We report two cases who presented with gall stone disease, which on histopathological evaluation was diagnosed as eosinophilic cholecystitis. Retrospective analysis of their case histories and investigation did not reveal any known etiology. These cases are being reported because of their rarity and to highlight the importance of complete workup to rule out other associated disorders that may be a manifestation of a more severe disease.
Case 1
A 30-year-old female presented with colicky pain off and
on for 2 years. Her investigations revealed hemoglobin
11gm/dl, total leucocyte count 4.5x103 /mm3, differential
leucocyte count neutrophils 55/mm3, lymphocyte 34/mm3,
eosinophils 8/mm3, monocytes 3/mm3, platelets 1.9 lac/
mm3, absolute eosinophil count 350/ mm3, blood sugar:
98 gm/dl, alkaline phosphatase/ aspartate transaminase/alanine transaminase 166/74/35 IU/ml, blood urea 23 mg/
dl, serum creatinine 0.5 ng/dl, and serum amylase 45 IU/
ml.
Ultrasound was suggestive of chronic cholecystitis. A clinical diagnosis of chronic cholecystitis was made. On gross examination, the gall bladder was 6 cm in length with a wall thickness of 2 mm. On opening, multiple mixed stones were present. Microscopically, in addition to chronic cholecystitis (Figure 1) there was a prominent eosinophilic infiltration (Figure 2) and a diagnosis of eosinophilic cholecystitis with cholelithiasis and focal pyloric metaplasia was reported.
Figure 1: Gall bladder wall showing features of chronic cholecystitis (H&E; x100).
Figure 2: Gall bladder wall showing eosinophilic infiltration (H&E; x400).
Case 2
A 22-year-old female presented with pain in the right
hypochondrium for the last 3 months. Her investigations
revealed hemoglobin 10.6 gm/dl, total leucocyte count
5.7x103/mm3, differential leucocyte count neutrophils 51/mm3, lymphocyte 33/mm3, eosinophils 10/mm3, monocyte
6/mm3, platelets 2.62 lac/mm3, absolute eosinophilic count
550/mm3, blood sugar: 105 gm/dl, alkaline phosphatase/
aspartate transaminase/ alanine transaminase 203/136/63
IU/ml, blood urea 12 mg/dl, serum creatinine 0.8 ng/dl,
and serum amylase 65 IU/ml.
Sonography was suggestive of acute cholecystitis with cholelithiasis. A clinical diagnosis of a possible acute pancreatitis or acute cholecystitis was made. On gross examination, the gall bladder was 7.8 cm in length with a wall thickness of 1-2 mm and multiple mixed stones were also observed. Thus a histopathological diagnosis of eosinophilic cholecystitis with cholelithiasis was made.
Dabbs et al.[1] reviewed 217 consecutive cholecystectomy specimens and found that a large number of eosinophils in the inflammatory infiltrate were three times more common in patients with acalculous cholelithiasis. In contrast, both of our patients had cholelithiasis.
Although there are quite few case reports describing EC[5,6,7] the etiopathogenesis of disease still remains obscure. The proposed etiologies include local allergic reaction to substances released at the foci of inflammation, local diathesis involving gall stones, acalculous cholecystitis, parasites, hypereosinophilic syndrome (HES), eosinophilic gastroenteritis and eosinophilia myalgia (EM) syndrome. Certain drugs such as cephalosporins and herbal medicines have been implicated in EC[5,6]. A subset of idiopathic EC has also been reported, after excluding the above etiologies. However we did not find any possible etiology even after a thorough workup in both of our cases.
Histopathology remains the mainstay for diagnosis of eosinophilic cholecystitis as there is no specific clinical presentation. The treatment of choice for eosinophilic cholecystitis is cholecystectomy. However, steroids may be used as an adjuvant therapy if the disorder is associated with gastroenteritis[7].
The importance of reporting EC lies in the fact that it may be the presenting feature of many conditions such as HES and EM syndrome that are much more severe than cholecystitis itself. I cholecystitis is the only presenting complaint and a post-operative diagnosis of EC is made on histopathology, the patient must therefore be evaluated meticulously to rule out other associated diseases. Treatment may warrant more than a simple cholecystectomy if an underlying causative factor is discovered.
1) Dabbs DJ. Eosinophilic and lymphoeosinophilic cholecystitis.
Am J Surg Pathol. 1993;17:497-501. [ Özet ]
2) Albot G, Poilleux, Olivier C, Libaude H, Cascarigny P. Les
cholecystites a eosinophils. Presse Med. 1949;39:558-9.
3) Sanchez-Pobre P, Lopez-Rios MF, Colina F, Yela C, Manzano M,
Rodriguez S, Martín A, Casís B, Garfia C, Castellano G, Solís-
Herruzo JA. Eosinophilic cholecystitis: An infrequent cause of
cholecystectomy. Gastroenterol Hepatol. 1997;20:21-3. [ Özet ]
4) Mohan H, Punia RP, Dhawan SB, Ahal S, Sekhon MS. Morphological
Spectrum of gall stone disease in 1100 cholecystectomies
in North India. Indian J Surg. 2005;67:140-2.
5) Shakov R, Simoni G, Villacin A, Baddoura W. Eosinophilic
Cholecystitis with a review of the literature. Ann Clin Lab Sci.
2007;37:182-5. [ Özet ]
6) Singh DK, Shankar R, Gondal R, Malhotra V, Mishra P. Idiopathic
eosinophilic cholecystitis with cholelithiasis: A case report and
review of literature. Internet Journal of Surgery. 2008;16:2.
7) Punia RP, Arya S, Jain P, Bal A, Mohan H. Eosinophilic and
Lympho-eosinophilic cholecystitis. Indian J Gastroenterol. 2003;
22:153-4. [ Özet ]