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Erythema induratum (nodular vasculitis)

Erythema induratum (nodular vasculitis)
Literature review current through: Jan 2024.
This topic last updated: Feb 10, 2022.

INTRODUCTION — Erythema induratum (EI) is an uncommon inflammatory disorder with alterations centered upon the subcutaneous fat tissue (panniculitis). The term "EI" was first proposed by Ernest Bazin in the mid-19th century, who recognized the association of the distinctive clinical and histologic changes with tuberculosis (TB) [1,2]. Subsequently, it was recognized that not all cases are associated with TB.

The three clinical subsets of EI are:

TB-associated EI

EI associated with other diseases or drugs

Idiopathic EI

EI most often occurs in adult females and is characterized by erythematous, tender, variably ulcerated subcutaneous nodules, classically arising on the posterior lower legs (picture 1A-D). Histologically, EI is a mostly lobular panniculitis associated with necrosis and a mixed granulomatous infiltrate with vasculitis (picture 2).

Treatment of the associated underlying disease can lead to resolution of EI and is the mainstay of treatment. Efficacy data for other treatments are limited.

The clinical features, diagnosis, and management of EI are reviewed in this topic review (algorithm 1). Other cutaneous disorders associated with TB and other forms of panniculitis are reviewed separately. (See "Cutaneous manifestations of tuberculosis" and "Panniculitis: Recognition and diagnosis".)

TERMINOLOGY — EI is closely related to or synonymous with "nodular vasculitis" (NV). Usage of the terms EI and NV varies worldwide, with many authorities using these terms interchangeably. Historically, EI has been regarded as the subset of NV that is associated with tuberculosis (TB). Some clinicians, including the authors who first coined the term NV in 1945, reserve the term EI for TB-associated cases and NV for non-TB-associated cases of panniculitis exhibiting identical histopathologic features [3]. TB-associated cases are classified as one of the true forms of "tuberculid." (See "Cutaneous manifestations of tuberculosis", section on 'Tuberculids'.)

The term EI itself is also subject to variation. Historically, "EI of Bazin" has been used to refer to TB-associated EI, in contrast to "EI of Whitfield," which recognizes non-TB-associated cases.

For the purposes of this topic review, the terms EI and NV will be regarded as interchangeable and without requirement to be used in conjunction with the names Bazin or Whitfield.

EPIDEMIOLOGY — EI is uncommon, although incidence and prevalence are unknown. The primary demographic for EI is adult females [4]. Both tuberculosis (TB)-associated and non-TB-associated variants of EI appear to be more common in females than in males. EI may be the most common cutaneous manifestation of TB in Brazil, Japan, mainland China, and Hong Kong [5-7].

The age range for EI is wide. In one of the largest series (86 patients with EI), the median age was 56 years (range 23 to 81 years) [8]. In a separate series of 32 patients with TB-associated EI, the mean age of presentation was 37 years (range 13 to 66 years) [9]. In addition, there are case reports of TB-associated EI in young children [10-12].

Data are insufficient for definitive conclusions about racial or ethnic predilections in EI, but cases have been reported from North America [4,13], Central America [6], South America [14], Europe [8], Asia [9], the Middle East [15,16], Africa [17], and Australia [18].

PATHOGENESIS — The pathogenesis of EI is poorly understood. Similar to other forms of noninfectious panniculitis, EI is regarded as an immune-mediated hypersensitivity reaction. In EI, the histologic reaction pattern is specifically characterized by a mixed granulomatous inflammatory process triggered by Mycobacterium tuberculosis or other antigens that induce similar or identical clinicopathologic features (see 'Associated disorders' below). In addition, given that vasculitis is a histologic hallmark, endothelial antigens may be the target of cell-mediated cytotoxicity. Based upon these concepts, EI has been characterized as having features of both type III (immune-complex vasculitis) and type IV (delayed) hypersensitivity. (See 'Histopathology' below.)

CLINICAL PRESENTATION — EI is typically confined to the lower legs, classically the posterior leg (calf) and/or lateral leg, and may be unilateral or bilateral (picture 1A-D). Atypical distributions can occur, including a predilection for the shins as described in a series of 25 patients in Singapore [19]. In addition, EI occasionally arises on the thighs or upper extremities, and rare truncal, facial, or disseminated involvement has been reported [20,21].

The earliest clinical manifestation of EI is one or more erythematous subcutaneous nodule(s). Individual lesions are typically no greater than 2 cm in diameter [4,22]. Nodules may or may not be scaly. Tenderness typically is present. Pain is variable but usually not excruciating, if present.

With sufficient severity or disease progression, ulceration is characteristic. Healed lesions may leave scars and, rarely, lipoatrophy [23].

