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Panniculitis: A Dermatopathologist's Perspective and Approach To Diagnosis
Panniculitis: A Dermatopathologist's Perspective and Approach To Diagnosis
228]
Review Article
A B S T R A C T
Panniculitis is the inflammation of subcutaneous fat. It poses a diagnostic challenge, both for the clinician as well as the histopathologist
owing to its diverse etiologies, overlapping morphological features, and dynamic nature of the lesions. The standard protocol
for histopathologic diagnosis is to examine deep skin biopsies after staining with hematoxylin and eosin. Sometimes, however,
special stains are also needed to rule out varied etiologies. A thorough histopathologic examination in conjunction with appropriate
clinical details is the key to identify different subtypes of panniculitis. In this review, we discuss the classification of panniculitis with
salient histopathologic features of the subtypes in each category. We also present a diagnostic algorithm for arriving at a definitive
histopathologic diagnosis of different panniculitis subtypes.
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DOI: Cite this article as: Gupta P, Saikia UN, Arora S, De D, Radotra BD.
10.4103/2349-6029.195224 Panniculitis: A dermatopathologist’s perspective and approach to diagnosis.
Indian J Dermatopathol Diagn Dermatol 2016;3:29-41.
29 © 2016 Indian Journal of Dermatopathology and Diagnostic Dermatology | Published by Wolters Kluwer - Medknow
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thin fibrous septa that divide the subcutaneous fat Table 1: Histopathologic classification of panniculitis
into lobules are constituted by collagen and reticulin Predominantly septal
fibers and contain the nerves, blood, and lymphatic With vasculitis
Leukocytoclastic vasculitis
channels. Each fat lobule is supplied by an arteriole Superficial thrombophlebitis
that branches into capillaries in the lobule. There Cutaneous polyarteritis nodosa
is a peculiar pattern of blood supply of the lobules. Without vasculitis
Erythema nodosum
The blood supply is terminal so that there are no Necrobiosis lipoidica
capillary communications between adjacent lobules or Scleroderma
between dermis and subcutaneous fat. This explains Rheumatoid nodule
Subcutaneous granuloma annulare
why large‑vessel vasculitis involving the septal vessels Necrobiotic xanthogranuloma
is commonly attended by little inflammation of the Predominantly lobular
fat lobules, whereas small‑vessel vasculitis displays With vasculitis
Erythema nodosum leprosum
extensive fat necrosis with centrilobular infarction and Lucio’s phenomenon
dense inflammation within the lobule.[8] Neutrophilic lobular panniculitis associated with rheumatoid
arthritis
Erythema induratum of Bazin
The subcutaneous fat has a poor repertoire of responses
Crohn’s disease
to noxious stimuli, with the most common response Without vasculitis
being fat necrosis on histopathology, which could in Sclerosing panniculitis
Calciphylaxis
turn be secondary to innumerable conditions.[9,10] It
Sclerema neonatorum
is also important to remember that the subcutaneous Cold panniculitis
fat may be involved secondarily in vasculitides, Lupus erythematosus profundus
Pancreatic panniculitis
trauma, deep cutaneous fungal infections, and many
Infective panniculitis
malignancies.[11‑20] Histopathologically, panniculitis can Traumatic panniculitis
predominantly affect lobules or septa, with/without Factitious panniculitis
Subcutaneous fat necrosis of newborn
vascular involvement. Accordingly, the panniculitis
Subcutaneous sarcoidosis
can be classified into following main classes: Post‑steroid panniculitis
1. Predominantly septal panniculitis without vasculitis Gout panniculitis
Postirradiation sclerodermatous panniculitis
2. Predominantly septal panniculitis with vasculitis
Crystal‑storing histiocytosis
3. Predominantly lobular panniculitis without Others
vasculitis Eosinophilic panniculitis
Subcutaneous panniculitis‑like T‑cell lymphoma
4. Predominantly lobular panniculitis with vasculitis
5. Others.
similar nodular lesions developing over months or
The detailed histopathologic classification of even years [Figure 1].[21‑24]
panniculitis is given in Table 1.[3,7‑9]
Histologically, EN shows widening of the septa due
SEPTAL PANNICULITIS WITHOUT VASCULITIS to edema and neutrophilic infiltrate admixed with
eosinophils. The infiltrate often extends into the
Erythema nodosum periphery of the fat lobules and between the individual
Erythema nodosum (EN) is the prototype of nodular fat cells in a lace‑like fashion in early stages [Figure 2a].
