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Measuring 24-OHase induction helps identify defects in vitamin D processing and predict treatment response.

Truncated LTBP-1 disrupts TGF-β signaling, affecting hair growth.

A Western diet may increase acne risk, while a Mediterranean diet and certain supplements can help reduce it.

A specific gene mutation causes vitamin D resistance, but certain vitamin D analogs might help.

Increased HSD11B1 enzyme expression is linked to higher body fat and insulin resistance.

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

Cortisone reductase deficiency can cause high androgen and cortisol levels and may be missed in women with similar symptoms.

Females with 5 alpha-reductase-2 deficiency have less body hair, no acne, normal fertility, and delayed menarche.

3βHSD2 is not useful for diagnosing PCOS.

Nonclassic 21-hydroxylase deficiency is a common, treatable genetic disorder causing reversible symptoms like acne and hair loss.

Patients with the same genetic mutation for vitamin D-resistant rickets showed different symptoms but all improved with treatment except for hair loss.

Inhibitors of 11β-HSD1 show potential for treating type 2 diabetes but require more testing for safety and effectiveness.

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.

Non-classical 21-hydroxylase deficiency can be missed in newborn screenings and should be considered in cases of early puberty or virilization.

A girl had rickets due to a gene mutation affecting vitamin D response.

Masculinization in affected individuals occurs gradually after puberty due to hormone changes.

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

Certain mutations in the H6PD gene cause Cortisone Reductase Deficiency by affecting hormone production.

A new gene mutation causes vitamin D resistance and rickets, treatable with calcium therapy.

Estrogen deficiency can reduce the enzyme activity needed to activate vitamin D.

Blocking the enzyme 11β-HSD1 might help treat obesity and metabolic issues.

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

A child with a rare vitamin D-resistant condition improved with treatment.

Increased 11β-HSD1 activity in skin may contribute to aging and could be targeted to reduce aging effects.

Two rare genetic diseases cause severe rickets in children due to defects in vitamin D metabolism.

Patients with the same vitamin D receptor mutation showed different symptoms due to other factors.

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

A woman's hyperandrogenism was caused by a genetic mutation leading to non-classic adrenogenital syndrome.

The enzyme 17β-HSD type 2 mainly performs oxidation in human sebaceous glands, which may help protect against acne.

Individuals with this condition often develop male traits and identities at puberty despite being raised as females.