Primary human immunodeficiency virus infection presenting as acute pancreatitis.

Abstract: Primary human immunodeficiency virus (HIV) infection can present in a variety of ways. It is important to recognize acute HIV infection, for personal and public health reasons. We present an unusual case of primary HIV infection manifesting as acute pancreatitis.

Key Words: pancreatitis, primary human immunodeficiency virus infection

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Although acute human immunodeficiency virus (HIV) infection may be asymptomatic, 40 to 90% of newly infacted patients will present with or recall symptoms, often suggestive of a mononucleosis-like illness. (1-3) We present a case of primary HIV infection manifesting as acute pancreatitis.

Case Report

A 40-year-old white man presented to our emergency room with a 2-day history of fevers, nausea, vomiting, and watery diarrhea. Two weeks earlier, he had been seen at another emergency room with 2 days of fever, myalgias, fatigue, and sore throat. A rapid group A streptococcal antigen test was positive, and he was subsequently treated with 10 days of penicillin. His fever and sore throat resolved, but myalgias and fatigue persisted. Two days after completing the course of penicillin, fevers recurred, associated with nausea, vomiting, diarrhea, and decreased oral intake. The patient denied any respiratory, genitourinary, cardiac, or rheumatologic symptoms. He had a distant history of hepatitis A and tested negative for HIV 2 months previously. He was taking no other medications or recreational drugs. In general, he rarely drank and had consumed no alcohol in the previous 3 weeks. He did not smoke. He was a sexually active homosexual who had been with two partners in the past several months, using condoms for anal but not oral intercourse.

Physical examination revealed a muscular man resting comfortably in bed. The patient's blood pressure was 130/80 mm Hg without orthostatic changes, his pulse was 100 to 110 beats/min and regular, his respiratory rate was 16 breaths/min, and his temperature was 39[degrees]C. There was diffuse blanching erythroderma of the neck and anterior chest; there was a small, nontender, shallow ulceration on the hard palate; there was no palpable lymphadenopathy; the lungs were clear to auscultation; and a Grade II/VI systolic murmur was heard throughout the precordium. There was no abdominal tenderness, guarding, organomegaly, or masses. There were no joint abnormalities, and the neurologic examination was unremarkable. Laboratory studies were significant for serum levels of sodium (119 mmol/L), amylase (510 U/L), lipase (6,902 U/L), aspartate aminotransferase (AST) (215 U/L), alanine aminotransferase (ALT) (606 U/L), triglycerides (100 mg/dL), and a white blood cell count of 4.1 X 1[0.sup.3]. The patient's arterial blood gas demonstrated a pH of 7.50, a PC[O.sub.2] of 25 mm Hg, a P[O.sub.2] of 79 mm Hg, and an oxygen saturation of 97%. Chest and abdominal radiographs were unremarkable; however, a computed tomographic scan of the abdomen demonstrated pancreatic prominence and multiple scattered hypodense lesions 2 cm or smaller in both hepatic lobes.

The patient was hospitalized with a diagnosis of pancreatitis of unknown cause. A right upper quadrant ultrasound examination demonstrated a normal gallbladder, with no stones, sludge, or dilated ducts. No intrahepatic lesions were noted. He was given nothing orally and was hydrated intravenously. The nausea, vomiting, and diarrhea resolved quickly, and he tolerated gradual reintroduction of oral intake. The nephrology department was consulted, and fluid restriction and salt tablet supplementation were started for euvolemic isotonic hyponatremia, deemed to be secondary to elevated antidiuretic hormone from the pancreatitis. HIV testing was negative according to enzyme-linked immunosorbent assay, but a viral load was greater than 750,000 viral particles/m[m.sup.3]. T-cell studies revealed a CD4 count of 93 cells/m[m.sup.3] (14%) and a CD4/CD8 ratio of 0.21. The patient was informed of his HIV status, and trimethoprim-sulfamethoxazole was started for prophylaxis against Pneumocystis carinii pneumonia. Antiretroviral therapy was deferred because of continued elevations in serum lipase and transaminases. Blood cultures and stool studies were negative. By hospital day 9, defervescence occurred in the patient, and 2 days later he was discharged to home. Laboratory values at discharge were as follows: sodium, 128 mmol/L; serum amylase, 512 U/L; serum lipase, 6,542 U/L (peak = 9,010 on the second hospital day); AST, 91 U/L; and ALT, 247 U/L. Before discharge, a repeat abdominal computed tomographic scan demonstrated no change in the hepatic lesions. Repeat laboratory tests performed 2 weeks after discharge showed the following: amylase, 233 U/L; lipase, 3,080 U/L; AST, 29 U/L; and ALT, 76 U/L.

