Signs of Vitamin D deficiency

Signs of Vitamin D Deficiency

General Signs

Frank deficiency of vitamin D affects several systems, most prominently skeletal and neuromuscular.

Vitamin D deficiency


Vitamin D Deficiency in Humans

Rickets

Rickets first appears in 6- to 24-month old children, but can manifest at any time until the closure of the bones’ epiphyseal growth plates. It is characterized by impaired mineralization of the growing bones with accompanying bone pain, muscular tenderness, and hypocalcemic tetany. Tooth eruption may be delayed, the fontanelle may close late, and knees and wrists may appear swollen. Affected children develop deformations of their softened, weight-bearing bones, particularly those of the rib cage legs and arms; hence the characteristic leg signs, bow-leg,151 knock knee,152 and sabre tibia, which occur in nearly half of cases. Radiography reveals enlarged epiphyseal growth plates resulting from their failure to mineralize and continue growth. Rickets is most frequently associated with low dietary intakes of calcium, as in the lack of access to or avoidance of milk products.

Osteomalacia

Osteomalacia occurs in older children and adults with formed bones whose epiphyseal closure has rendered that region of the bone unaffected by vitamin D deficiency. The signs and symptoms of osteomalacia are more generalized than those of rickets; e.g., muscular weakness and bone tenderness and pain, particularly in the spine, shoulder, ribs or pelvis. Lesions involve the failure to mineralize bone matrix, which continues to be synthesized by functional osteoblasts; therefore, the condition characterized by an increase in the ratio of non-mineralized bone to mineralized bone. Radiographic examination reveals abnormally low bone density (osteopenia) and the presence of pseudofractures, especially in the spine, femur, and humerus. Patients with osteomalacia are at increased risk of fractures of all types, but particularly those of the wrist and pelvis.

Osteoporosis

Although it is sometimes confused with osteomalacia, osteoporosis is a very different disease, being characterized by decreased bone mass with retention of normal histological appearance. Its etiology (loss of trabecular bone with retention of bone structure) is not fully understood; it is considered a multifactorial disease associated with aging and involving impaired vitamin D metabolism and/or function associated with low or decreasing estrogen levels. The disease is the most common bone disease of postmenopausal women, and also occurs in older men154 (e.g., non-ambulatory geriatrics, postmenopausal women) and in people receiving chronic steroid therapy, which groups show high incidences of fractures, especially of the vertebrae, hip, distal radius, and proximal femur. In women, osteoporosis is characterized by rapid loss of bone (e.g., 0.5–1.5%/year) in the first 5–7 years after menopause.156 The increased skeletal fragility observed in osteoporosis appears not to be due solely to reductions in bone mass, but also involves changes in skeletal architecture and bone remodeling (e.g., losses of trabecular connectivity, as well as inefficient and incomplete microdamage repair). Affected individuals show abnormally low circulating levels of 1,25-(OH)2-D3, suggesting that  estrogen loss may impair the renal 1-hydroxylation step – i.e., that the disease may involve a bihormonal deficiency.

Musculoskeletal Pain

Deep pain is common among rickets and osteoporosis patients. Some reports have indicated persistent, non-specific musculoskeletal pain among asymptomatic adults with low circulating levels of 25-OH-D3; however, a systematic review of published data159 found no convincing evidence of either low vitamin D status or latitude being associated with chronic pain prevalence in non-cases. Similarly, well controlled intervention trials have largely been negative.

Vitamin D Deficiency in Renal Patients

Low circulating levels of 25-OH-D3 are frequently observed in patients with chronic renal disease and those with nephrotic syndrome and normal renal function. Some studies have found treatment with vitamin D analogs to reduce proteinuria in patients with chronic renal disease

VITAMIN D TOXICITY

Excessive intakes of vitamin D are associated with increases in circulating levels of 25-OH-D3; this is especially true for vitamin D3, exposure to high levels of which produces higher serum levels of the 25-OH metabolite than do comparable intakes of vitamin D2.162 The 25-OH metabolite is believed to be the critical metabolite in vitamin D intoxication. At high levels163 it appears to compete successfully for VDR binding, thus bypassing the regulation of the 25-OH-D3 1-hydroxylase to induce transcriptional responses normally signaled only by 1,25-(OH)2-D3. Therefore, risk to hypervitaminosis D is increased under conditions such as chronic inflammation, in which the normal feedback regulation of the renal 25-OH-D3 1-hydroxylase is compromised.

 

REFERENCE

The Vitamins

Fourth Edition

Gerald F. Combs, Jr

Professor Emeritus

Cornell University

Ithaca, NY

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