septal panniculitis. It is a clinical syndrome with Vascular changes and hemorrhage are commonly seen
varied symptoms and etiologies. It typically affects but no definite vasculitis is present. In later stages,
young adults with a predilection for females. There the infiltrate is replaced by collections of histiocytes,
are two clinical forms of EN ‑ acute and chronic, especially around slit‑like spaces or blood vessels
which differ in their clinical manifestations but forming Miescher’s radial nodules, which are considered
do not exhibit much histopathological difference. to be a characteristic feature of EN and can be found in
Acute EN also known as migratory panniculitis or all stages of EN. Further progression of the lesion leads
subacute nodular migratory panniculitis is typically to the development of a granulomatous response with
asymmetrical, unilateral, and predominantly involves giant cells [Figure 3]. However, fat necrosis is usually
legs. It exhibits a female preponderance and tends to not seen. The older lesions of EN show widening of the
affect older age groups, in contrast to classical EN. septa due to fibrosis and inflammation at the edges of
The chronic form is less recognized, however, shows the septa and mainly involve the periphery of the fat
b
b
Figure 2: Histopathologic features of erythema nodosum. (a) Sparse inflammatory
infiltrate involving septa of subcutaneous fat with no inflammation of the
lobules (H and E, ×40), (b) older lesion showing fibrosis of the widened septa
with sparse chronic inflammatory infiltrate (H and E, ×200)
no increased mucin in NL and plasma cell collections with hyalinosis and thickened collagen bundles. In the
can be seen in the deeper dermis.[7,25,26] later stages, the inflammatory infiltrate extends from
the septa into the periphery of the fat lobules causing
Scleroderma reduction in the fat lobules, which is replaced by newly
The word scleroderma is derived from skleros ‑ hard formed pale collagen. In the late sclerotic stage, the
and derma ‑ skin (Greek) is a connective tissue disorder, inflammation disappears and the collagen bundles in
which leads to thickening and fibrosis of the skin. There the reticular dermis are thickened, hypocellular and
are two types of scleroderma, i.e., localized (morphea) stain more deeply eosinophilic. The eccrine glands
and systemic (progressive systemic sclerosis). The too appear atrophic and surrounded by newly formed
thickening and hardening of skin may also be associated collagen [Figure 6].[7,26]
with metabolic, genetic, immunologic, or occupational
disorders.[37] Subcutaneous granuloma annulare
SGA is an idiopathic condition characterized by
In nearly all forms of scleroderma, the inflammatory palisaded granulomatous infiltration in the dermis
changes involve both the dermis as well as the commonly occurring in children and young adults with
subcutaneous fat and cannot be differentiated female predilection. The common sites of involvement
histologically. In the localized form, early stages show are hands, arms, legs, and feet. It is a chronic condition
lymphoplasmacytic perivascular infiltrate throughout with variants including (a) generalized popular form,
the dermis, extending into thickened fibrous septa along
b
b Figure 4: Clinical images of (a) necrobiosis lipoidica (b) erythema nodosum
Figure 3: Histopathologic features of erythema nodosum. (a and b) leprosum
Granulomatous inflammation with scattered multinucleate giant cells involving
predominantly the septa with extension into the lobules (H and E, ×200)
a b
Figure 5: Histopathologic features of necrobiosis lipoidica. (a and b)
Granulomatous inflammation with occasional multinucleate giant cells Figure 6: Histopathologic features of scleroderma. Deeply eosinophilic collagen
surrounding degenerating pale collagen and involving predominantly the fibers in reticular dermis surrounding atrophic eccrine glands with reduced
septa (H and E, [a] ×40, [b] ×200) subcutaneous fat (H and E, ×40)
(b) perforating, (c) erythematous, and (d) deep GA which Old lesions show dense fibrosis, clefts, and cystic
involves the subcutis.[38,39] degeneration.[7,8]
b
Figure 7: Histopathologic features of subcutaneous granuloma annulare.
