Service for paediatricians

Only in rare cases is the cause of obesity hormonal. However hypothroidism and overproduction of cortisol should be ruled out.

Recommended analyses in the case of adipositas:

Cortisol in the serum and free corticoids in 24-hour urine collection as well as TSH, fT3, fT4, (TPO –AB).

It is also important to recognise established secondary diseases deriving from the adipositas and as such to better justify the necessity of a loss of weight or, in the case of children who are still growing, a stabilisation of weight.

Also recommended in the case of adipositas a blood sample taken on an empty stomach:

Cholesterol, HDL cholesterol, triglyceride, LDL cholesterol, lipoprotein a, intact proinsulin, cortisol in the serum, Got, GPT, GGT, Hba1c, TSH, fT3, fT4, LH, FSH, testosterone, estradiol, SHBG, homocysteine, prolactin, 17-hydroxyprogesteron, uric acid

An oral-glucose-tolerance-test OGTT with insulin determination should also be conducted to recognise insulin resistance and to justify possible treatment with metformin.

Macrosomie can often be traced back to a family disposition. Growth reducing hormone therapy can be considered for boys with a growth prognosis of over 203 cm and for girls of over 187 cm. It is advisable that boys measuring 165-170 cm or girls measuring 160-165 cm attend a paediatric endocrinological consultation session with their parents.

Macrosomie can also be attributed to a genetic syndrome such as for example Klinefelter’s or Marfan syndrome. You can find more information under Human genetics.

Percentile-cutting growth can also be the result of premature puberty development or a continuous exogenous supply of sexual hormones. Children with macrosomie may become conspicuous in these cases. Precocious puberty must be ruled out when growth acceleration is above average.

It is important to recognise percentile-cutting growth due to premature puberty development.

Recommended analyses in the case of macrosomie, which is not solely derived from the family:

LH, FSH, estradiol/17-β-oestradiol, testosterone, 17-OH-progesteron,

Ursachen für gestörtes Wachstum

• Any chronic disease (prolonged nutritional problems, oncological diseases, heart, stomach, bowel or kidney diseases, coeliac disease)
• Hormone disorders:
  Deficiency of growth hormone
  Thyroid gland diseases
  Disorders of puberty
  Adrenal gland diseases
  Hormone deficiency due to tumors
• Genetically causes (the most common cause in girls is an Ullrich-Turner syndrome, Shox-Gen defects and many more.

Recommended endocrinological analyses on suspicion of a primary endocrinological growth disorder:

• IGF-1 and IGF-BP3;
• TSH, free T3, free T4.
• In adolescence: LH, FSH, testosterone, oestradiol;
• Sodium, potassium, cortisol, prolactin.

We also recommend the following parameters in clinical chemistry:

GOT, GPT, GGT, urea, creatinine, uric acid, Na, Ca, K, phosphate, iron, ferritin, CRP, differential blood count, and IgA, trans anti glutaminase-AB, gliadin/endomysium-AB.

Clarification of possible genetic causes should be left to the specialists. The general conditions outlined in the German genetic diagnostics law (GenDG) should be adhered to. See our department for Human Genetics.

Note:

• Urgent clarification in the case of percentile deviating growth!
• Does the growth correspond to the calculated target height range?
• Average target height boys: (Height father (in cm) plus height mother (in cm) divided by 2 plus 6.5 cm.
• Average target height girls: (Height father (in cm) plus height mother (in cm) divided by 2 minus 6.5 cm.
• It is to be expected that the final height of the children lies in the range of ± 8.5 cm from the calculated average target height.

Growth hormone determination (GH/STH) above and beyond a stimulation test is unnecessary. Physiologically GH is only distributed selectively/peak-like, meaning a low value outside a stimulation test bears no significance. There is generally a lowered IGF-1-level in children with a delay in development; the IGF-BP3- level for these children is however at a normal level for their age.

The symptoms are always the decisive criteria.

Percentile deviating growth has to be clarified.

