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Following factors which
should be considered when assessing granulomatous inflammation of the
lung in the histological section:
(a)
The granulomas :
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Are they distinct and well formed, as in
sarcoidosis, or rather soft and diffuse, as in extrinsic allergic
alveolitis (EAA)?
Are they necrotising or non-necrotising?
If necrotising, are they "caseous",
abscess-like with inflammatory cells or just degenerate?
Caseous or abscess-like necrosis are
strong pointers to an infectious etiology.
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The term
caseous , though commonly used to describe a characteristic
form of combined coagulative/liquefactive
necrosis, is actually used in gross description of "cheesy" necrotic
material.
Histologically,
this dead material has a distinctive granular amorphous appearance with
cellular features barely maintained.
(b)
Other features/pathology:
- A "cause" for the granuloma- Eg.
Foreign bodies (polarisable or not), microorganisms, tumour.
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- Vasculitis, tissue necrosis. Seen
in various sections. The more important are Wegener’s granulomatosis (WG)
and infection.
- Interstitial inflammation
around/adjacent to the granuloma. This helps distinguish EEA from
sarcoidosis.
(c) Location or distribution of
granulomas:
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Does this appear to
be diffuse granulomatous process or is there a distinct mass, lesion
which is granulomatous?
Radiological
correlation is very helpful in this situation.
Mass lesions are
commoner in infection, usual in WG, unusual in sarcoidosis and not seen
in EAA.
If the granulomas are relatively diffuse
or scattered in the lung parenchyma, do they have a particular location
related to the acinus or other recognizable locations. Eg:
Are they centriacinar, broncentric, perivascular or septal/lymphatic in
their distribution?
Granulomas in EAA are characteristically
centriacinar while in sarcoidosis a bronchial and vascular/septal
distribution is common.
Rheumatoid nodules are characterized by
palisaded histiocytes together with the necrobiotic center and are
regarded as ‘granulomatous’ by some pathologists and these lesions enter
the differential diagnosis of necrotizing granulomatous masses.
Sarcoid-like granulomas may very rarely
be seen around an otherwise typical rheumatoid nodule or pulmonary
hyalinising granuloma in the lung.
Visit:
Infectious Granuloma of the Lung
;
Pathological Diagnosis of Granulomatous Lung
Diseases ;
Non-necrotising Granulomatous Inflammation of the
Lung ;
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Necrotising sarcoidal granulomatosis: a problem of identity. A
study of seven cases.
Sarcoidosis. 1987 Sep;4(2):94-100.
We report
on a study of 6 cases of Necrotising Sarcoidal Granulomatosis (NSG)
and details of another problem case illustrating the difficulties
of classification. We have compared the clinical and pathological
features with those of sarcoidosis, Wegener's Granulomatosis (WG),
Churg Strauss Granulomatosis (CSG), Pulmonary Hyalinizing
Granuloma (PHG) and various metal lung diseases. We distinguish
NSG from sarcoidosis, in particular by the prominence of
vasculitis, necrosis and the rarity of extrapulmonary
manifestations, but accept that problem cases can occur. We see no
difficulty in separating NSG from CSG, PHG and metal lung
granulomatous diseases, but on occasion WG may cause considerable
difficulty. For the present NSG is best regarded as a distinct
entity.
Necrotizing
sarcoid granulomatosis--is it different from nodular sarcoidosis?
Pneumologie. 2003 May;57(5):268-71.
BACKGROUND: Necrotizing sarcoid granulomatosis (NSG) was initially
defined as a granulomatosis with features in between sarcoidosis
and Wegener's granulomatosis (WG), but without extrapulmonary
involvement. Subsequent reports have shown that extrapulmonary
involvement does exist, and some have suggested NSG as a variant
of sarcoidosis. MATERIAL AND METHODS: We studied 10 cases from 3
institutions, and compared clinical and histologic features with
those of nodular sarcoidosis and WG. We have analyzed the 10 cases
for mycobacterial chaperonin and for the insertion sequence 6110
by PCR. RESULTS AND CONCLUSIONS: Nodular aggregates of granulomas
in NSG were similar to those seen in nodular sarcoidosis.
Granulocytic vasculitis, a hallmark of WG was not seen in any of
the NSG cases. Granulomatous vasculitis was a common feature in
cases of NSG, and did not differ from that seen in sarcoidosis.
The only unique feature of NSG is infarct-like necrosis, induced
by the vasculitis, which might also be interpreted as a function
of the duration of the vasculitis, leading ultimately to vascular
obstruction. NSG based on our morphologic findings is best
classified as a variant of nodular sarcoidosis. In contrast to our
findings in sarcoidosis mycobacterial DNA was not found in any of
the 10 cases.
Pulmonary
angitis and granulomatosis.Zhonghua
Nei Ke Za Zhi. 1992 Jul;31(7):424-7,
445.
16
patients of Wegener's granulomatosis, 4 of allergic angiitis and
granulomatosis, 3 of lymphomatoid granulomatosis and 1 of
necrotizing sarcoid granulomatosis were reported. In this group of
different diseases, characteristic pathological manifestations are
inflammatory cellular infiltration of vessel wall combined with
destruction and necrosis of pulmonary parenchyma. There was little
difference in their clinical features. In most of the cases, fever
and systemic symptoms related to lung and extrapulmonary organs
were present. Correct diagnosis of these diseases is very
important, because both the prognosis and therapy are different.
As for the prognosis, it ranges from benign (necrotizing sarcoidal
granulomatosis) to very malignant (lymphomatoid granulomatosis).
The clinical features of each illness were reviewed with emphasis
on their histopathologic findings. The therapeutic effect and
final outcome were followed.
Pathomorphogenesis of tubercular histologic changes: mechanisms of
granuloma formation, maintenance and necrosis.
Internist (Berl). 2003 Nov;44(11):1363-73.
The
histopathological hallmark of infections with Mycobacterium
tuberculosis is the development of centrally necrotizing
granulomatous lesions. Granulomas are focal accumulations of
mononuclear cells in various states of differentiation, in which
the local activation of mycobacteria-infected macrophages by
specific T cells takes place. On the one hand, this assures
efficient containment of mycobacterial growth and demarcation of
the infectious focus. On the other hand this is associated with
the displacement of and irreversible damage to functionally vital
organ tissue (predominantly in the lungs). New insights, emerging
from animal models of infection, into the dynamic mechanisms
regulating the induction, maintenance and caseation of tuberculous
granulomas explain why highly effective anti-inflammatory
therapies, e. g. administration of anti-TNF monoclonal antibodies,
may result in reactivation of tuberculosis.
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