ETIOLOGI

Penyakit Fibromyalgia rheumatica berhubungan dengan kejadian infeksi dari adenovirus,

respiratory synctical virus, virus parainfluenza tipe 1, parvovirus B19, Mycoplasma pneumoniae dan
Chlamidia pneumoniae. Terdapat juga faktor genetik. HLA DRB1*04 dan HLA DRB1*01 berhubungan
dengan tingkat keparahan penyakit ini. Polimorfisme dari ICAM-1, TNF-, dan Reseptor IL-1
berhubngan dengan tingkat perkembangan penyakit. Sekresi yang berkurang dari kortisol, ACTH dan
dehydroepiandrosteron sulfat menunjukkan adanya peran patogenensis pada kelenjar adrenal. 2
PATOGENESIS
Although the temporal artery is most frequently involved in giant cell arteritis, patients often

have a systemic vasculitis of multiple medium and large-sized arteries which may go undetected.

Histopathologically, the disease is a panarteritis with inflammatory mononuclear cell infiltrates within

the vessel wall with frequent giant cell formation. There is proliferation of the intima and agmentation

of the internal elastic lamina. Pathophysiologic findings in organs result from the ischemia related to the
involved vessels. Experimental data support that giant cell arteritis is an antigen driven disease in which

actirated T Iymphocytes macrophages and dendritic cells play a critical role in the disease

pathogenesis. Sequence analysis of the T cell receptor of tissue-infiltrating T cells in lesions of giant

cell arteritis indicates restricted clonal expansion suggesting the presence of an antigen residing in the

arterial wall. Giant cell arteritis is believed to be initiated in the adventitia where CD4+ T cells enter

through the vasa vasorum become activated and orchestrate macrophage differentiation. T cells

recruited to vasculitic lesions in patients with giant cell arteritis produce predominantly IL-2 and IFN-y

and the latter has been suggested to be involved in the progresson to overt arteritis. Recent data

demonstrate that at least two separate lineages of CD4 T cells--IFN-y-producing TH l cells and IL- 1 7-
producing TH 1 7 cells-participate i n vascular inflammation and may have differing levels of
responsiveness to glucocorticoids1

DIAGNOSIS
Polimialgia reumatika ditegakkan berdasarkan kriteria Healey :
1. Usia > 50 tahun
2. Nyeri dan kaku berlangsung sekurang-kurangnya satu bulan, melibatkan sekurang-
kurangnya 2 dari 3 area leher, bahu dan panggul.
3. Kaku pagi hari berlangsung sekurang-kurangnya 1 jam.
4. LED > 40 mm/jam
5. Penyakit lain dieksklusi kecuali GCA
6. Berespon terhadap pemberian prednison (20 mg/hari)3
Daftar Pustaka :
1. Harrison,
2. Soubrier, M. Dubost, J.J. dan Ristori, J.M.2006. Polymialgia rheumatica, Joint bone spine
73 : 599-605.
3. Ilmu penyakit dalam, FKUI.