Discussion

A mononucleosis-like illness has been described in primary HIV infection since 1985. (2) The most common symptoms and findings in patients with acute HIV infection are fever, fatigue, rash, pharyngitis, headache, and lymphadenopathy. Myalgias, nausea, vomiting, and diarrhea also occur frequently. (1-4) Oral ulcers are present in 10 to 30% of patients. (1,3) Symptoms typically last less than 14 days but can range from a few days to several months. (3,4) Thrombocytopenia, leukopenia, and elevated hepatic enzymes are common laboratory abnormalities. (4)

Our patient is unusual in that his primary HIV infection manifested as acute pancreatitis. In light of the evidence for acute HIV infection and the exclusion of other causes of acute pancreatitis, his pancreatitis appears to be due to primary HIV infection. Whether this represents direct invasion of the pancreas by the virus or just an association with the systemic infection is unclear. Textbook chapters and review articles on primary HIV infection do not mention acute pancreatitis, and primary HIV infection associated with acute pancreatitis has been described in only two other patients. (5) Our patient was also somewhat unusual in the extent of his CD4 cell depletion. The two previously described patients with acute HIV-associated pancreatitis both had CD4 counts greater than 600 cells/mL (5) at the time of presentation. Schacker et al (4) found only 3 (7%) of 46 of their acute seroconverters to have CD4 counts less than 300 cells/mL, with the lowest being 210 cells/mL.

There are data demonstrating that early initiation of antiretroviral treatment can preserve HIV-specific immune responses, thereby possibly improving prognosis. Early treatment may also limit the emergence of resistant virus. (1,6) In addition, from a public health perspective, patients have markedly elevated viral loads and are highly contagious during acute HIV seroconversion. Therefore, a disproportionate amount of HIV transmission occurs during primary infection. (7)

Conclusion

The potential to modulate the course of the disease and to limit further transmission and emergence of resistance should place early detection and treatment of HIV seroconversion at the forefront of physicians' minds. However, due to the myriad and varying manifestations of primary HIV infection, a high index of suspicion is required to make this diagnosis. This case illustrates the importance of inquiring about HIV risk factors and considering primary HIV infection even in unusual clinical settings.

Accepted August 13, 2003.

Copyright [c] 2004 by The Southern Medical Association

0038-4348/04/9704-0393

References

1. Kahn JO, Walker BD. Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33-39.

2. Cooper DA, Gold J, Maclean P, et al. Acute AIDS retrovirus infection: definition of a clinical illness associated with seroconversion. Lancet 1985;1:537-540.

3. Vanhems P, Allard R, Cooper DA, et al. Acute human immunodeficiency virus type 1 disease as a mononucleosis-like illness: is the diagnosis too restrictive? Clin Infect Dis 1997;24:965-970.

4. Schacker T, Collier AC, Hughes J, et al. Clinical and epidemiologic features of primary HIV infection. Ann Intern Med 1996;125:257-264.

5. Rizzardi GP, Tambussi G, Lazzarin A. Acute pancreatitis during primary HIV-1 infection. N Engl J Med 1997;336:1836-1837 (letter).

6. Hurtado R, Rosenberg ES. Before seroconversion: the clinical and scientific events of acute HIV infection and immunologic benefits of treatment. AIDS Clin Care 2001;13:1-7.

7. Cates W Jr, Chesney MA, Cohen MS. Primary HIV infection: a public health opportunity. Am J Public Health 1997;87:1928-1930.

RELATED ARTICLE: Key Points

* This case illustrates an unusual presentation of primary human immunodeficiency virus (HIV) infection: acute pancreatitis.

* Diagnosing primary HIV infection and early intervention can be of great benefit to the individual's, as well as the public's, health.

* Clinicians must maintain a high index of suspicion and inquire about HIV risk factors, even in patients with unusual presentations, to diagnose primary HIV infection.

Ryan Tyner, MD, and Glenn Turett, MD

From the Section of Infectious Diseases, Department of Medicine, St. Vincent's Catholic Medical Center, New York, NY, and New York Medical College, Valhalla, NY.

No financial support was received for this work. Neither author has any commercial or proprietary interest in anything mentioned in this article.

Reprint requests to Glenn Turett, MD, St. Vincent's Catholic Medical Center, 153 W. 11th Street, Cronin Building, Room 1003, New York, NY 10011. Email: [e-mail]