A Giant Pancreatic Pseudocyst in a Patient with HIV Infection

Abstract

This article describes the first case of a giant pancreatic pseudocyst in a 48-year-old man with HIV infection under combination antiretroviral therapy. The patient presented with an abdominal mass involving the epigastrium, left hypochondrium, and left flank. An enhanced abdominal computed tomography (CT) scan showed a well-defined cyst of 21 cm in diameter, with a liquid content that dislocated adjacent viscera. Microbiological and cytological tests on fluid were negative, confirming diagnosis of pancreatic pseudocyst. The CT-guided percutaneous drainage was carried out and the patient’s clinical condition gradually improved.

Introduction

With the drop in AIDS-related diseases, HIV-infected concerns are growing about diagnosis and treatment of non-AIDS-related morbidity due to the patients’ higher risk of complications and complex regimen of drugs. To our knowledge, this article presents the first case of a giant pseudocyst in a patient with AIDS. A giant pancreatic pseudocyst is defined as a 10-cm or more accumulation of pancreatic fluid enclosed within a well-defined capsule, persisting for more than 4 weeks. It usually follows an episode of acute pancreatitis. ¹

Case Report

A 48-year-old man with HIV infection (stage Centers for Disease Control-C3) and depression was admitted to the Infectious Diseases Unit in November 2011 because of an abdominal mass in the epigastrium and left hypochondrium. He had been suffering from fatigue, abdominal discomfort and distension, anorexia, early satiety, lack of appetite, and weight loss for 1 month. He had been on second-line combination antiretroviral therapy (cART), with darunavir/ritonavir (RTV) and tenofovir (TDF)/emtricitabine until January 2011, when he developed hypophosphatemic osteomalacia secondary to proximal renal tubulopathy, thus replacing TDF/emtricitabine with abacavir (ABC)/lamivudine (3TC). He was also on oral alendronic acid, cholecalciferol, valproic acid, levetiracetam, escitalopram, and fenofibrate. At the last checkup, HIV-1 RNA was undetectable, and the CD4 count was 471 cells per mL; laboratory tests showed increased amylase (242 IU/L) and lipase (113 IU/L) levels. The patient was known since 6 years when advanced HIV disease was diagnosed and first cART was started with lopinavir/ritonavir (LPV/r) and zidovudine (ZDV)/3TC. His past medical history was negative for abdominal pain, alcohol abuse, or gallstones. A low level of hyperamylasemia (103-210 IU/L) associated with high triglycerides (189-610 mg/dL) were present when HIV infection was identified and subsequently during follow-up. Lipase level was normal at HIV diagnosis and slightly increased in the last 3 years of therapy (75-100 IU/L). An abdominal ultrasound scan performed on March 2010 was normal. At hospital admission (November 2011), an abdominal computed tomography (CT) scan showed pancreatic calcifications consistent with a diagnosis of chronic pancreatitis and a well-defined pancreatic cyst (21 cm diameter), with liquid content, displacing adjacent viscera (Figure 1A and B). The esophagogastroduodenoscopy was negative. Calcium level (8.7 mg/dL), intact parathyroid hormone (42.1 ng/L), and 25-hydroxyvitamin D (31 ng/mL) were in the normal range and thus hyperparathyreoidism was excluded. The CT-guided percutaneous drainage was carried out (Figure 2). Fluid microbiology and cytology were negative for bacteria, fungi, mycobacteria, and atypical cells; biochemical analysis and tumor marker in cyst fluid and in serum were carcinoembryonic antigen (CEA): 21.7/3.9 ng/mL, carbohydrate antigen (CA) 19-9: 1900/15.8 U/mL, and amylase: 5213/395 U/L. These data supported the diagnosis of a pancreatic pseudocyst.

Figure 1.

A, Enhanced computed tomography (CT) before drainage (transverse axial section) showed a well-demarcated pancreatic cyst (diameter of 21 cm), with liquid contents, that displaced stomach, left kidney, spleen, and aorta. B, Coronal maximum intensity projection reconstruction frontal section of enhanced CT before drainage. Pancreatic pseudocyst displaced aorta considerably.

Figure 2.

A computed tomography-guided percutaneous drainage with a pigtail of 10F.

Seven days after drainage, the catheter was removed. There were no complications and the patient was well at the 2-month checkup, during which an abdominal CT showed that the pancreatic cyst had disappeared (Figure 3A and B). To our knowledge, a simple giant pseudocyst had never been described in a patient with AIDS.

Figure 3.

A, Enhanced computed tomography (CT) after drainage (transverse axial section) showed the resolution of pancreatic cyst. B, Coronal maximum intensity projection reconstruction frontal section of enhanced CT after drainage. Pancreatic pseudocyst is absent.

Discussion

In the real world, HIV-infected patients undergo accelerated biological aging. ² They are frequently affected by difficult-to-treat comorbidities and take complex regimen of drugs. All these factors can contribute to severe atypical or new diseases.

Although the annual incidence of acute pancreatitis in the non-HIV-infected general population is relatively low, it is considerably high in HIV population (0.61 per 100 person-years), ³ with the main factors being alcohol use, gallstones, high triglyceride levels, and drugs. Drug-induced acute pancreatitis appears to be relatively rare but may be underestimated, perhaps because it is not always recognized and the diagnosis is difficult to establish. ⁴ Drug etiology is even more difficult to establish for chronic pancreatitis. Our patient had long been treated with many drugs, such as valproic acid, and fenofibrates that are known to induce pancreatic disorders. ⁵ In addition, although specific information is missing, TDF appeared to have induced hypophosphatemic osteomalacia secondary to proximal renal tubulopathy. One might hypothesize that the treatment with oral alendronic acid and cholecalciferol was implicated in pancreatic calcifications in this patient. In any case, the role of these drugs was not proved.

In the differential diagnosis of pancreatic cysts, the first step is to identify them as neoplastic or not. A pancreatic pseudocyst is a cystic cavity surrounded by inflammatory tissue, containing fluid that is rich in pancreatic enzymes and is often blood-tinged or frankly hemorrhagic. The cavity wall is usually fibrous and lacks an epithelial lining, making it different from a true pancreatic cyst. The most frequent cystic lesion of the pancreas, the pseudocyst, may be single or multiple and is usually related to pancreatic trauma or an acute or chronic inflammation. ⁶

Symptoms of pancreatic pseudocysts are related to the underlying pancreatic disease (eg, chronic pancreatitis) or, as in the present case, the dislocation effects of the pseudocyst mass on adjacent viscera (eg, gastric compression and Wirsung duct obstruction). The most frequent symptoms are pain, especially epigastric pain; early satisfaction; and dyspeptic disease. Although the majority of acute pancreatic pseudocysts resolve spontaneously, in some cases, it may hemorrhage, rupture, develop into fistulas, or become infected. Treatment is mandatory when the pancreatic pseudocyst is >6 cm in size and persists for more than 6 weeks. ⁴ Management options include conservative, percutaneous, endoscopic, and surgical treatment ⁷ but optimal management in HIV patients has not yet been established and the role of different drugs should be investigated.

In our patient, conservative management was not possible as the mass had major effects on adjacent viscera. Surgery would have led to a longer hospitalization and a higher risk of infection. Percutaneous access helped in the diagnosis and proved to be the best choice therapy for this giant pancreatic pseudocyst in a patient with AIDS.