Other Types of Panniculitis

Slide 1 · Other Types of Panniculitis

Patterns, causes, and pathological mimics

A clinicopathologic approach to deep subcutaneous inflammation

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Localize panniculitis to fat septa or fat lobules.

Distinguish nonvasculitic from vasculitic inflammation.

Recognize four less-common etiologic settings.

Explain why lymphoma can imitate inflammatory panniculitis.

Slide 3 · What this lecture includes

Four explicitly named entities: Weber–Christian disease, factitial panniculitis, T-cell lymphoma mimics, and lupus-associated panniculitis.

Necessary anatomical and clinical comparisons with erythema nodosum and erythema induratum.

Interpretative questions derived from the textbook descriptions—not additional unverified diagnostic criteria.

Slide 4 · Panniculitis involves the subcutaneous adipose tissue

Dermis

Subcutaneous fat

Epidermal or superficial dermal abnormalities do not define the central site of panniculitis.

SCHEMATIC

Slide 5 · Two major anatomical patterns: Septal and lobular

Dermis

Subcutaneous fat

Septal

Connective tissue between adipose lobules

Lobular

Fat lobules themselves

Slide 6 · A pattern is not yet an etiologic diagnosis

The anatomical pattern describes where inflammation is concentrated.

Vasculitis indicates inflammatory injury to blood vessels and is a separate observation.

Clinical context and possible underlying processes must still be considered.

A malignancy may produce a similar inflammatory appearance.

Slide 7 · Four questions for a panniculitis specimen

Compartment

Is inflammation mainly septal or lobular?

Vessels

Is a vasculitic process described or absent?

Injury

Are necrosis and other tissue effects identified?

Context

Is a trigger, systemic disease, or mimic known?

Slide 8 · Why sampling the subcutis matters

Surface lesion

A nodule may be the clinical clue.

Deep biopsy

Adequate subcutaneous fat is required.

Assessment

Evaluate septa, lobules, and vessels.

Robbins explicitly stresses a generous deep wedge of subcutis for diagnosing erythema nodosum.

Slide 9 · Classification axes serve different purposes

Morphologic description

Etiologic interpretation

Septal or lobular localization

Vasculitis: Present or absent

Necrosis and inflammatory cell types

Immune-associated inflammation

Factitial injury or injected substance

Lymphoma producing a mimic

Slide 10 · Why erythema nodosum is an important comparator

Erythema nodosum as the most common panniculitis.

It frequently occurs on the lower legs and typically presents subacutely.

Its defining histologic pattern is septal inflammation without vasculitis.

Slide 11 · Erythema nodosum: Clinical phenotype

Poorly defined, exquisitely tender erythematous plaques or nodules.

They may be more readily palpable than visible.

Fever and malaise can accompany the skin findings.

Slide 12 · Erythema nodosum: Associated settings

Reported associations include infections and several drugs.

Sarcoidosis, inflammatory bowel disease, and certain neoplasms are also associated.

In many patients, the specific cause remains unidentified.

Slide 13 · Erythema nodosum: Mechanism is not fully resolved

Possible antigen

Microbial or drug-related exposures

Immune response

Proposed delayed hypersensitivity

Tissue injury

Septal panniculitis

Immune complexes have been implicated in some cases; The persisting uncertainty.

Slide 14 · Erythema nodosum: Early septal morphology

Connective septa

Widening in early lesions

Early changes

Edema and fibrin exudation

Cells

Neutrophilic infiltration

This is a septal-centered pattern, not a primary lobular process.

Slide 15 · Erythema nodosum: Later changes

Cells

Lymphocytes and macrophages

Additional cells

Giant cells; Occasional eosinophils

Repair

Septal fibrosis

Histologic appearance varies with the age of a lesion.

Slide 16 · Erythema nodosum: Vasculitis is absent

The reference description explicitly states that vasculitis is not present.

This negative finding supports comparison with vasculitic panniculitides.

It must be interpreted alongside the positive septal features and the clinical presentation.

Slide 17 · Erythema induratum: Clinical clues

An uncommon panniculitis, described particularly in adolescent and menopausal females.

