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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Medicine+(Baltimore)
2014 ; 93
(24
): 405-413
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Single-organ gallbladder vasculitis: characterization and distinction from
systemic vasculitis involving the gallbladder An analysis of 61 patients
#MMPMID25500710
Hernández-Rodríguez J
; Tan CD
; Rodríguez ER
; Hoffman GS
Medicine (Baltimore)
2014[Nov]; 93
(24
): 405-413
PMID25500710
show ga
Systemic vasculitis (SV) involving abdominal structures usually has a poor
prognosis. Gallbladder vasculitis (GV) has been reported as part of SV (GB-SV)
and focal single-organ vasculitis (GB-SOV). We analyzed clinical and histologic
characteristics of patients with GV to identify features that differentiate
GB-SOV from the systemic forms of GV. To identify affected patients with GV we
used pathology databases from our institution and an English-language PubMed
search. Clinical manifestations, laboratory and histologic features, treatment
administered, and outcomes were recorded. Patients were divided in 2 groups,
GB-SOV and GB-SV. As in previous studies of single-organ vasculitis, GB-SOV was
only considered to be a sustainable diagnosis if disease beyond the gallbladder
was not apparent after a follow-up period of at least 6 months. Sixty-one
well-characterized patients with GV were included (6 from our institution). There
was no significant sex bias (32 female patients, 29 male). Median age was 52
years (range, 18-94 yr). GB-SOV was found in 20 (33%) and GB-SV in 41 (67%)
patients. No differences were observed in age, sex frequency, or duration of
gallbladder symptoms between groups. Past episodes of recurrent right-upper
quadrant or abdominal pain and lithiasic cholecystitis were more frequent in
GB-SOV patients, whereas acalculous cholecystitis occurred more often in GB-SV.
In GB-SV, gallbladder-related symptoms occurred more often concomitantly with or
after the systemic features, but they sometimes appeared before SV was fully
developed (13.5%). Constitutional and musculoskeletal symptoms were reported only
in GB-SV patients. Compared to GB-SOV, GB-SV patients presented more often with
fever (62.5% vs 20%; p?=?0.003) and exhibited higher erythrocyte sedimentation
rate levels (80?±?28 vs 37?±?25?mm/h, respectively; p?=?0.006). All GB-SV
patients required glucocorticoids and 50% of them also received cytotoxic agents.
Mortality in GB-SV was higher than in GB-SOV (35.5% vs 10%; p?=?0.05).
Nongranulomatous inflammation with fibrinoid necrosis of medium-sized vessels
occurred equally in both groups (>90%). Forms of SV affecting the gallbladder
included polyarteritis nodosa (n?=?10), hepatitis B virus-associated vasculitis
(n?=?8), cryoglobulinemic (essential or hepatitis C virus-associated) vasculitis
(n?=?6), vasculitis associated with autoimmune diseases (n?=?6), microscopic
polyangiitis (n?=?4), eosinophilic granulomatosis with polyangiitis
(Churg-Strauss) (n?=?4), IgA vasculitis (Henoch-Schönlein) (n?=?2), and giant
cell arteritis (n?=?1).GV is uncommon. Its histology most often consists of a
nongranulomatous necrotizing vasculitis affecting medium-sized vessels. GB-SOV is
usually discovered after routine cholecystectomy performed because of the
presence of local symptoms, gallstone-associated cholecystitis, and contrary to
GB-SV, GB-SOV is usually not associated with systemic symptoms. Acute phase
reactants and surrogate markers of autoimmunity are usually normal or negative in
GB-SOV. GB-SOV does not require systemic antiinflammatory or immunosuppressive
therapy; surgery is adequate to achieve cure. GB-SV always warrants
immunosuppressant therapy and is associated with high mortality. The finding of
GV may precede the generalized manifestations of SV. Therefore, once GV is
discovered, studies to determine disease extent and a vigilant follow-up are
mandatory.