(a) Nodular infiltrates in the dermis composed of palisading histiocytes b
surrounding degenerating collagen (H and E, ×100), (b) Periodic acid‑Schiff Alcian Figure 8: Histopathologic features of rheumatoid nodule. (a and b) Nodular
blue stain highlighting the increased mucin interspersed between degenerating infiltrates in the dermis composed of palisading histiocytes surrounding central
collagen fibers (Periodic acid‑Schiff Alcian blue, ×200) fibrin (inset, ×200) and degenerating collagen (H and E, [a] ×40, [b] ×200)
in and around the vessels involving the panniculus vasculitis and thrombosis occluding the lumina.[52‑55] In
causing lobular panniculitis. In the later stages, there early stages, there is leukocytic infiltrate accompanied
is intimal proliferation with thrombosis leading to with edema, and in later stages, lymphocytes,
ischemia and ulceration sometimes. In the healed or histiocytes, and occasional giant cells are seen in the
healing stage, there is fibrovascular proliferation and wall of the veins.[7,29] The differential diagnosis includes
nonspecific lymphocytic infiltrate in the perivascular PAN; however, there is no involvement of arteries.
area.[7,8] In a series of 16 cases with cutaneous PAN, it A Gram stain is always advised to rule out common
was observed that all cases manifested lesions in the bacteria causing suppurative thrombophlebitis, and a
form of nodules and/or indurated erythematous patches history of trauma is needed to exclude traumatic fat
over their lower extremities, and on histopathologic necrosis.[52‑54]
examination, all cases exhibited necrotizing vasculitis
of small, subcutaneous, muscular arteries with/without LOBULAR PANNICULITIS WITHOUT VASCULITIS
luminal occlusion. Eight of these cases were followed
Lupus erythematosus panniculitis (lupus profundus)
up for at least 5 years, with the longest follow‑up period
This is defined as a specific involvement of
being 19 years and displayed good prognoses without
the subcutaneous fat in patients with lupus
any systemic involvement.[46]
erythematosus (LE). It is a rare manifestation of the
Superficial thrombophlebitis disease, occurring approximately in 1%–3% of patients
Superficial thrombophlebitis usually involves lower with cutaneous LE. It may be observed in patients with
extremities, presenting as tender, erythematous nodule, discoid LE or SLE or as an isolated phenomenon without
or cord‑like structure. Often there is the presence systemic or other cutaneous findings [Figure 1a].
of predisposing factors such as varicose veins, A patchy lymphoplasmacytic infiltrate in the lobules
hypercoagulable state, oral contraceptive intake, or of the subcutaneous fat along with lymphocytic
underlying malignancy.[49‑51] nuclear dust is a clue for the histopathological
diagnosis of LE panniculitis (LEP) [Figure 10]. The
There is involvement of small‑ or medium‑sized veins in diagnosis of LEP may be especially problematic
the deeper dermis and subcutaneous fat causing acute in cases where the involvement of subcutaneous
fat is the only manifestation of the disease.
Clinically, LEP and subcutaneous panniculitis‑like
T‑cell lymphoma (SPTCL) are indistinguishable;
however, in SPTCL, the presence of atypical
CD8‑positive T‑lymphocytes and the absence of septal
fibrosis, B‑cell follicles, and plasma cells clinch the
diagnosis.[53‑58]
a b
c d
Figure 9: Histopathologic features of cutaneous polyarteritis nodosa.
b
(a and b) Inflammatory infiltrate involving medium‑ and large‑sized arteries in Figure 10: Histopathologic features of lupus erythematosus panniculitis.
the dermis and septa of subcutaneous fat (H and E, [a] ×40, [b] ×200). (c and d) (a) Dense collections of lymphocytes and few plasma cells in the lobules with
fibrinoid necrosis and neutrophilic infiltrate involving full thickness of vessel hyalinized fat necrosis (H and E, ×100), (b) scattered lymphoid follicles with
wall (H and E, [c] ×100, [d] ×200) germinal centers (inset, ×200) (H and E, ×200)
LOBULAR PANNICULITIS WITH VASCULITIS Neutrophilic lobular panniculitis associated with rheumatoid
arthritis
Erythema nodosum leprosum Rheumatoid arthritis may be accompanied by cutaneous
This is a Type 2 reaction occurs most commonly in manifestations such as rheumatoid granuloma,
lepromatous leprosy (LL) followed by borderline leukocytoclastic vasculitis, and rheumatoid neutrophilic
leprosy. Clinically, the patients present with tender dermatitis.
