Diagnostic and Contributing Factors of Adult Rickets

A physician would begin a trial of adult rickets by looking for any growth or orthopedic issues, hypocalcemic symptoms (muscle cramps, paresthesia, numbness, seizures, and tetany), family history (retarded growth, short statures, alopecia, and consanguineous marriage of parents), dietary habits (only vegetarian), and about sunlight exposure. Diagnostic investigations are as follows:

Clinical tests: Blood tests and urinalysis estimate serum calcium, phosphate, alkaline phosphatase (ALP), parathyroid hormone (PTH), vitamin D (25OHD) levels, and urine calcium and phosphate levels. Clinical markers include decreased serum calcium, phosphate, calcidiol, calcitriol levels, and urinary calcium, along with increased serum PTH and ALP and urinary phosphate levels.

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X-Rays: Radiographic features can include physeal widening with bowing, coxa vara, physeal cupping, lordosis, scoliosis, kyphosis, dental abnormalities.

Bone biopsy for the histologic study of bone matrix cells.

Contributing factors are as follows:

The main contributors of adult rickets are deficiency of vitamin D, calcium, and phosphorous.

Therefore, adult rickets can arise from nutritional deficiency.

Calcium or phosphate deficiency:

Calcipenic rickets: Underlying conditions, such as any abdominal surgery, celiac disease, pancreatitis, renal diseases, or biliary tract obstruction can hinder calcium absorption and cause rickets.

Phosphopenic rickets: From genetic mutations, dietary deficiency, malabsorption, renal Fanconi syndrome.

Mineral deficiency results in decreased mineralization of bones and the formation of soft bones susceptible to rickets.

Other causes are as follows:

Genetic disorders (hypophosphatemic rickets)

Hereditary disorders (pseudovitamin D deficiency rickets)

Drugs (anticonvulsants)

Burns or injuries

Multiple pregnancies

Types of adult rickets are as follows:

Nutritional deficiency: Vitamin D, calcium, or phosphate deficiency

Vitamin D dependent: Type 1 (gene defect) and type 2 (autosomal mutation)

Vitamin D resistant: Familial hypophosphatemic rickets

Role of Vitamin D in Adult Rickets
Vitamin D plays a vital role in maintaining calcium and bone homeostasis in the body. It aids in absorbing calcium and phosphate in the small intestines, reduces resorption in bones, and decreases excretion through kidneys. Vitamin D circulates as 250HD, and its average serum value is 25 nmol/L; anything less than that reflects deficiency. Phosphate excretion in the kidneys increases with PTH signaling in response to lower calcium levels from poor absorption because of vitamin D deficiency. A failure of mineralization or hardening of the immature young bones, or osteoids occurs due to the decrease in minerals. It leads to the accumulation of these soft immature bones and preventing osteoclast formation, and further hardening of bones. It results in adult rickets with soft, brittle bones with less mineral content. Therefore, a deficiency in vitamin D directly affects mineral absorption, and lower mineral content leads to weak and soft bones resulting in rickets. Factors contributing to vitamin D deficiency are as follows:

Vitamin D production from cholesterol in the skin requires sunlight to activate. When there is a lack of sunlight exposure, vitamin D production reduces. A lack of sunlight exposure arises in cold countries, wearing too much protective clothing, using too many sunscreen lotions that block sunlight, and poor absorption of sunlight by dark complexed people, such as Africans and Asians.

Malabsorption of vitamin D can occur with conditions, such as Crohn’s disease, pancreatitis, celiac disease, abdominal surgery, chronic kidney disease, and cirrhosis.

Deficiency in newborns can occur from vitamin D deficient mothers during pregnancy, prolonged breastfeeding (exclusive), and lack of vitamin D in supplemental infant formula.

Vitamin D is an essential nutrient and a fat-soluble vitamin mainly found in animal dietary sources, such as dairy products. Hence, vegetarians or vegans will have problems choosing vitamin D foods, and vitamin D supplementation may be necessary.

Clinical Manifestation of Adult Rickets and Its Management
Rickets can cause general pain and weakness or severe excruciating pain in the bones. In addition, the soft and brittle bones become highly susceptible to breaks or fractures. Furthermore, structural deformities can change a person’s overall physical appearance, leading to physical and emotional stress.

Clinical features are as follows:

Bone deformities: Bowing of long bones, codfish vertebrae, dorsal kyphosis, a curvature of the spine, and bulging chest wall (pigeon chest)

Growth restriction

Gait disturbances

Dental problems

Muscle hypotonia

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