The rash may appear reddish, tan, or brown, with flaking, rippling, peeling, iridescence, or cracking skin.If the person is hairy, hair follicles can become inflamed resulting in some bumps (papules, nodules and pustules) within the plaque. The plaque may reach the scrotum in men and the labia majora and mons pubis in women. The penis is usually unaffected unless there is immunodeficiency or there has been use of steroids.Affected people usually experience intense itching in the groin which can extend to the anus. Causes
Tinea cruris is often associated with athletes foot and fungal nail infections. Rubbing from clothing, excessive sweating, diabetes and obesity are risk factors. It is contagious and can be transmitted person-to-person by skin-to-skin contact or by contact with contaminated sports clothing and sharing towels.The type of fungus involved may vary in different parts of the world; for example, Trichophyton rubrum and Epidermophyton floccosum are common in New Zealand. Less commonly Trichophyton mentagrophytes and Trichophyton verrucosum are involved. Trichophyton interdigitale has also been implicated. Diagnosis
Tests are usually not needed to make a diagnosis, but if required, may include microscopy and culture of skin scrapings, a KOH examination to check for fungus or skin biopsy. Differential diagnosis
The symptoms of tinea cruris may be similar to other causes of itch in the groin. Its appearance may be similar to some other rashes that occur in skin folds including candidal intertrigo, erythrasma, inverse psoriasis and seborrhoeic dermatitis. Prevention
To prevent recurrences of tinea cruris, concurrent fungal infections such as athletes foot need to be treated.
Urinary calcium excretion balances intestinal calcium absorption and does not increase with calcifediol levels up to ~400 nmol/L (160 ng/mL). Supplementation
Calcifediol supplements have been used in some studies to improve vitamin D status. Indications for their use include vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia, hypoparathyroidism, hypocalcemia and renal osteodystrophy and, with calcium, in primary or corticosteroid-induced osteoporosis.Calcifediol may have advantages over cholecalciferol for the correction of vitamin D deficiency states. A review of the results of nine randomized control trials which compared oral doses of both, found that calcifediol was 3.2-fold more potent than cholecalciferol. Calcifediol is better absorbed from the intestine and has greater affinity for the vitamin-D-binding protein, both of which increase its bioavailability. Orally administered calcifediol has a much shorter half-life with faster elimination. These properties may be beneficial in people with intestinal malabsorption, obesity, or treated with certain other medications.In 2016, the FDA approved a formulation of calcifediol (Rayaldee) 60 microgram daily as a prescription medication to treat secondary hyperparathyroidism in patients with chronic kidney disease. Interactive pathway map
History
Research in the laboratory of Hector DeLuca identified 25(OH)D in 1968 and showed that the liver was necessary for its formation. The enzyme responsible for this synthesis, cholecalciferol 25-hydroxylase, was isolated in the same laboratory by Michael F. Holick in 1972. Research
Studies are ongoing comparing the effects of calcifediol with other forms of vitamin D including cholecalciferol in prevention and treatment of osteoporosis. See also
Hypervitaminosis D
Hypovitaminosis D
Vitamin D

References
External links
"Calcifediol". Drug Information Portal. U.S. National Library of Medicine.