Typically presents as a slightly tender erythematous nodule.

The nodule commonly progresses to ulceration.

Slide 18 · Erythema induratum: Vessel-centered mechanism

Deep vessels

Necrotizing vasculitis described

Compromised flow

Vascular supply to fat lobules

Consequence

Fat necrosis and inflammation

Primary deep-vessel vasculitis as the prevailing interpretation.

Slide 19 · Erythema induratum: Characteristic morphology

Lobular granulomatous inflammation.

Zones of caseous necrosis in fat lobules.

Early necrotizing vasculitis in deep dermal and subcutaneous small- to medium-sized vessels.

Slide 20 · Erythema nodosum versus erythema induratum

Feature

Erythema nodosum

Erythema induratum

Main location

Septa

Lobules

Vasculitis

Not present

Necrotizing vasculitis

Selected findings

Edema, fibrin, evolving fibrosis

Granulomas and caseous necrosis

Typical course

Bruise-like resolution; No scar

Nodule often ulcerates

Slide 21 · The four “other” entities require different reasoning

Weber–Christian disease is described as a relapsing, nonvasculitic lobular form.

Factitial panniculitis is defined by deliberate physical or injected injury.

T-cell lymphomas can infiltrate fat and mimic panniculitis.

Systemic lupus erythematosus may cause inflammation of the subcutis.

Slide 22 · Weber–Christian disease: Source-defined identity

Also termed relapsing febrile nodular panniculitis.

Described as a rare lobular, nonvasculitic panniculitis.

Occurs in children and adults.

Slide 23 · Weber–Christian disease: Clinical distribution

Crops of erythematous plaques or nodules.

Predominant involvement of the lower extremities.

The source describes a relapsing presentation rather than a single fixed lesion.

Slide 24 · Weber–Christian disease: Episodic lesion pattern

Crops

Erythematous nodules or plaques

Recurrence

Relapsing presentation

Deep substrate

Foci of subcutaneous inflammation

“Relapsing febrile nodular panniculitis” is the textbook synonym; The excerpt gives no specific fever frequency.

Slide 25 · Weber–Christian disease is lobular, not septal

Dermis

Subcutaneous fat

The fat lobule is the central compartment in the Robbins description.

Schematic anatomy, not a patient specimen

Slide 26 · Weber–Christian disease: Absence of vasculitis

The term nonvasculitic is part of the source definition.

This contrasts with the deep necrotizing vasculitis of erythema induratum.

Anatomical location and vascular status must both be described.

Slide 27 · Weber–Christian disease: Foamy macrophage aggregates

Deep-seated inflammatory foci contain aggregated foamy macrophages.

These macrophages form part of a broader mixed inflammatory population.

A macrophage-rich lobular infiltrate is descriptive, not sufficient by itself to specify etiology.

Slide 28 · Weber–Christian disease: The associated cell mixture

Foamy macrophages coexist with lymphocytes.

Neutrophils are also included in the infiltrate.

Giant cells are part of the source description.

Slide 29 · Mixed inflammatory cells in Weber–Christian disease

Foamy macrophages

Lymphocytes

Neutrophils

Giant cells

Schematic cell mixture — not histology

These populations together in deep lobular inflammatory foci.

Slide 30 · Integrated description of Weber–Christian disease

Location

Fat lobules

Inflammation

Foamy macrophages + mixed cells

Vascular status

No vasculitis described

Combine clinical relapses and lower-extremity nodules with the histologic pattern.

Slide 31 · Weber–Christian disease versus erythema nodosum

Weber–Christian

Erythema nodosum

Relapsing crops of nodules or plaques

Lobular panniculitis

Nonvasculitic; Foamy macrophages and mixed cells

Exquisitely tender nodules

Septal panniculitis

No vasculitis; Stage-related septal fibrosis

Slide 32 · Weber–Christian disease versus erythema induratum

Weber–Christian

Erythema induratum

Fat-lobule involvement

Nonvasculitic

Mixed inflammatory infiltrate

Fat-lobule involvement

Deep necrotizing vasculitis

Granulomas and caseous necrosis

Slide 33 · Weber–Christian disease: Limit the inference

The excerpt does not supply a specific initiating cause.