Patients with EI typically lack constitutional symptoms with the exception of those related to underlying disease. Associated peripheral neuropathy has been reported [24,25].

ASSOCIATED DISORDERS — EI may be subclassified into three clinical subsets:

Tuberculosis (TB)-associated EI

EI associated with other diseases or drugs

Idiopathic EI

These subsets cannot be distinguished by clinical morphology or histopathology.

Based upon published reports, latent or active TB is the most commonly reported identifiable cause of EI. In a review of 26 patients diagnosed with EI between 1966 and 1986 in England, all patients had a positive tuberculin skin test [4]. In a Spanish retrospective study that included 65 patients given a histologic diagnosis of EI between 1976 and 1994, 89 percent had a positive tuberculin skin test [26]. A Singaporean retrospective study of 25 patients diagnosed with EI between 1989 and 1995 found active pulmonary tuberculosis in 28 percent [19].

EI may present in association with other forms of tuberculid, most commonly with papulonecrotic tuberculid [27-29]. (See "Cutaneous manifestations of tuberculosis", section on 'Tuberculids'.)

Disease associations other than TB are much less common but have been documented in case reports. Examples include:

Superficial thrombophlebitis [8,30]

Autoimmune diseases (systemic lupus erythematosus [31], rheumatoid arthritis [8,30], hypothyroidism [8,30], Addison disease [32]) and Takayasu arteritis [33]

Inflammatory bowel disease (Crohn disease [34], ulcerative colitis [35]), including development of EI in the setting of vedolizumab therapy for Crohn disease [36,37]

Hematologic disorders (chronic lymphocytic leukemia, antiphospholipid antibodies [38])

Lung cancer [39]

Viral infections (hepatitis C virus [40], hepatitis C virus in association with red fingers syndrome [41], hepatitis B virus [8])

Bacterial infections (Nocardia, Pseudomonas, Fusarium, Chlamydophila pneumoniae [42])

Mycobacterial infections (Mycobacterium chelonae [43], Mycobacterium avium [44], and Mycobacterium monacense [45])

Medication associations described in case reports include etanercept [46], infliximab [47], intravesical Bacillus Calmette-Guérin immunotherapy [48], and propylthiouracil [49]. In addition, EI has occurred in association with new-onset tuberculous lymphadenitis in a patient treated with certolizumab pegol for rheumatoid arthritis [50]. Recurrence of EI during chemotherapy for breast cancer also is reported [51].

A minority of cases of EI have no plausible cause or association (idiopathic EI).

HISTOPATHOLOGY — Typical pathology findings in EI include panniculitis and vasculitis (picture 2):

Panniculitis – At scanning magnification, the inflammatory infiltrate exhibits a predominantly lobular pattern. The inflammatory infiltrate is "mixed," typically containing lymphocytes, plasma cells, histiocytes forming granulomas, neutrophils, and eosinophils. Extravascular foci of fibrinoid necrosis are typically present, although these may represent nondiagnostic sections through centrilobular venules affected and possibly obscured by venulitis (vasculitis involving venules). Neutrophil-rich granulomas typify early lesions, whereas histiocytes may predominate in later stages [52].

Vasculitis – The vasculitis may involve a variety of vessel types including arteries, arterioles, veins, and venules in the subcutaneous septa and/or lobules. In the largest series of histologically confirmed cases of EI (101 biopsies from 86 patients), small centrilobular venules were most commonly involved, with less frequent involvement of septal veins and/or septal arteries [8]. Vasculitis is not always seen in specimens of EI. In the series, vasculitis was not identified in 10 percent of biopsies [8].

The associated infiltrate exhibits leukocytoclasis and may appear neutrophilic or lymphocytic. The appearance of lymphocytic vasculitis in EI has been interpreted as a late stage of a primarily neutrophilic vasculitis. Granulomatous vasculitis, a histologic hallmark of nodular tuberculid that also occurs in EI, may represent an even later stage of the vasculitic process [53,54].

Ulceration in EI is attributed to ischemic necrosis secondary to occluding vasculitis. The presence of ulceration does not clearly correlate with a particular type of vessel involvement.

DIAGNOSIS — The diagnosis of EI is made based upon a composite assessment of the clinical and skin biopsy findings combined with negative test results for lesional infection (algorithm 1).

In sum, key features that support a diagnosis of EI are:

Erythematous, tender nodules on the lower legs, particularly the calf (with or without ulceration)

Skin biopsy demonstrating:

Predominantly lobular panniculitis

Mixed inflammatory infiltrate containing lymphocytes, plasma cells, histiocytes forming granulomas, neutrophils, and eosinophils

Vasculitis (examination of multiple sections may be required)

Negative stains and cultures for bacteria, mycobacteria, and fungi

A diagnosis of EI should be followed by an evaluation for tuberculosis. (See 'Additional studies' below.)