Vitamin-D-deficiency-rickets with impaired mineralization and structural disorders of the growth plate can originate from:

• An insufficient supply of Vitamin D
• Insufficient endogenous synthesis
• Malabsorption of Vitamin D in the intestine

A deficiency of Vitamin-D leads to reduced absorption of calcium in the bowel. According to the differential diagnosis the Vitamin-D dependent forms of rickets (VDAR) and the phosphorpenic forms must be differentiated. Infants/ small children and shrouded adolescents, people with a migrational background and/or dark skin are particularly at risk. Overweight children and adolescents also have a higher risk of Vitamin D deficiency. If Vitamin D deficiency rickets is diagnosed chronic malabsorption disorders (coeliac disease, cystic fibrosis, Crohn’s disease), liver synthesis disorders, bile duct diseases or a chronic kidney insufficiency should be ruled out. In the case of prolonged rickets there are corresponding changes in the x-ray image of the left hand.

Recommended analyses on suspicion of a bone metabolism dysfunction:

Calcium, phosphate, alkaline phosphatase (AP), Vitamin D3/1,25-OH, Vitamin D2/25-OH, parathyroid hormone intact (EB°+)

Additional analyses on confirmation of rickets:

Calcium (serum & 24h-urine), phosphate (serum & 24h-urine), creatinine (serum & 24h-urine), urea, calculation of calcium/creatinine, procentual phosphate reabsorption (TRP), IgA, TGLUA, GLIA, GGT, GPT, bilirubin total & direct.

Note

Intact parathyroid hormone normal to lowered indicates phosphorpenic rickets. The calculation for tubular phosphate reabsorption is necessary in this case.

A normal AP rules out rickets (Exception: normal to lowered AP in the case of hypophosphatemic, renal tubular acidosis). Normal PTH rules out osteomalacia (Vitamin-D deficiency, VDAR I and II).

The appearance of secondary sexual features before the 8th birthday for girls and before the 9th birthday for boys always requires diagnostic clarification.

In every case of percentile-cutting growth premature puberty development in particular should be considered.

Recommended screening parameters:

• LH, FSH (increased values, central precocious puberty)
• Oestradiol, testosterone
• 17-hydroxyprogesterone, ACTH, androstendione, DHEAS (Adrenal androgens), sodium, potassium

Note

Selective pre-puberty values do not rule out precocious puberty. If central precocious puberty is suspected the LHRH test can provide further information. In the hormonal resting phase, approx. from the 2nd year of life until the beginning of the endogenous puberty, the pituitary gland does not react until the LHRH has been repeatedly pulsed from a pulse generator in the hypothalamus. Therefore the individual administering of LHRH in the LHRH test does not cause a rise in gonadotropine.

In the case of a premature pubarche and an acceleration in development an ACTH test should be conducted even for selective non-increased androgens.

In the case of absent puberty development further diagnostics are necessary at the latest at an age of approx. 13.5 years for girls and 14.5 years for boys.

Recommended analyses on suspicion of absent puberty development:

• LH, FSH, testosterone, oestradiol;
• TSH, fT3, fT4 (hypothroidism can lead to a delay in development),
• prolactin, cortisol in the serum

We also recommend the following

Parameters of clinical chemistry:

GOT, GPT, GGT, urea, creatinine, uric acid, Na, Ca, K, phosphate, iron, ferritin, CRP, differential blood count.

To rule out a pituitary cause a buserelin test should be conducted.

The presence of a hyperthyroidism should be ruled out for an increasing number of patients with childhood hyperactivity. The paediatrician can detect this simply and easily. Should definite indications of Morbus Basedow be apparent, this constitutes an endocrinological „emergency“, which should be brought to the immediate attention of a paediatric endocrinologist. The most important clinical indications are a tachycardia, increased sweating („moist-warm“ hands), nervousness (increased reflexes) and an enlarged thyroid gland.

Recommended analyses on suspicion of a hyperthyreose:

TSH (suppressed), fT3, fT4, TSH receptor antibodies (T-R-AB; raised in the case of M. Basedow), thyroid gland peroxidase anti bodies (TPO-AB; hyperthyroidism at the beginning of an autoimmunthyreoiditis).

In many cases a hypothroidism should be ruled out as the cause for adipositas. Even if Cushing syndrome is extremely rare, cortisol levels in the serum should be determined or, even better; the level of free corticoids in the 24-hour urine collection should be identified.

Recommended analyses on suspicion of a hypothroidism:

TSH, fT3, fT4, (TPO –AB).