No diagnostic biomarker, staging system, or laboratory cutoff is provided.

The named microscopic pattern should not be expanded into unverified molecular mechanisms.

Slide 34 · Factitial panniculitis: Definition

A secondary form of panniculitis.

Caused by self-inflicted trauma or injection of foreign or toxic material.

The causal history—not merely septal/lobular anatomy—is central to the designation.

Slide 35 · Factitial panniculitis: Trauma pathway

Exposure

Self-inflicted trauma

Anatomic target

Subcutaneous tissue

Effect

Secondary panniculitis

This is an etiologic linkage reported; No specific biopsy cell pattern is stated.

Slide 36 · Factitial panniculitis: Injection pathway

Exposure

Foreign or toxic material injected

Anatomic target

Subcutaneous tissue

Effect

Secondary inflammation

The source does not specify any particular substance or histologic signature.

Slide 37 · Factitial panniculitis: What the name tells us

Established from the excerpt

Not specified in the excerpt

The process is secondary

Trauma or injection is causal

Foreign or toxic materials may be involved

A pathognomonic cell type

A defined vasculitic status

Any laboratory confirmation threshold

Slide 38 · Avoid inferring factitial causation from morphology alone

The excerpt defines the exposure-based cause, but gives no unique morphology.

A compatible inflammatory biopsy is not itself proof of self-injury.

Establishing a causal history requires evidence beyond a nonspecific pattern.

Slide 39 · Application: Evidence for factitial panniculitis

CLINICAL / PATHOLOGY SCENARIO

A patient has nodular subcutaneous inflammation and a verified history of repeated injections of a foreign material at the same locations.

REASONING

The injection exposure supports a secondary, factitial etiology. The excerpt does not justify assigning a unique septal/lobular or cellular pattern.

Slide 40 · T-cell lymphoma may mimic panniculitis

Cells

A rare T-cell lymphoma

Distribution

Homing to subcutaneous fat lobules

Appearance

Fat injury + inflammatory changes

The source directly describes an inflammatory mimic of a malignant infiltrate.

Slide 41 · T-cell lymphoma: Preferential fat-lobule localization

Rare T-cell lymphomas with a tendency to home to fat lobules.

Their presence produces a lobule-centered process.

The appearance may overlap with non-neoplastic lobular panniculitis.

Slide 42 · T-cell lymphoma: Resulting tissue injury

T-cell infiltrate

Cells localize in fat lobules

Fat necrosis

Injury to the adipose tissue

Inflammation

Superimposed inflammatory infiltrate

The necrosis and accompanying inflammation produce the panniculitis-like mimic.

Slide 43 · Why panniculitis-like lymphoma is an important mimic

The inflammatory component can dominate the perceived pattern.

A tissue reaction that resembles panniculitis is not necessarily non-neoplastic.

The textbook explicitly identifies lymphoma as a cause of deceptive lobular inflammation.

Slide 44 · T-cell lymphoma mimic versus Weber–Christian disease

Lymphoma mimic

Weber–Christian description

Lymphomatous T cells target fat lobules

Fat necrosis develops

Superimposed inflammation imitates panniculitis

Lobular nonvasculitic panniculitis

Foamy macrophages and mixed inflammatory cells

Relapsing crops of lower-leg lesions

Slide 45 · Do not convert a mimic into a benign diagnosis

“Panniculitis-like” describes morphology, not behavior.

The differential diagnosis must preserve the possibility of neoplasia.

Robbins provides no immunophenotypic panel or molecular test in this short section.

Slide 46 · Application: The malignant mimic

CLINICAL / PATHOLOGY SCENARIO

A biopsy shows a lobule-centered process with fat necrosis and inflammation; A rare T-cell lymphoma is also being considered.

REASONING

The morphologic description alone does not exclude lymphoma. Robbins specifically warns that a fat-homing T-cell lymphoma can mimic panniculitis.

Slide 47 · Systemic lupus erythematosus and panniculitis

Systemic lupus erythematosus can occasionally be associated with subcutaneous inflammation.

The involvement may present as an associated panniculitis.

