Chronic giardiasis: a rare cause of exocrine pancreatic insufficiency (2024)

Abstract

Exocrine pancreatic insufficiency (EPI) is a major cause of maldigestion/malabsorption syndromes. It is routinely diagnosed in clinical practice with the use of faecal elastase 1 levels, and pancreatic enzyme replacement therapy continues to be the mainstay of treatment. Numerous primary pancreatic and extrapancreatic causes for EPI have been established. Chronic giardiasis is a common condition with symptoms similar to EPI; however, it has also been described as an infrequent cause of EPI. Much remains to be understood about the pathobiology of this association. Here, we present our experience of an intriguing case of severe pancreatic insufficiency in the setting of chronic giardiasis. The patient showed improvement in symptoms over weeks after completion of treatment for chronic giardiasis.

Keywords: malabsorption, hepatitis and other GI infections

Background

Exocrine pancreatic insufficiency (EPI) is one of the main causes of maldigestion/malabsorption syndromes. Patients with EPI may be asymptomatic or have abdominal symptoms despite normal appearing bowel movements. Steatorrhoea and malabsorption are usually seen with severe EPI. The aetiology of EPI includes pancreatic parenchymal conditions such as chronic pancreatitis, pancreatic neoplasms, cystic fibrosis, hereditary haemochromatosis, alpha-1 antitrypsin deficiency and Shwachman-Diamond-Oski syndrome, and secondary (extrapancreatic) causes such as coeliac disease, inflammatory bowel disease, gastrinoma and short bowel syndrome. Giardiasis is a common waterborne parasitic infection mainly causing acute gastrointestinal symptoms. However, chronic giardia infection may cause prolonged steatorrhoea, abdominal cramping, weight loss and vitamin deficiencies resembling other diseases associated with malabsorption. Chronic giardiasis not only is an important differential diagnosis to EPI but also is reported to be a cause.^{1 2}

Through this case report, we present an intriguing case of severe pancreatic insufficiency in the setting of chronic giardia infection.

Case presentation

A 28-year-old woman with a medical history of iron deficiency anaemia presented to the hospital due to worsening of diarrhoea and abdominal pain which began 8 months before presentation. The patient reported having multiple loose, yellow-brown, oily stools three to four times a day that would float in the toilet accompanied by crampy left-sided abdominal pain and tenesmus. She also had intermittent nausea and rare episodes of vomiting. Over the 8 months, the patient lost about 8 pounds. She did not report melaena, haematochezia, fever and chills. She was evaluated by her primary care doctor who tested for malabsorption syndromes and advised her on targeted diet restrictions. However, the symptoms persisted despite changes in her diet. The patient also developed iron deficiency anaemia which was refractory to oral iron supplementation.

Laboratory investigations were significant for normal serum levels of vitamins A, D, E and K. Serum tissue transglutaminase IgG/IgA antibody levels were not elevated. HIV testing was negative. Stool studies showed an elevated faecal fat content; faecal elastase 1 (FE1) was 65 µg/g and calprotectin was 343 µg/g. A single stool ova and parasite screen was negative. Given the decreased FE1, the patient was diagnosed with severe pancreatic insufficiency and prescribed pancreatic enzyme replacement therapy. However, the patient began experiencing syncopal episodes at home, which prevented her from obtaining the medication. These worsening symptoms prompted the patient to come to hospital for further evaluation.

On arrival to the hospital, the patient’s vitals were stable. Her physical examination was significant for a tender lower abdomen. There were no oral cavity ulcers visualised. Bedside rectal examination was normal.

Investigations

Laboratory investigations were impressive for haemoglobin of 113 g/L, white cell count of 7.5 ×10⁹/L, erythrocyte sedimentation rate of 17 mm/hour, C reactive protein of 0.5 mg/dL, serum amylase of 85 U/L and lipase of 48 U/L. The patient underwent MR cholangiopancreatography which showed a normal-appearing pancreas. Endoscopy and colonoscopy were performed, which did not show any signs of an inflammatory bowel disease. Duodenal mucosal biopsy showed preserved villous architecture, and colonic biopsy showed mucosa with prominent lymphoid aggregates but no evidence of microscopic colitis. Later, an infectious gastroenteritis PCR panel was sent, which returned positive for Giardia lamblia.