erythematous plaques or nodules [Figure 4b]. It is often
accompanied with fever, malaise, and arthralgia. Histopathology shows a predominantly lobular
panniculitis, severe necrosis of the adipocytes in the
Histologically, the lesions show neutrophilic infiltrates lobule, and an inflammatory infiltrate composed of
superimposed on chronic multibacillary leprosy. An neutrophils, foamy histiocytes, and multinucleate
associated necrotizing vasculitis affecting arterioles, giant cells. Small cystic spaces lined by amorphous
venules, and capillaries can be seen in some cases eosinophilic material were seen in some cases as an
of erythema nodosum leprosum (ENL) [Figure 11]. early expression of lipomembranous or membranocystic
Sometimes, the neutrophilic infiltration is scanty with panniculitis. Neutrophilic lobular panniculitis should
a predominance of macrophages containing fragmented be differentiated from the suppurative variant of EN,
bacilli. [86‑89] In a series of 32 patients with ENL, in which numerous neutrophils extend into the lobule
22 patients developed ENL before the commencement from fibrous septa.[93,94]
of chemotherapy, thereby highlighting the fact that
Erythema induratum of Bazin/nodular vasculitis
development of ENL in the absence of chemotherapy
NV is a multifactorial syndrome with lobular
is not an infrequent event and early recognition of this
panniculitis and vasculitis, in which tuberculosis
event is important. The authors concluded that ENL
may or may not be one of its many etiologies. Thus,
should be looked upon as a manifestation of leprosy, and
erythema induratum/NV complex is classified into
not essentially as a mere complication of its therapy.[87]
two variants: EIB type and NV or erythema induratum
of Whitfield type [Figure 1c]. The Bazin type has a
tuberculous etiology.
or septal vessels, 9.9% biopsies showed predominantly SPTCL is histologically characterized by neoplastic
lobular panniculitis with vasculitis involving large lymphoid cells infiltrating mainly the lobules of the
septal vessels, both arteries and veins, and necrotizing subcutaneous tissue with or without the involvement
vasculitis of the centrilobular venules, and 8.9% of the epidermis and dermis. The neoplastic
biopsies displayed lobular panniculitis with vasculitis lymphoid cells have hyperchromatic, angulated
involving larger septal vessels (both arteries and nuclei, scant cytoplasm, and indistinct cell borders.
veins), but without any involvement of the smaller In addition, interspersed histiocytes, plasma cells,
centrilobular vessels. There were 9.9% biopsies with neutrophils, mitoses, apoptotic bodies, karyorrhectic
a predominantly lobular panniculitis but without debris, and areas of fat necrosis are also seen. The
any obvious evidence of septal or lobular vasculitis, atypical cells often show rimming of individual fat
even in serial sections.[28] The differential diagnosis cells [Figure 12].
of EIB/NV typically includes PAN, which can be
differentiated clinically and by the presence of all Based on T‑cell receptor (TCR) phenotype and
stages of the lesion in the biopsy.[95‑97] immunophenotypic characteristics, there are two
types of SPTCL. One is TCR‑αβ, associated with an
Subcutaneous panniculitis‑like T‑cell lymphoma indolent course and the neoplastic T‑cells are usually
SPTCL is a very rare form of skin lymphoma and CD4−, CD8+, and CD56−. The second type is TCR‑γδ,
accounts for <1% of all non‑Hodgkin’s lymphomas. It is characterized by rapid clinical deterioration and
localized primarily to the subcutaneous adipose tissue CD4−, CD8−, and CD56+ neoplastic T‑cells. Nowadays,
without the involvement of the lymph nodes. diagnosis of SPTCL is used for patients with TCR‑αβ,
Predominantly septal
Vasculitis?
Yes No
Small Large
Vessel Vessel
Artery/Vein
LCV
Cut. PAN(Art)
Sup. TB(Vn)
Predominantly lobular
Vasculitis?
Yes No
Small Large
Vessel Vessel
ENL
Artery
NP-RA
CD
EIB
Gout Traumatic
Sclerosing Sclerema Cold Pancreatic Infective Factitious panniculitis
Calciphylaxis LEP Post steroid
Panniculitis neonatorum panniculitis panniculitis panniculitis panniculitis
SFN S/C Sarcoidosis
while TCR‑γδ type is designated as cutaneous gamma/ In any given case of panniculitis, a diagnostic
delta positive T‑cell lymphoma (Cγδ‑TCL).[98‑104] algorithm should be followed to reach to an appropriate
histopathologic diagnosis with adequate clinical
CONCLUSION information [Tables 2 and 3].
Some important points to remember in cases with Financial support and sponsorship
clinically suspected panniculitis: Nil.
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