Polyarteritis Nodosa

Necrotising vasculitis of medium-sized arteries with characteristic microaneurysm formation. Distinguished from ANCA-associated vasculitis by the absence of glomerulonephritis and ANCA negativity. Historically associated with hepatitis B, though idiopathic cases are now more common.

Key Facts

PAN is a medium-vessel vasculitis characterised by necrotising arteritis with microaneurysm formation on angiography ANCA negative and no glomerulonephritis (unlike AAV); distinguishing features from MPA Hepatitis B association: historically ~30%; now <10% due to vaccination; HBsAg-positive PAN treated with antivirals + plasma exchange Mesenteric angiography: shows microaneurysms (beaded appearance), stenoses, and occlusions – diagnostic Clinical features: systemic (fever, weight loss), skin (livedo, nodules, ulcers), peripheral neuropathy (mononeuritis multiplex, 70%), GI (mesenteric ischaemia), renal (hypertension from renal artery involvement) Treatment: prednisolone ± cyclophosphamide for severe disease (FFS ≥1); HBV-related: antivirals + plasma exchange + short steroids Rare: incidence ~2-9 per million/year; M:F slight male predominance

Overview

Key Facts

PAN is becoming rarer as hepatitis B prevalence decreases. It is distinguished from AAV by medium-vessel involvement without glomerulonephritis.

Epidemiology

  • Incidence: ~2-9 per million/year (declining)
  • Peak age: 40-60; slight male predominance
  • Declining incidence due to HBV vaccination

Pathophysiology

  • Necrotising inflammation of medium-sized arteries (segmental, at vessel bifurcations)
  • Transmural inflammation with fibrinoid necrosis → microaneurysm formation
  • Vessel occlusion → tissue ischaemia and infarction
  • NO venous involvement, NO granulomata, NO small-vessel involvement

Clinical Presentation

Constitutional (>90%)

  • Fever, malaise, weight loss, myalgia, arthralgia

Neurological (70%)

  • Mononeuritis multiplex: most common manifestation; foot drop, wrist drop
  • Peripheral neuropathy (sensorimotor)

Skin (50%)

  • Livedo reticularis, subcutaneous nodules
  • Skin ulcers, digital gangrene
  • Purpura (non-palpable, unlike small-vessel vasculitis)

GI (50%)

  • Abdominal pain (mesenteric ischaemia)
  • GI bleeding, perforation, cholecystitis
  • Mesenteric vasculitis is the most serious visceral manifestation

Renal

  • Renal artery involvement → renovascular hypertension, renal infarction
  • NO glomerulonephritis (key distinction from AAV)

Cardiac

  • Coronary arteritis → MI
  • Pericarditis, heart failure

Testicular

  • Orchitis (~20% of males): testicular pain and swelling

Red Flags

  • Abdominal pain → mesenteric ischaemia → surgical emergency if infarction
  • Severe hypertension → renal artery involvement
  • Testicular pain → consider PAN

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
MPAANCA positive, GN, small vesselANCA, urine
GPAUpper airway, ANCA positive, GNANCA
SLE vasculitisANA/dsDNA positive, multi-systemImmunology
Cholesterol emboliPost-catheterisation, blue toes, eosinophiliaBiopsy
Infective endocarditisMurmur, embolic phenomenaBlood cultures, echo

Diagnosis / Investigation

Bloods

  • ANCA: negative (essential for diagnosis)
  • HBsAg: hepatitis B screen (positive in <10% now)
  • CRP/ESR: elevated
  • FBC: anaemia, leucocytosis, thrombocytosis
  • U&Es: renal function (may show renovascular hypertension)

Angiography

  • Mesenteric or renal angiography: microaneurysms, stenoses, occlusions at vessel bifurcations (diagnostic)
  • CT angiography or MR angiography: less sensitive but non-invasive alternatives

Biopsy

  • Tissue biopsy (skin, sural nerve, muscle, testis): transmural necrotising vasculitis of medium arteries, fibrinoid necrosis
  • No granulomata, no venous involvement

Urinalysis

  • No active sediment (no GN); may show proteinuria from renovascular disease

Management

Idiopathic PAN

FFS = 0:

  • Prednisolone 1mg/kg/day alone; taper over 12-18 months

FFS ≥1 (cardiac, GI, renal, CNS):

  • Prednisolone + IV cyclophosphamide induction
  • Azathioprine maintenance

HBV-Associated PAN

  • Short course prednisolone (2-4 weeks only)
  • Antiviral therapy: entecavir or tenofovir (aim for HBV seroconversion)
  • Plasma exchange: to remove immune complexes
  • Prolonged immunosuppression avoided (risk of HBV reactivation)

Supportive

  • Antihypertensives for renovascular hypertension
  • Neuropathic pain management
  • Surgical intervention for bowel ischaemia/infarction

Referral

  • All PAN → rheumatology
  • Mesenteric ischaemia → surgery
  • HBV-positive → hepatology

Prognosis

  • 5-year survival: 80-90% with treatment
  • Untreated: ~50% mortality at 1 year (historical)
  • FFS score predicts outcome (higher = worse)
  • HBV-related PAN: antiviral-induced seroconversion can lead to complete remission
  • Relapse: less common than AAV (~10-20%)
  • Mononeuritis multiplex: may cause permanent neuropathy despite treatment

Other Relevant Information

PAN vs MPA

FeaturePANMPA
Vessel sizeMediumSmall
ANCANegativePositive (MPO 70%)
GNNoYes (crescentic)
AngiographyMicroaneurysmsNormal
HBV associationYes (historically)No
PulmonaryRareDAH common

Five-Factor Score (FFS) for PAN

FactorSignificance
CardiacPoor prognosis
GIPoor prognosis
Renal (creatinine >141)Poor prognosis
Proteinuria >1g/dayPoor prognosis
CNSPoor prognosis