Physical examination — The physical examination is focused on the lower extremities since involvement of other sites is uncommon. Involvement of other body sites does not rule out EI but should prompt consideration of other disorders. (See 'Clinical presentation' above.)

Biopsy — A biopsy is required to confirm the diagnosis. The biopsy type can be critical. Small biopsies or superficial punch biopsies are more likely to render the specimen nondiagnostic or misinterpreted. Ideally, an incisional biopsy or full-thickness punch biopsy should be taken from lesional skin. (See "Skin biopsy techniques", section on 'Punch biopsy'.)

In addition, stains and cultures for bacteria, mycobacteria, and fungi should be obtained. By definition, lesional histochemical stains and lesional cultures are negative for pathogens in EI.

ADDITIONAL STUDIES — Patients with EI should be evaluated for underlying disease, particularly tuberculosis (TB). An appropriate work-up for patients without a known history of TB includes:

Tuberculin skin test or interferon gamma release assay [13,55,56]

Review of systems

Chest radiograph

If available, polymerase chain reaction (PCR) for M. tuberculosis from lesional formalin-fixed tissue can be used to support an association of EI with TB [13]. However, the diagnostic sensitivity is variable and likely affected by technical factors as well as the prevalence of EI and TB in the population. In a retrospective study from the United States, PCR-based testing of biopsy specimens of EI for TB was positive in 5 of 20 patients (25 percent) with positive tuberculin skin tests and characteristic lesions that responded to antituberculous treatment [57]. In a larger retrospective study from Spain, PCR was positive for evidence of TB in 77 percent of 72 specimens from 65 patients with EI (including 57 with positive tuberculin skin tests) [26]. In this series, there was a correlation between a positive test and the degree of tissue necrosis but not with any other histopathologic attributes [26]. In another study, multiplex PCR followed by nested PCR identified TB in tissue specimens from 8 of 10 patients considered to have TB-associated EI in Mexico City [58].

Reasonable additional initial tests for other associated diseases in patients without evidence of TB include [2]:

Complete blood count with differential

Erythrocyte sedimentation rate

Liver function tests

Hepatitis C virus serology

The need for additional tests is guided by the findings on the review of symptoms. (See 'Associated disorders' above.)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis for EI includes other forms of panniculitis that typically affect the lower extremities:

Erythema nodosum – Erythema nodosum (EN) is the most common cause of primary panniculitis. Patients with EN typically present with nonulcerating bilateral nodules on the anterior legs (shins) rather than posterior legs. Considering the higher incidence of EN, nonclassic cases of EI are not infrequently clinically misdiagnosed as EN [59].

Pathologic findings that support EN include a mostly septal pattern of subcutaneous inflammation. Histiocytic aggregates surrounding clefts (Miescher's radial granuloma) are characteristic of EN. Similar to EI, EN is a reaction pattern with numerous possible disease associations including some that overlap with those of EI, including tuberculosis (TB) and possibly hepatitis C. (See "Erythema nodosum".)

Infectious (infective) panniculitis – EI is characterized by neutrophilic granulomatous infiltrates, which is also the typical host response against most pathogens, particularly fungi, mycobacteria, and parasites. Since histochemical stains have limited sensitivity and negative stains do not exclude infection, lesional cultures and/or ancillary molecular diagnostic testing are required if infection is a clinical concern. For example, a case of panniculitis secondary to Mycobacterium massiliense was reported to mimic EI [60]. (See "Panniculitis: Recognition and diagnosis", section on 'Infection'.)

Cutaneous polyarteritis nodosa – Cutaneous polyarteritis nodosa (PAN) is characterized by tender, erythematous, purpuric macules, papules, and nodules, often occurring in a livedoid pattern on the lower extremities. Histologically, the changes in PAN are stereotypically centered upon small subcutaneous arteries, whereas prominent, extravascular, lobular subcutaneous inflammation affecting a wider range of vessel types is typical of EI. (See "Cutaneous polyarteritis nodosa".)

Traumatic panniculitis – Similar to EI and infectious panniculitis, traumatic panniculitis presents as one or a few tender or asymptomatic nodule(s), usually on the lower extremities. Any site can be traumatized, the anterior leg (shin) being typical. Factitial panniculitis is regarded as a subset of traumatic panniculitis. Histologically, traumatic panniculitis shows prominent fat necrosis with lipophagic fat necrosis and lipomembranous fat necrosis predominating; vasculitis is not a feature.

