- Rickets
- A disease of infants and children that disturbs normal bone formation (ossification). Rickets is a failure to mineralize bone. This softens bone (producing osteomalacia) and permits marked bending and distortion of bones. Up through the first third of the 20th century, rickets was largely due to lack of direct exposure to sunlight or lack of vitamin D. Sunlight provides the necessary ultraviolet rays. These rays do not pass through ordinary window glass. Once the role of vitamin D in rickets was discovered, cod liver oil (which is rich in vitamin D) became a favored, if not too tasty, remedy. Thanks to such supplements of vitamin D, nutritional rickets has become relatively rare in industrialized nations. It still occurs, for example, in breast-fed babies whose mothers are underexposed to sunlight and in dark-skinned babies who are not given vitamin D supplements. And in unindustrialized countries, vitamin D deficiency rickets continues to be a problem. Rickets in North America and Europe now is usually not nutritional. It is due to other causes, namely: {{}}Disorders that create vitamin D deficiency by interfering with the absorption of vitamin D through the intestines. Diseases (for example, of the liver or kidney) that impair the normal metabolic conversion and activation of vitamin D. Conditions that disrupt the normal balance in the body (the homeostasis) between calcium and phosphorus. No matter what causes rickets, the features are the same. They include softness of the infant’s skull (formally known as craniotabes and informally as “Ping-Pong ball skull”), enlargement of the front end of the ribs (creating the “rachitic rosary”), thickening of the wrists and ankles, lateral curving of the spine (scoliosis) and abnormal forward-backward curving of the spine (kyphosis and lumbar lordosis), and deforming and narrowing of the pelvis (which in the female interferes later with delivering vaginally). As the child begins to walk, the weight on the soft shafts of the legs results in knock-knees or, more often, bowlegs. The deformities of the spine, pelvis and legs reduce height leading to short stature. The deformities of the spine impair posture and gait. A person with rickets seemed to walk in a shaky or tottering way so “rickety” came to mean just that, shaky and tottering. The word “rickets” is probably a corruption of “rachitis” which came from the Greek “rhachis” (spine) + the suffix -“itis” (inflammation). Before the causes of rickets were discovered, rickets (which is also called “rachitis”) was believed to be an inflammatory disease of the spine.
* * *A disease due to vitamin D deficiency and characterized by overproduction and deficient calcification of osteoid tissue, with associated skeletal deformities, disturbances in growth, hypocalcemia, and sometimes tetany; usually accompanied by irritability, listlessness, and generalized muscular weakness; fractures are frequent. SYN: infantile osteomalacia, juvenile osteomalacia, rachitis. [E. wrick, to twist]- acute r. SYN: hemorrhagic r..- adult r. SYN: osteomalacia.- celiac r. arrested growth and osseous deformities associated with defective absorption of fat and calcium in celiac disease.- hemorrhagic r. bone changes seen in infantile scurvy, consisting of subperiosteal hemorrhage and deficient osteoid tissue formation; often used to indicate simultaneous occurrence of r. and scurvy. SYN: acute r..- hereditary hypophosphatemic r. with hypercalciuria, an inherited disorder in which there is a defect in renal tubular reabsorption.- late r. SYN: osteomalacia.- refractory r. r. that does not respond to treatment with usual doses of vitamin D and adequate dietary calcium and phosphorus; most often due to inherited renal tubular disorder, e.g., Fanconi syndrome.- renal r. a form of r. occurring in children in association with and apparently caused by renal disease with hyperphosphatemia. SYN: pseudorickets, renal fibrocystic osteosis, renal infantilism, renal osteitis fibrosa.- vitamin D-resistant r. a group of metabolic disorders characterized by renal tubular defect in phosphate transport and bone abnormalities resulting in hypophosphatemic r. or osteomalacia; hypocalcemia and tetany are not features. There is an autosomal dominant form [MIM*193100] and an X-linked dominant form [MIM*307800], the latter caused by mutation in the phosphate-regulating gene with homologies to endopeptidases (PHEX) on chromosome Xp. Both forms are not responsive to standard therapeutic doses of vitamin D but they may respond to very large doses of phosphate and/or vitamin D. There is also an autosomal recessive form [MIM*277440] caused by mutation in the vitamin D receptor gene (VDR) on 12q. SYN: familial hypophosphatemic r..
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rick·ets 'rik-əts n pl but sing in constr a deficiency disease that affects the young during the period of skeletal growth, is characterized esp. by soft and deformed bones, and is caused by failure to assimilate and use calcium and phosphorus normally due to inadequate sunlight or vitamin D called also rachitis* * *
n.a disease of childhood in which the bones do not harden due to a deficiency of vitamin D. Without vitamin D, not enough calcium salts are deposited in the bones to make them rigid: consequently they become soft and malformed. This is particularly noticeable in the long bones, which become bowed, and in the front of the ribcage, where a characteristic rickety 'rosary' may become apparent. The deficiency of vitamin D may be dietary or due to lack of exposure to sunlight, which is important in the conversion of vitamin D to its active form. In the UK rickets is more common in Asian immigrant families.Renal rickets is due to impaired kidney function causing bone-forming minerals to be excreted in the urine, which results in softening of the bones.* * *
rick·ets (rikґəts) [thought to be a corruption of Gr. rhachitis a spinal complaint] an interruption in the development and mineralization of the growth plate of bone, with radiographic abnormalities, osteomalacia, bone pain, fatigability, growth retardation, and often hypotonia, convulsions, and tetany. Biochemical abnormalities include hypocalcemia, elevated serum alkaline phosphatase, hypophosphatemia, and decreased intestinal absorption of calcium and phosphorus. It is caused by a variety of defects in vitamin D, calcium, and phosphorus homeostasis, including dietary deficiencies or malabsorption, primary disorders of bone matrix, and acquired or inherited metabolic and hormonal abnormalities. See also osteomalacia.
Rickets, with characteristic cupping and fraying of the metaphyseal ends of the radius and ulna.
Medical dictionary. 2011.
