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A Chinese family had a child with a specific gene mutation causing vitamin D-resistant rickets, but the child improved with calcium and low-dose calcitriol.

A boy with severe Vitamin D-resistant rickets did not respond to treatment and lacked a common symptom, suggesting a need for alternative treatments.

Three new gene mutations cause rickets and hair loss, treatable with high calcium and calcidol, but hair regrowth is rare.

Certain genetic variants impair enzyme activity, contributing to non-classic congenital adrenal hyperplasia.

Treating classic 21-hydroxylase deficiency requires precise glucocorticoid dosing and attention to individual patient needs, with new treatments showing promise.

HSD11b1 affects skin nerves and increases non-histaminergic itch.

Certain inhibitors can potentially treat prostate cancer and other hormone-dependent conditions by controlling sex hormone levels in cells.

Different enzymes are active in different parts of developing mouse organs.

Severe genetic variants in children with a specific adrenal condition match predicted symptoms well, but milder variants do not.

Hirsute women have lower type 2 17β-HSD enzyme levels, which improve with treatment.

Early detection of specific VDR mutations is crucial for effective treatment and better dental outcomes in children with hereditary vitamin D–resistant rickets.

Certain hormone levels can help diagnose P450 oxidoreductase deficiency.

A child with a rare type of rickets showed some improvement with high doses of vitamin D, but such conditions often respond poorly to treatment.

Adolescents with PCOS have higher levels of certain androgens, which are linked to hair growth but don't help diagnose PCOS better than testosterone levels.

Two siblings with a genetic mutation had a form of rickets that doesn't respond to vitamin D.

A single amino acid change in the vitamin D receptor can disrupt its function and lead to hair loss.

Non-classical 21 hydroxylase deficiency is an underdiagnosed cause of female hair loss and polycystic ovarian syndrome.

Vitamin D receptor is crucial for bone health and mineral metabolism.

Identifying nonclassic congenital adrenal hyperplasia and carriers of CYP21 mutations is challenging, and genetic counseling is recommended due to their prevalence.

Researchers created a mouse model of a type of rickets that does not cause hair loss.

Measuring 17-hydroxyprogesterone in hair can help monitor androgen levels in people with congenital adrenal hyperplasia.

A rare genetic mutation causes resistance to vitamin D, leading to severe rickets and requiring high doses of calcium and vitamin D for treatment.

Some women with excess hair growth have a hormone condition that can't be diagnosed by blood or urine tests alone.

New genotype linked to non-classical congenital adrenal hyperplasia found in Italian siblings.

Mutations in the HEPHL1 gene cause abnormal hair and cognitive issues.

The document's conclusion cannot be provided because the document is not available or cannot be read.

A mutation in the vitamin D receptor causes severe resistance to vitamin D, affecting bone health but not hair growth.

A genetic mutation in a specific gene causes a salt-wasting condition in a Pakistani girl and her family.

DDR-II hair follicle cells don't respond to 1, 25-dihydroxyvitamin D3, aiding diagnosis.

Mutations in the vitamin D receptor cause hereditary vitamin D-resistant rickets, leading to poor bone health and requiring high calcium doses for treatment.