Correlation of Insulin resistance and development of metabolic syndrome in the 4th and 5th Decades of life in PCOS Women

What % of PCOS are the effects of IR? Is primary can result into secondary PCOS: Etiologyof PCOS?

Insulin resistance (IR) is the cause of up to 25% of PCOS.

How do we differentiate it (such phenotype) from conventional?

This hyperinsulinaemia- induced- PCOS is differentiated from “classic” PCOS by elevated insulin levels, a normal LH-to-FSH ratio and failure to respond to clomiphene until insulin levels return to normal. What is the cause’s ofCC resistance in India? Therefore all CLINICIANS SHOULD Seriously CONSIDER POSIBILITY OF IR ETILOGY OF IN pcos INFERTIE WOMEN WHO ARE cc RESISTANCE. In such cases primary THERAPY WILL BE Metformin or other OAD. The first line of treatment for women with borderline and mild IR should be weight loss. Metformin 500-1,000 mg twice a day with meals is indicated for anovulatory women who continue to have elevated insulin levels after weight loss. Addition of CC is often necessary for ovulation.

What is Met syndrome? Syndrome X?

Hyperinsulinemia, if left untreated, leads to hypertension, an increased risk of cardiovascular disease and gestational diabetes. Insulin resistance is considered to be one component of a condition formerly called syndrome X and now labeled metabolic syndrome. In addition to insulin resistance and obesity, the metabolic syndrome requires there to be three or more of the following.

Hypertension 130/85 mmHg or higher

Triglyceride levels 150mg/dL or higher

HDL cholesterol levels less than 50mg/dL

Abdominal obesity: waist circumference greater than 35 inches (89 cm)

Fasting glucose 110mg/dL or higher.

What are the Lab findings of IR? Laboratory findings in IR are: fasting insulin levels greater than 20 μU/mL and a fasting glucose-to-insulin ratio less than 4.5[9]. Due to wide variability among different ethnic groups, the 2-hour glucose/insulin response to a 75 g glucose load is considered more reliable. A 2-hour insulin level of 100-150 μU/mL indicates probable IR; 150-300 μU/mL is diagnostic of IR; and above 300 μU/mL indicates severe IR. 2-hour glucose of 140-199mg/dL indicates impaired glucose tolerance. 2-hour glucose above 200 mg/dL indicates non-insulin-dependent diabetes (type II diabetes). Patients with IR should not be labeled as type II diabetes unless, in addition to elevated insulin, the 2-hour glucose is also elevated.

Adrenal hyperplasia

Congenital adrenal hyperplasia is an inherited autosomal recessive enzyme defect that results in metabolic disorders and masculinization of newborn females. It is fortunately rare. A milder form, with onset at or following menarche, is variously labeled late-onset, adult-onset, acquired, partial, attenuated and non-classical adrenal hyperplasia.

Cause of Late onset CAH?

The most common form is due to 21-hydroxylase deficiency; other forms are due to 11β-hydroxylase deficiency and 3β-hydroxysteroid dehydrogenase deficiency. Clinical signs include mild hirsutism, increased skin sebum causing mild acne, increased scalp sebum making daily hair washing necessary and mild hypertension.

How to diagnose CAH? The diagnosis is confirmed by 17-hydroxyprogesterone (17OHP) levels ≥ 200 ng/dL or dehydroepiandrosterone sulfate (DHEAS) levels ≥ 180 μg/dL, which may also originate in the ovary. Elevated DHEAS is more common in mild cases and can be measured first. 17OHP should be measured first if there is virilization (hirsutism, male-pattern baldness or clitoral enlargement).

How to treat CAH? Treatment for either defect (congenital/ LATE ONSET) is low-dose corticosteroid (0.5 mg dexamethasone or 5 mg prednisone) daily at bedtime. The addition of CC is often necessary or ovulation. Corticosteroids should be discontinued after ovulation, because of the risk of birth defects. Amenorrhea and excess androgen may be due to Cushing’s syndrome or acromegaly. Rapid development of virilization may be due to an androgen-producing tumor.