Gastroduodenal involvement in disseminated strongyloidiasis.

Here, we report the case of a 57-year-old Peruvian man on long-term corticosteroid therapy for a drug allergy and proton pump inhibitors for chronic dyspepsia symptoms. Upper gastrointestinal endoscopy showed multiple white granular lesions and widespread erosions in the stomach. Our findings indicate that gastric strongyloidiasis should be carefully considered in high-risk patients even if endoscopic findings are nonspecific.

A 57‐year‐old Peruvian man was admitted to our hospital with upper abdominal pain and fever. He had been diagnosed with gastroduodenal mantle cell lymphoma 9 months previously and achieved complete remission following 6 cycles of bendamustine plus rituximab therapy. During chemotherapy, he developed eosinophilia, which was thought to be caused by a drug allergy to bendamustine, and was taking low‐dose prednisolone (10 mg/day). He exhibited chronic dyspepsia symptoms and had also taken proton pump inhibitors for years.

Physical examination on admission showed mild tenderness in the upper abdomen without peritoneal irritation signs. The differential white blood cell count showed severe eosinophilia (5640/μL; normal range: 0–500/μL). He was negative for human T‐lymphotropic virus‐1 (HTLV‐1) and human immunodeficiency virus. Abdominal computed tomography did not show any specific findings.

Upper gastrointestinal endoscopy showed multiple white granular lesions resembling xanthoma in the antrum (Fig. 1a,b) and widespread erosion surrounded by granular lesions in the gastric body (Fig. 1c). Diffuse duodenal white villi and edematous papilla of Vater were also observed (Fig. 1e). None of these endoscopic findings existed 8 months previously (Fig. 1d,f). A parasite‐specific immunoglobulin G antibody screening test did not detect significant abnormalities, and biopsy specimens taken from white granular lesions in the antrum showed nonspecific histopathological findings such as atrophic gastric mucosa and lymphocytic infiltration (Fig. 1g). However, direct microscopic examination of gastric fluid obtained from the gastric tube revealed crawling filariform larvae consistent with Strongyloides stercoralis (Fig. 1h).

Figure 1

Upper gastrointestinal endoscopy showed multiple white granular lesions resembling xanthoma in the antrum (a, b) and widespread erosion surrounded by granular lesions in the gastric body (c). None of these endoscopic findings existed 8 months previously (d). Upper gastrointestinal endoscopy also showed diffuse duodenal white villi and edematous papilla of Vater (e), which did not exist 8 months previously (f). Biopsy specimens taken from white granular lesions in the antrum showed nonspecific histopathological findings such as atrophic gastric mucosa and lymphocytic infiltration (g). Direct microscopic examination of gastric fluid revealed crawling filariform larvae of Strongyloides stercoralis (white arrow) (h).

Under a diagnosis of strongyloidiasis, ivermectin (200 μg/kg/day) therapy was initiated. Meropenem and vancomycin were also initiated to prevent secondary bacterial infection. The patient was treated with ivermectin for 10 consecutive days; however, he developed bilateral pneumonia and meningitis, also caused by S. stercoralis infection. Unfortunately, he died of disseminated strongyloidiasis on day 36.

Strongyloidiasis is an intestinal parasitic infection caused by S. stercoralis, which infects humans transcutaneously. Through autoinfection, rhabditiform larvae grow into filariform larvae in the gastrointestinal tract. Latin America, including Peru, is considered an endemic area of strongyloidiasis. Clinical manifestations vary from asymptomatic eosinophilia to multiorgan symptoms, such as gastrointestinal, pulmonary, and dermatological symptoms. Similar to the present case, fatal hyperinfection syndrome and disseminated strongyloidiasis can occur as a result of an immunosuppressed state, including corticosteroid use, HTLV‐1 infection, acquired immunodeficiency syndrome, malignancy, and malnutrition. Even if stool and serological tests are negative, strongyloidiasis should be ruled out by examination of gastrointestinal fluid before administering immunosuppressive treatment. The treatments of choice for strongyloidiasis are ivermectin and albendazole, and the former is the most effective therapy.

Gastric involvement in strongyloidiasis is uncommon; however, chronic acid suppression by long‐term medication with proton pump inhibitors can be a predisposing factor.1 Duodenal edematous mucosa, white villi, and erythematous mucosa are reported as endoscopic findings, whereas thickened folds and mucosal erosions may be seen in the stomach.2, 3 Multiple white granular lesions, as seen in our patient, have been rarely reported as gastric findings. Although these endoscopic findings are nonspecific, gastric strongyloidiasis should be carefully considered in high‐risk patients as early diagnosis and treatment can decrease the risk of mortality.