e., holes in the bones does not cause bone pain. In contrast, osteomalacia can cause isolated or generalized bone aches and pains. Although the mechanism for bone pain is not well understood, it is possible that the unmineralized collagen matrix becomes hydrated and expands, causing outward pressure on the periosteal covering, which is innervated by pain fibers. On physical examination the application of minimum pressure with the thumb on the sternum, anterior tibia or radius and ulna will often elicit pain and discomfort, which is a helpful diagnostic sign for osteomalacia. Vitamin D deficiency also causes muscle weakness and muscle aches and pains. Glerup et al.4 reported that 88% of Danish women of Arab decent who presented with muscle pains and weakness (symptoms similar to fibromyalgia) were severely vitamin D deficient.