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Case Report
 
Chylous Ascites Caused by Histoplasmosis
Keywords :
Akash Mathur1, Ankur Yadav1, Vinita Agrawal2, Manoj Jain2, Uday C Ghoshal1
Departments of 1Gastroenterology and 2Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow-226014, India.


Corresponding Author
:
Dr Uday C Ghoshal 
Email: udayghoshal@gmail.com


DOI: http://dx.doi.org/10.7869/tg.634

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48uep6bbph|2000F98CTab_Articles|Fulltext
Triglyceride rich peritoneal fluid with milky appearance has traditionally been defined as chylous ascites.1 Chylous ascites is an uncommon finding with a reported incidence of approximately 1 per 20,000 admissions at a large university-based hospital from United States of America over a two-decade period.2 While abdominal malignancy, lymphatic abnormalities, and cirrhosis account for over two-thirds of all cases in western countries, in developing countries, infections like tuberculosis are often responsible.3 Most of the reported cases of chylous ascites have been due to Mycobacterium tuberculosis infection with only a single case being reported due to fungal infection with paracoccidioidomycosis. We present here a case of chylous ascites due to histoplasmosis. 

Case Report

A 53-year female with undifferentiated connective tissue disorder and hypothyroidism presented with a 3-month history of anasarca initially responding transiently to prednisolone and diuretics. However, ascites and anasarca recurred along with breathlessness. 25-year ago, she received anti-tubercular drugs (ATD) for tubercular lymphadenitis. Examination revealed cervical lymphadenopathy, right-sided pleural effusion (confirmed on chest radiography) and ascites. Echocardiography did not reveal pericardial effusion. Investigations: Hb 14.7 gm/dL (normal 12-15.5 gm/dL), serum total protein and albumin 4.1 and 2.3 g/dL, respectively (normal 6-8.4 g/dL, and 3.5-5.5 g/dL). 24-h urinary protein: 118 mg.  Endoscopic duodenal biopsy (for possible protein-losing enteropathy) was unremarkable. Pleural and ascitic fluids were milky white, had low serum ascitic fluid albumin gradient with high triglyceride (437 mg/dL). The fluid cleared on applying the ether clearance test. A contrast-enhanced computerized tomography (CT) scan showed bilateral pleural effusion, ascites, and subcutaneous edema (Figure 1A and 1B). Cervical lymph node aspiration cytology showed necrosis, no granuloma but acid-fast bacilli (ZiehlNeelsen stain). As she did not respond to 1-mo ATD, histopathology of an excisional biopsy of the cervical lymph node was done, which showed necrosis, effaced nodal architecture and capsulated fungal elements in histiocytes suggesting histoplasmosis (Figure 1C). A rectal biopsy also showed histoplasmosis (Figure 1D). Serology for the human immunodeficiency virus (HIV) was negative. With a diagnosis of histoplasmosis, liposomal amphotericin B was started. Though she showed some initial improvement, she left against medical advice from our centre, admitted at a private hospital in New Delhi, where exploratory laparotomy with thoracic duct ligation, and repeated pleurodesis were done. However, the patient died of sepsis in post-operative period.





Discussion

We report here a case of chylous ascites in a female with underlying connective tissue disease on immunosuppression. A review of literature was done excluding the pediatric cases and cases with non-infective etiology. While dealing with a milky white appearing ascitic fluid, before making the diagnosis of chylous ascites, differentiation should be done from pseudo-chylous ascites, which is marked by low level of triglyceride in chylous fluid (<200 mg/dl).4 Clinically chylous and pseudo-chylous ascites can be differentiated by the ether clearance test. The milky white fluid is taken in two test tubes and two drops of 10% potassium hydroxide are added to both the tubes. A volume of ethyl ether equivalent to the amount of suspect fluid is added in one tube while water is added to the other. The tubes are inverted to allow mixing, and then compared. If the fluid is chyle, the chylomicrons will be dissolved by the ethyl ether and the fluid will clear. The tube to which water is added is diluted and serves as a control. Usually multiple mechanisms contribute in the pathogenesis of chylous ascites including lymph nodal fibrosis and infiltration obstructing the flow of chyle, congenital abnormalities leading to chyle leak through a fistula into peritoneum and acquired thoracic duct obstruction due to various etiologies.5
Chylous ascites is often caused by cirrhosis, malignancy and trauma or surgical injury; however, infections, though rare, are also important causes of chylous ascites especially in the setting of an immunocompromised state in the developing countries. Although most cases reported so far had underlying HIV infection causing immunosuppression but our patient was on long-term steroid therapy.  
Out of the total 23 cases from the literature, 21 were due to Mycobacterium tuberculosis and Mycobacterium avium intracellularae (MAC) infections (Table 1). Since MAC infection is usually associated with HIV infection, in all patients with chylous ascites, HIV should be ruled out. Also, MAC infection should be carefully differentiated from tuberculosis as both the organisms could demonstrate AFB positivity. Therefore, appropriate cultures from peritoneal or tissue specimen must be done in every case with underlying HIV infection.5 In conclusion, our patient highlights the need for increasing awareness among physicians about histoplasmosis, especially in immunocompromised subjects and the lesson that all acid-fast organisms are not tubercle bacillus.




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