Treatment

The patient was treated with a 7-day course of metronidazole.

Outcome and follow-up

After completing the treatment for giardiasis, the symptoms resolved over a period of few weeks.

Discussion

Giardiasis is a form of infectious diarrhoea caused by the flagellated protozoan G. lamblia. It is common globally and estimated to cause 280 million infections every year.³ The most common route of infection is ingestion of contaminated water. Transmission from contaminated food and feco-oral route of infection are well established. Symptoms of giardiasis include watery diarrhoea, abdominal pain, nausea and weight loss. Chronic infection with G. lamblia can give rise to multiple gastrointestinal and extraintestinal consequences. Some of the extraintestinal complications include iridocycl*tis, choroiditis, retinal haemorrhages, arthritis, myopathy, failure to thrive, growth stunting, impaired cognition and chronic fatigue syndrome. Gastrointestinal complications of chronic giardiasis include functional dyspepsia and postinfectious irritable bowel syndrome.⁴ Secondary impairment of pancreatic function as a cause of severe malabsorption in intestinal giardiasis has been reported by Carroccio et al in adults¹ and in children.²

EPI primarily is caused by the destruction of pancreatic parenchyma or ducts, causing reduced enzyme production or transport. Furthermore, EPI can also be associated with conditions that affect the enteropancreatic feedback mechanism, leading to decreased pancreatic stimulation and secretion (secondary EPI).⁵ Clinical manifestations of EPI include steatorrhoea, abdominal pain and signs of malnutrition. Severe EPI cases with malnutrition have a high morbidity and mortality with an increased risk of cardiovascular adverse events due to deficiency of essential micronutrients and fat-soluble vitamins A, D, E and K.⁶ The gold standard for evaluation of pancreatic exocrine function is secretin test. However, it is an invasive test and is not always practical. Diagnosis of EPI is commonly made in clinical practice by measuring FE1. It is an indirect assessment of pancreatic exocrine function and is highly sensitive and specific (93% and 93%, respectively).⁷ FE1 of <200 µg/g is diagnostic of EPI. However, in a study by Walkowiak et al, the authors show that the specificity of FE1 in differentiation between primary EPI and intestinal malabsorption with mucosal atrophy is low and that FE1 regains its specificity after mucosal regeneration.⁸ The mainstay of treatment for EPI is pancreatic enzyme replacement therapy.

Our patient showed symptoms including steatorrhoea, abdominal pain and weight loss for about 8 months. There were no overt signs of fat-soluble vitamin deficiency on physical examination and investigations. She was diagnosed with EPI based on the severely reduced FE1 levels (65 µg/g). However, the patient had no risk factors or a history suggestive of a primary pancreatic disorder. Imaging of the pancreas was also normal. A thorough work-up for inflammatory bowel disease including endo-colonoscopy was normal. Small intestinal mucosal biopsy showed normal villous architecture which excluded coeliac disease. Colonic biopsy showed prominent lymphoid aggregates that can be seen in giardiasis.⁹ There was no evidence of mucosal atrophy, which would potentially decrease the specificity of FE1 according to the study by Walkowiak et al. Although our suspicion for an infectious diarrhoea was low given the chronicity of symptoms and absence of risk factors for chronic infectious diseases such as HIV or immunosuppression, the infectious gastroenteritis panel proved to be a decisive test.

FE1 levels in the context of giardiasis has not been studied; however, in a subgroup analysis of a study by Carroccio et al, two of five patients with intestinal giardiasis had low FE1 levels, while faecal chymotrypsin, a test with lower sensitivity and specificity for diagnosis of EPI,¹⁰ was normal in both patients.¹¹ This only indicates that newer diagnostic markers are required to assess pancreatic exocrine function.

Chronic giardiasis remains an important differential diagnosis while assessing maldigestion/malabsorption syndromes. However, our case report contributes to the evidence^{1 2} that it can also be a cause of secondary EPI. The mechanism by which giardiasis causes EPI is not fully understood and needs to be studied. Currently, there is no evidence for or against whether pancreatic exocrine function fully recovers after the treatment of giardiasis, and therefore the role of pancreatic enzyme replacement therapy in EPI associated with giardiasis is unclear.

Footnotes

References