The short Robbins subsection does not give an entity-specific cellular or vascular profile.

Slide 48 · Lupus-associated panniculitis involves the subcutis

Dermis

Subcutaneous fat

SLE

Subcutaneous inflammation and panniculitis

Schematic only

Slide 49 · Lupus-associated panniculitis: Limits of this excerpt

No frequency, preferred body site, or distinctive microscopic pattern is specified.

No lupus panniculitis-specific immunohistochemical finding is listed.

The claim supported here is the clinical association with SLE and inflammation of subcutis.

Slide 50 · Why the systemic disease context matters

A subcutaneous inflammatory nodule can be considered in the setting of known SLE.

The systemic context gives an etiologic lead, not a standalone tissue diagnosis.

Robbins does not claim all panniculitis in patients with SLE is caused by lupus.

Slide 51 · Application: Panniculitis with known SLE

CLINICAL / PATHOLOGY SCENARIO

A patient with systemic lupus erythematosus develops a subcutaneous inflammatory process. Which Robbins association is relevant?

REASONING

SLE is explicitly listed as a condition that can occasionally cause subcutaneous inflammation and an associated panniculitis. No further histologic specificity is justified from the excerpt.

Slide 52 · Integrated comparison of the four named entities

Entity

Source-defined mechanism / context

Anatomy / injury

Weber–Christian

Relapsing febrile nodular form

Lobular; Nonvasculitic; Mixed cells

Factitial

Self-inflicted trauma or injection

Secondary inflammation; Pattern unspecified

T-cell lymphoma

Lymphoma homes to fat

Lobular; Necrosis; Inflammation mimic

SLE-associated

SLE with subcutis inflammation

Panniculitis; Pattern unspecified

Slide 53 · Different causes can converge on a nodule

Inflammatory form

Relapsing nonvasculitic lobular panniculitis

External injury

Trauma or injected material

Neoplastic mimic

T-cell lymphoma producing fat necrosis

Systemic disease

SLE-associated subcutaneous inflammation

Slide 54 · Morphology-first interpretation of panniculitis

Localize

Septal versus lobular

Evaluate

Vasculitis, necrosis, cell mix

Integrate

History and systemic context

Do not treat a pattern as a complete etiologic diagnosis.

Slide 55 · Case comparison: Septal versus lobular

CLINICAL / PATHOLOGY SCENARIO

Two biopsies show subcutaneous inflammation. One is septal with fibrosis; The other is lobular, nonvasculitic, and rich in foamy macrophages.

REASONING

The first better fits the later erythema nodosum pattern. The second resembles the Weber–Christian description; Location and cell composition provide discrimination.

Slide 56 · Case comparison: Vascular involvement

CLINICAL / PATHOLOGY SCENARIO

Two lobular lesions are considered. One has deep necrotizing vasculitis and caseous necrosis; The other is defined as nonvasculitic with a mixed inflammatory infiltrate.

REASONING

The first favors the Robbins description of erythema induratum; The second is compatible with the Weber–Christian description. Vasculitis is the crucial distinguishing axis.

Slide 57 · Three common interpretive pitfalls

Calling every lobular inflammatory process an idiopathic panniculitis despite a possible lymphoma mimic.

Attributing factitial causation without supporting exposure evidence.

Claiming specific lupus panniculitis histology that is not supplied by this source.

Slide 58 · Integrated knowledge check

CLINICAL / PATHOLOGY SCENARIO

A recurrent lower-extremity nodular process is lobular and nonvasculitic; Foamy macrophages, lymphocytes, neutrophils, and giant cells are described. Which source-defined entity does this match?

REASONING

Weber–Christian disease (relapsing febrile nodular panniculitis). The description combines recurrence, localization, absence of vasculitis, and the mixed-cell pattern.

Slide 59 · Clinicopathologic synthesis

Localize disease to the subcutaneous septa or lobules.

Ask whether vasculitis, fat necrosis, and distinct inflammatory populations are reported.

Recognize injury, malignancy, and systemic disease as alternative etiologic contexts.

Preserve uncertainty when the source supplies only an association or descriptive pattern.