Endocrine Abstracts (2011) 26 P423

The regulatory role of neuroprotective nerve growth factor in Graves' ophthalmopathy

Ildiko Molnar1 & Agota Bokk2


1EndoMed, Debrecen, Hungary; 2Genzyme Europe BV, Budapest, Hungary.


Nerve growth factor (NGF) belongs to the neurotrophic family and maintains the normal function of peripheral sympathetic and sensory neurons. NGF can synthesize locally in the neuronal and nonneuronal tissues. The main cell sources of NGF restrict to bone-marrow derived cells (lymphocytes, mast cells, eosinophils, monocytes, macrophages) as well as to structural cells (fibroblasts, epithelial cells, smooth muscle cells, adipocytes, keratinocytes). The sympathoadrenal activity initiated NGF-liberation is linked to the hormone-releases from the anterior pituitary. NGF plays a potent role in the highly sympathetic innervated organs such as in glands, adipose tissues and orbits, where it participates in the development of retina, corneal and conjunctival epithelium, lens, iris, ciliary bodies and optic nerves. NGF can induce a local inflammation with the liberation of cytokines, chemokines, active peptides and influence the cell survival and apoptosis processes via its two classes of receptors, tyrosine kinase A and p75. Maintaining the integrity of the sympathetic innervation, NGF contributes to tissue reparative responses.

Graves’ ophthalmopathy represents a complexity of endocrine, autoimmune and inflammatory events with an increased sympathoadrenal activity. We investigated the serum NGF levels in the patients with Graves’ disease (n=95), Hashimoto’s thyroiditis (n=19), toxic nodular goitre (n=17) and controls (n=20). Our findings demonstrated elevated NGF levels in Graves’ hyperthyroidism in comparison with Graves’ euthyroidism (1831.29±39.32 vs 1649.33±75.63 pg/ml, P<0.023). The presence of TSH receptor autoantibodies (P<0.009) and the levels of FT3 (P<0.01) gave a strict association with the elevation of NGF. Surprising, hyperthyroid Graves’patients with ophthalmopathy showed lower NGF levels than those who had no eye symptoms (1910.47±55.62 vs 1746.65±51.98 pg/ml, P<0.036).

The results support, that the lower serum NGF due to a failed neuroprotectivity may contribute to the onset of ophthalmopathy.

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