What genetic mechanism causes Prader-Willi syndrome?

Paternal deletion 15q11-q13 (70%): often larger BMI increase and more behavioral challenges; maternal UPD (25%): higher rate of autism-spectrum features, psychosis; IC defects (2%): variable severity.

What caloric restriction is required to prevent obesity in PWS?

Energy restriction 60-80% of normal intake (for males often 1000-1200 kcal/day) is required to maintain a healthy weight; combined with vigorous food security measures and structured environment; dietary management is lifelong.

What growth outcomes does GH therapy provide in PWS?

GH 0.035 mg/kg/day improves height velocity, body composition (reduces fat mass, increases lean mass), and cognitive function; start as early as 6 months; sleep apnea screening required before and during GH.

What age does hyperphagia begin in PWS?

Hyperphagia typically begins between ages 2-5 years; before that, infants have profound hypotonia and feeding difficulties requiring NG tube; the transition from hypo- to hyperphagia is sudden and dramatic.

What psychiatric complications occur in PWS?

Skin picking, obsessive-compulsive behaviors, temper tantrums, and psychosis (more common in UPD subtype) are psychiatric features; SSRIs reduce OCD and skin picking; antipsychotics for psychosis with caution given metabolic risk.

Prader-Willi Syndrome Obesity Risk and GH Response Calculator

Calculates obesity risk trajectory in Prader-Willi syndrome using genotype (deletion vs UPD), age at hyperphagia onset, BMI trajectory, and growth hormone therapy response monitoring.

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Frequently Asked Questions

What genetic mechanism causes Prader-Willi syndrome?

What caloric restriction is required to prevent obesity in PWS?

What growth outcomes does GH therapy provide in PWS?

What age does hyperphagia begin in PWS?

What psychiatric complications occur in PWS?