Discussion
Hernandez-Rodriguez et al. described and validated 4 main histological
patterns among TAB from GCA patients. Patterns of inflammation were
defined according to the extent and distribution of inflammatory
infiltrates through the artery wall as follows :
- Adventitial pattern : presence of inflammatory cells
only in the adventicia and preservation of media and intima layers
(5.6%) ;
- Advential invasive pattern : adventitial infiltration
followed by local invasion of the muscular layer with integrity of the
intima (7.3%) ;
- Concentric bilayer pattern : inflammatory cells
infiltrate the adventitia and the intima with preservation of the
media (18.2%) ;
- Panarteritic pattern : inflammatory infiltrates are
distributed through the 3 arterial layers (68.8%).
They also proposed a scoring system according to the severity of the
vessel invasion : « mild infiltrative pattern » including adventitial
pattern and adventitial invasive pattern, scored as 1 and 2 ; and
« extensive infiltrative pattern » including concentric bilayer pattern
and panarteritic pattern, scored as 3 and 4 (Figure 3 )
(5).
Figure 3. Histological Patterns involving the Temporal Artery
in GCA and scoring system according to Hernandez-Rodriguez et al.
Another important point of Hernandez-Rodriguez et al. is the proposition
of a dynamic model of arterial inflammation in GCA based on the fact
that different histological patterns are observed in TAB from GCA
patients and that those different inflammatory patterns may coexist in a
same artery with the presence of normal and/or healing sections
(Figure 4 ) (5).
Figure 4. Dynamic model of arterial invasion adapted from
Hernandez-Rodriguez et al.
Besides the 4 histological patterns, the scoring system and the proposal
of a dynamic model of arterial invasion, Hernandez-Rodriguez et al did
not find clear correlation between the different patterns and clinical
or biological findings at disease diagnosis although abnormalities on
temporal artery palpation and some cranial symptoms seems to occur
mostly in patients with panarteritic pattern on TAB (5).
The main clinical features in this patient were the deterioration in the
general status and visual blurring. Permanent visual loss is the most
severe complication of GCA and is often an early manifestation of the
disease (7). Chatelain et al found that the presence of giant cells on
TAB was associated with permanent vision loss and also found a positive
correlation between the quantity of giant cells and the risk of
blindness. However, they found no association between the abundance of
the inflammatory infiltrate, and the presence of arterial thrombosis
(7). Makkuni et al showed that the degree of intimal hyperplasia on TAB
seems to be closely associated with neuro-ophtalmic complications of GCA
(8). Hernandez-Rodriguez et al showed that the presence or absence of
giant cells and the extent of intimal hyperplasia did not correlate with
cranial and neuro-ophtalmic ischemic manifestations (5).
The young age of our patient has contributed to the relative delay of
GCA diagnosis, making it less likely. Indeed, GCA is well described in
patients of 50 years and older with incidence of the disease increasing
with age (9,10) making the diagnosis here more challenging.