Clinical examination
| Signs and findings | |
|---|---|
| 1. Assessment of fat mass | Accurate height and weight and waist circumference. We find other measures of fat mass (e.g. skinfold thicknesses) are of little use in the clinical situation. Bioimpedance is becoming useful now that normative data are available |
| 2. Distribution of fat | For example, whether generalised or abdominal or other pattern. The presence or absence of the “buffalo hump” is a poor sign of Cushing’s syndrome, as a prominent nuchal fat pad is common in simple obesity |
| 3. Presence and degree of acanthosis nigricans | Acanthosis nigricans, the presence of dark greasy thickening of the skin around the neck and in skin creases, is suggestive of hyperinsulinism but is neither sensitive or specific |
| 4. Accurate blood pressure | Using an appropriate size cuff (two readings, lying and sitting) |
| 5. Pubertal and growth assessment | Those obese before 2 years are tall for age. Many obese girls develop early in puberty. Pubertal and growth assessment is particularly important to assess whether weight maintenance (i.e. growing into their weight) is a viable option for treatment |
| 6. Signs of hypothyroidism | Short stature, goitre, yellowish skin, dry skin and hair |
| 7. Signs of Cushing’s syndrome or polycystic ovarian syndrome (PCOS) | Glucocorticoid and androgen excess in Cushing’s syndrome produce striae, acne, telangiectasia, hirsutism, and virilisation. The androgen excess in polycystic ovarian syndrome (PCOS) in girls produces hirsutism and acne. However striae are almost universal in obese children and adolescence and we have not found that the distribution or colour of the striae can help distinguish between the extremely common simple obesity and the extremely rare Cushing’s syndrome. Obesity by itself is practically never the presenting sign of Cushing’s syndrome |
| 8. Signs of genetic obesity syndromes | For example, Prader Willi, Bardet Biedl, leptin deficiency, melanocortin 4 receptor (MC4R) deficiency and other monogenic forms of obesity. Monogenic forms of obesity remain a very rare cause of obesity in the general population, although such syndrome should be considered in those who have very early onset of extremely obesity.23 See table 3 |