Acute Disseminated Histoplasmosis in a Recovering Alcoholic

November 1, 2004
Virendra Parikh, MD
Virendra Parikh, MD

A 48-year-old man with jaundice, nausea, vomiting, and abdominal pain was hospitalized. The patient- a recovering alcoholic- was afebrile and reported abstinence from alcohol for 6 months.

A 48-year-old man with jaundice, nausea, vomiting, and abdominal pain was hospitalized. The patient- a recovering alcoholic- was afebrile and reported abstinence from alcohol for 6 months. Laboratory analyses were significant for a serum lipase level of 3105 U/L (normal, 23 to 240 U/L); amylase, 354 U/L (normal, 30 to 130 U/L); total calcium, 7.6 mg/dL (normal, 8.4 to 10.2 mg/dL); albumin, 1.6 g/dL (normal, 3.6 to 5.0 g/dL); and total bilirubin, 10.2 mg/dL (normal, 0.2 to 1.3 mg/dL). Serum glucose levels were normal. Levels of aspartate aminotransferase and alanine aminotransferase were elevated at 273 U/L (normal, 15 to 46 U/L) and 69 U/L (normal, 11 to 66 U/L), respectively. The alkaline phosphatase level was 626 U/L (normal, 28 to 126 U/L). Results of testing for viral hepatitis, including hepatitis A, B, and C viruses, were negative. An abdominal ultrasonogram demonstrated hepatosplenomegaly and peripancreatic inflammation. A day after hospitalization, refractory hypotension, renal insufficiency, and coagulopathy developed, and the patient died. The postmortem examination demonstrated extensive peripancreatic fat necrosis and a mixed inflammatory infiltrate, without significant acute or chronic pancreatitis (A). Grocott-Gomori methenamine–silver nitrate stain highlighted simple, budding fungal yeast elements in the peripancreatic fat and, only occasionally, in macrophages (B). Cultures identified Histoplasma capsulatum. Nathan C. Birch, MD, of the University of Nebraska Medical Center, Omaha, writes that acute disseminated histoplasmosis typically occurs in immunocompromised patients, although it has been reported in those who are immunocompetent.1 Disseminated histoplasmosis may mimic miliary tuberculosis with fever, hepatosplenomegaly, lymphadenopathy, leukopenia, and jaundice. Pancreatic involvement has been reported in patients with histoplasmosis, but it is highly uncommon.2,3 In this patient, the lack of granuloma formation and paucity of macrophages in the necrotic foci suggested the possibility of HIV infection.4 An enzyme-linked immunosorbent assay of postmortem serum was positive for antibodies to HIV. The positive result was confirmed with a Western blot analysis.

References:

REFERENCES:


1.

Schlech WF 3rd, Wheat LJ, Ho JL, et al. Recurrenturban histoplasmosis, Indianapolis, Indiana,1980-1981.

Am J Epidemiol.

1983;118:301-312.

2.

Farber S, Craig JM. Clinical pathological conference.

J Pediatr.

1957;60:77-90.

3.

Pinkerton H, Iverson L. Histoplasmosis: threefatal cases with disseminated sarcoid-like lesions.

Arch Intern Med.

1952;90:456-467.

4.

Research News. HIV’s other immune system targets:macrophages.

Science.

1997;24:1464.