Swiss Med Wkly. 2017;147:w14476
Full text here smw.ch/article/doi/smw.2017...
Summary
Although Graves’ disease has been recognised for more
than 100 years, its physiopathological mechanisms are incompletely
understood. Treatment strategies today mainly
focus on suppression of thyroid hormone production by
use of antithyroid drugs or radio-iodine, but neglect the
underlying immunological mechanisms. Although Graves’
disease is often seen as a prototype for an autoimmune
mechanism, it is more likely to be a heterogeneous syndrome
showing characteristics of both autoimmunity and
immunodeficiency. The interplay of these two mechanisms
may well characterise the physiopathology of this disease
and its complications. Immunodeficiency may be either
genetically determined or secondarily acquired. Various
triggering events lead to autoimmunity with stimulation of
the thyroid gland resulting in the clinical syndrome of hyperthyroidism.
Also, relapse risk differs from patient to patient
and can be estimated from clinical parameters incorporated
into the Graves’ Recurrent Events After Therapy
(GREAT) score. Accurate risk stratification may help to
distinguish high-risk patients for whom a more definitive
treatment approach should be used from others where
there is a high probability that the disease will recover
with medical treatment alone. Several smaller trials having
found positive effects of immunosuppressive drugs on recurrence
risk in Graves’ disease; therefoore, there is great
potential in the use of novel immunomodulating drugs in
addition to the currently used antithyroid drugs for the successful
treatment of this condition. Further in-depth exploration
of susceptibility, triggering factors and immunological
mechanisms has the potential to improve treatment
of Graves’ disease, with more personalised, risk-adapted
treatment strategies based on the different physiopathological
concepts of this heterogeneous condition.