Strongyloidiasis as a Hidden Cause of Protein Losing ‎Enteropathy

INTRODUCTION

The prevalence of S. stercoralis varies between countries worldwide. It was ‎found to be 11.1% in Egypt [1]. In endemic areas, the parasite can persist ‎and replicate in the host for years causing various clinical presentations ‎including diarrhea, abdominal pain, vomiting, fever, GI hemorrhage, ‎weight loss, adynamic ileus, skin manifestations and pneumonia. In ‎hyperinfection , strongyloidiasis could be a strong etiological factor for ‎chronic diarrhea and protein losing enteropathy [2]. Disseminated infection ‎occurs when larvae invade organs other than GIT and lungs i.e, beyond the ‎autoinfection range. Hyperinfection can be encountered in any host but ‎disseminated infection is usually encountered in immunocmpromised ‎patients [3]. The prognosis of Strongyloidiasis is usually benign except in ‎hyperinfection and disseminated infection. Disseminated infection can be ‎also complicated by secondary Gram- negative bacterial infection that adds ‎to the bad prognosis of the condition [4]. Mortality rate can reach 71% in ‎disseminated disease [5].

Case Presentation

Five years ago, we were astonished by an interesting case of chronic diarrhea that was discovered to be caused by strongyloidiasis. A female villager patient of 62 years’ old, presented to Tropical Medicine Department, Zagazig University Hospitals, with severe abdominal pain, distention, anorexia, nausea, vomiting, watery diarrhea (3-5 times / day) and progressive loss of weight. Her complaint was of about 10 weeks duration and developed into bilateral pitting lower limp oedema. The patient denied any past history of chronic illness including diabetes mellitus and hypertension. Apart from the marked emaciation, abdominal distention and bilateral pitting lower limp oedema, the patient showed no clinical abnormality. 

The patient was subjected to some investigations where CBC showed mild eosinophilia, stool analysis showed only mild Entamoeba coli (E. coli) infection, liver profile showed hypoproteinemia with hypoalbuminemia and serum electrolytes showed hyponatremia and hypokalemia. Abdominal ultrasonography showed minimal ascites that was confirmed by CT scanning of abdomen and pelvis.‎

The patient received albendazole as a single daily dose of 400 mg / day for two weeks. The patient dramatically improved and reported complete recovery at her last visit - after 5 years of the first presentation - for another different complaint.  

DISCUSSION

The clinical presentation of the patient was not such classical picture of strongyloidiasis especially with the absence of criteria of immunocompromisation. The direct disappearance of the patient for 5 years after receiving albendazole therapy did not give us the chance to complete her investigations and exclude immunocompromising conditions including chronic illness, immunosuppressive therapy and HIV. However, a nearly similar clinical presentation was reported by Lakshmanan et al [2]. Moreover, the mere advanced age and malnutrition - manifested in this patient - can be considered as a cause of immunocompromisation that leads to enhancing the autoinfection, hyperinfection and even ultimately disseminated infection [4].

The absence of some clinical manifestations such as dermatological and respiratory symptoms. However, these symptoms are usually suffered in acute stage. Even in chronic strongyloidiasis, these symptoms - if happen - take usually mild intermittent course in most instances. The combined effect of chronic diarrhea, malabsorption and protein losing enteropathy in this patient may augment the hypoproteinemia and hypoalbuminemia causing refractory oedema [6].

The patient presented by hypoproteinemia and hypoalbuminemia that stressed the need to exclude the most suggested causes such as nutritional, hepatic and renal disorders to confirm the protein losing enteropathy syndrome. Some investigations were missed after disappearance of the patient, but the upper GI endoscopy with duodenal biopsy taking and histopathological examination saved the time and effort in the way of diagnosis.

S. stercoralis larvae can be detected in stool especially in hyperinfection and disseminated infection. However, stool analysis for this patient did not detect S. stercoralis larvae. This can be expected since single direct stool analysis is able to detect the infection in only 30 % of specimens in chronic disease [7,8].

The endoscopic findings of duodenum - including inflammation and ulceration of the mucosa were reported also by Lakshmanan et al [2]. They may be not pathognomonic for strongyloidiasis but they can be considered good diagnostic signs for strongyloidiasis in endemic areas [9]. Moreover, S. stercoralis colonizes the duodenum and the detection of parasitic larvae in duodenal biopsy is the most accurate method for the diagnosis [10]. Despite absence of a clue of immunocompromisation, the protein losing enteritis in this patient can be classified as the most severe form owing to the presence of ulceration and parasitic larvae in the mucosa of duodenum [11].

Even though E. coli is a non- pathogenic organism, its presence in stool analysis of an old age patient could be a sign of the non- uncommon concomitant mixed parasitic infection especially in immunocompromised patients [12- 14].

The association between strongyloidiasis and malabsorption was previously reported in a diarrheal case of uncontrolled celiac disease despite adopting a strict gluten- free diet by the patient a situation that provoke the etiologic role of S. stercoralis infection in the malabsorption [15]. Another case of malabsorption was reported presenting with severe weight loss (more than 20% of the total body mass) and the patient was salvaged by discovering strongyloidiasis as an etiologic cause of the illness [16].

The patient was treated successfully with albendazole for two weeks. Ivermectin is the first line therapeutic medicine for strongyloidiasis. However, albendazole is a reliable alternative. The duration of treatment is usually modified according to the severity of the case and should be continued until symptomatic relief and repeated negative stool samples for 2 weeks.  This management helps to guard against autoinfection and hyperinfection [9, 17]. Fortunately, this patient informed that she was improved dramatically after albendazole therapy despite her disappearance that time - 5 years ago - a situation that did not enable us to follow up her and confirm her recovery.

CONCLUSION

Protein losing enteropathy can be caused by strongyloidiasis even in absence of overt immune suppression. In endemic areas, parasitic infections including strongyloidiasis should be put into consideration in every case of protein losing enteropathy especially in immunocompromised patients.

Financial support: Nil.

Conflicts of interest: There is no conflict of interest.

Ethical consideration: An informed consent was freely given by the patient.