TREATMENT — EI is not a life-threatening disorder; however, treatment is usually given because EI can be painful and disfiguring (algorithm 1). In addition, untreated underlying diseases such as tuberculosis (TB) can cause death or significant morbidity.

First-line treatment — EI can be cured if the underlying cause is identified and successfully treated (algorithm 1). Patients with evidence for latent or active TB should receive standard treatment for TB in accordance with current guidelines. As with other tuberculids, TB-associated EI generally responds to anti-TB therapy. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection" and "Treatment of tuberculosis infection (latent tuberculosis) in nonpregnant adults without HIV infection".)

In addition, nonsteroidal anti-inflammatory drugs, rest, elevation, and compression can be helpful for improving symptoms [2,30].

If an underlying disease cannot be identified and treated, management of EI can be challenging. (See 'Other interventions' below.)

Other interventions — Limited data from case reports and case series suggest that other interventions may be useful for idiopathic EI or EI that cannot be cured through treatment of an underlying disease. Oral potassium iodide is our preferred first-line treatment for these patients [61] and may result in remission [62-64]. In one series, 16 of 17 patients with non-TB-associated EI responded to potassium iodide (360 to 900 mg per day) [62]. Patients were generally treated for three to four weeks because shorter courses seemed to promote relapse. Decreased pain and swelling occurred within two days, and complete resolution occurred within four weeks. In another series, 7 of 10 patients with EI achieved resolution of symptoms within 24 hours and complete resolution of lesions within two weeks with potassium iodide (300 mg three times per day) [64]. In both series, recurrences responded to retreatment.

Treatment with potassium iodide is generally well tolerated. Long-term treatment is associated with risk for hypothyroidism. Other potential side effects of potassium iodide include gastrointestinal symptoms, salivary gland enlargement, and potassium toxicity. Given that a rapid response is expected, if there is no response within two to three weeks, treatment can be discontinued [64].

Other treatments have been suggested, including systemic glucocorticoids (provided infection has been ruled out) [30], clofazimine [65] or colchicine [18] as a glucocorticoid-sparing agent, gold salts [66], mycophenolate mofetil [67], and topical anti-TB therapy [68]. However, evidence for benefit is limited to case reports. The efficacy of local therapies, such as topical or intralesional corticosteroids, is unclear.

Although some authors have suggested treatment with antituberculous drugs even in the absence of evidence for TB, given the potential side effects of antituberculous treatment, this is generally reserved for patients with evidence of latent or active TB [2].

PROGNOSIS — Prognostic data have not been reported. As a reaction pattern, EI is a heterogeneous entity with a correspondingly variable clinical course. Successful treatment of an associated underlying disease usually leads to resolution, although relapsing disease in patients with TB-associated EI has been reported [5]. Idiopathic EI can progress for months to years but may eventually stabilize or remit in association with treatment such as potassium iodide.

SUMMARY AND RECOMMENDATIONS

Erythema induratum (EI) is an uncommon form of panniculitis that may occur in association with tuberculosis (most common), other diseases or drugs, or as an idiopathic condition. EI is regarded as an immune-mediated hypersensitivity reaction. (See 'Pathogenesis' above and 'Associated disorders' above.)

EI most frequently occurs in adult females but may also occur in males and children. (See 'Epidemiology' above.)

The most common clinical presentation of EI is single or multiple erythematous nodule(s) on the posterior or lateral lower legs (picture 1A-D). Thigh and upper extremity involvement occurs occasionally. Truncal, facial, or disseminated EI is rare. Ulceration of nodules is common. (See 'Clinical presentation' above.)

The diagnosis of EI is made based upon the presence of consistent clinical and histologic findings. Skin biopsies demonstrate a predominantly lobular panniculitis with a mixed and granulomatous inflammatory infiltrate with vasculitis (picture 2). Multiple sections or multiple specimens may be required to identify vasculitis. (See 'Histopathology' above and 'Diagnosis' above.)

Given the strong association of EI with tuberculosis, all patients with EI should be evaluated for tuberculosis. (See 'Additional studies' above.)

First-line treatment for nonidiopathic EI is treatment of the underlying associated disease (algorithm 1). Nonsteroidal anti-inflammatory drugs, rest, elevation, and compression may aid with symptomatic improvement. (See 'First-line treatment' above.)

When an underlying disease cannot be identified and treated, treatment may be challenging. Data on therapeutic options are limited. We suggest a trial of oral potassium iodide for these patients (Grade 2C). Other treatments that may be beneficial include systemic glucocorticoids, clofazimine, colchicine, gold salts, and mycophenolate mofetil. (See 'Other interventions' above.)

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Topic 109264 Version 4.0

References

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