Acute Quadriparesis From Concurrent Celiac Crisis and Giardiasis

ABSTRACT

The coexistence of celiac disease and giardiasis is an uncommon and potentially dangerous clinical scenario that presents diagnostic and therapeutic challenges. We describe a 48-year-old man with persistent diarrhea for 3 weeks and new onset bilateral upper and lower extremity weakness. Laboratory results revealed severe hypokalemia and positive celiac serologies. In addition, stool testing was positive for Giardia lamblia, which likely contributed to the severity of his symptoms and resulting electrolyte abnormalities. This unique presentation reinforces the recommendation to combine serologic, histologic, and infectious workup when evaluating severe diarrhea, even in cases of suspected celiac disease.

INTRODUCTION

Celiac disease (CD) is a systemic autoimmune-mediated condition affecting an estimated 1% of the U.S. population.¹ In patients with CD, nonadherence to a strict gluten-free diet can cause symptoms such as diarrhea, weight loss, abdominal pain, and bloating.¹ Celiac crisis is a rare but potentially dangerous complication with severe acute diarrhea and/or vomiting leading to dehydration and multiple metabolic disturbances, often including hypokalemia.² In clinical situations with severely low potassium, the mechanism of muscle cell repolarization can be altered resulting in clinical weakness, paraparesis, and even paralysis.³ Giardiasis, or infection by Giardia lamblia, is the most prevalent protozoal infection worldwide.⁴ Interestingly, symptomatology, serology, endoscopy, and histopathologic findings in giardiasis can mimic CD.^5–7 Alternatively, patients with underlying CD can have severe gastrointestinal symptoms exacerbated or unmasked by concomitant infection with G. lamblia.^7,8

CASE REPORT

A 48-year-old man with a medical history of Type II diabetes mellitus, hyperlipidemia, and obstructive sleep apnea presented to the emergency department with worsening bilateral upper and lower extremity weakness and persistent diarrhea of 3 weeks duration. He reported at least 3 daily episodes of watery, nonbloody diarrhea. He denied abdominal pain, nausea, or vomiting. He experienced progressive weakness of his bilateral legs resulting in multiple falls. He additionally developed upper extremity weakness bilaterally, prompting presentation to the emergency department. He was not taking any current medications and denied initiation of new supplements, sick contacts, recent travel, or use of alcohol, nonsteroidal anti-inflammatories, or tobacco products. His neurologic examination demonstrated diminished strength with bilateral hip flexion, plantar flexion and extension, shoulder flexion, and grip strength. He had intact reflexes and sensation to light touch. Laboratory studies revealed severe hypokalemia (potassium of 1.6 mmol/L), leukocytosis (white blood cell count of 19.9 × 10⁹/L), normocytic anemia (hemoglobin of 12.8 g/dL with a mean corpuscular volume of 86.4 fL), hypophosphatemia (1.4 mg/dL), and magnesium of 1.9 mg/dL. Further laboratory testing revealed an antitissue transglutaminase IgA antibody (tTG IgA) of 1,973.2 U/mL (normal <15 U/mL) and an endomysial IgA antibody (EMA) titer of 1:320 (normal <1:10). Workup including computed tomography of the head, chest, abdomen, and pelvis were unremarkable.

Esophagogastroduodenoscopy revealed a normal appearing esophagus and stomach. Scalloping of the duodenal mucosa was observed (Figure 1). Duodenal biopsies revealed villous atrophy with increased intraepithelial lymphocytes.

Figure 1.

Third portion of the duodenum with evidence of scalloped folds.

Due to the strongly positive CD serology and diarrhea with severe electrolyte derangements requiring intensive care admission, the patient met diagnostic criteria for celiac crisis. He was instructed to eliminate gluten from his diet and was prescribed a budesonide taper. Stool testing revealed a positive polymerase chain reaction for G. lamblia. He was prescribed metronidazole 500 mg twice daily for 1 week. With correction of electrolytes, modification of diet, and initiation of budesonide and metronidazole, his diarrhea improved and weakness resolved. The patient was scheduled to establish care with a gastroenterology clinic to repeat serologic testing and endoscopy. Unfortunately, the patient was lost to follow-up.

DISCUSSION

CD is an immune-mediated enteropathy triggered by gluten ingestion in genetically predisposed individuals.¹ The onset of CD can occur at any age and may present with symptoms such as nausea, vomiting, constipation, diarrhea, and weight loss.⁹ Celiac crisis is a clinical diagnosis characterized by severe diarrhea, dehydration, and metabolic derangements from CD often requiring hospitalization.³ Although more common in children, celiac crisis can occur in adults with undiagnosed or untreated disease. Prompt recognition is essential, as delayed treatment can lead to hemodynamic instability or neurologic complications.³ Prednisone or open-capsule budesonide are recommended as first-line treatments in patients with celiac crisis.² Budesonide was chosen in this case for its lower risk of systemic adverse effects.

G. lamblia is transmitted through contaminated water and can cause diarrhea, bloating, and steatorrhea.⁴ In an interesting diagnostic dilemma, case reports have demonstrated that infection with G. lamblia can mimic CD symptomatically, endoscopically, and histologically. The infection can even cause transient elevations in both tTG IgA and EMA, more commonly reported in pediatric cases, which demonstrate mild elevations of these serological markers that resolve after treatment of the G. lamblia without adhering to a gluten-free diet.^5,6 This phenomenon has been more rarely reported in adults.⁷ In addition, G. lamblia most commonly inhabits the duodenum and causes damage that is histologically and endoscopically similar to CD. The inflammation from the protozoa can cause epithelial hyperplasia, villous blunting, and increased intraepithelial lymphocytes.^4,5,10 Endoscopists have observed chronic mucosal changes including scalloped folds due to the villous atrophy within the duodenum.¹¹ There are cases of G. lamblia infection exacerbating CD symptoms or precipitating the onset of previously latent disease with concurrent mucosal injury to the duodenum.⁸ Although simultaneous CD and giardiasis has been studied, we believe this to be the first reported case of an adult with celiac crisis with concurrent giardiasis.¹² Although without repeated serologies, a transient elevation of CD antibodies from giardiasis cannot be ruled out, we believe the significant elevations in both tTG IgA and EMA indicate a component of CD as reported cases of transient elevations from giardiasis tend to be mild (for example a tTG IgA of only 15 u/mL in a previously reported case).⁷ Concurrent infection with G. lamblia is thought to have further exacerbated the symptoms and triggered the celiac crisis. Due to the generalized nature of the weakness, the rapid improvement with correction of potassium, and lack of identification of an alternative neuromuscular cause, the weakness was fully attributed to the electrolyte derangements. This unique presentation reinforces the recommendation to combine serologic, histologic, and infectious workup when evaluating severe gastrointestinal symptoms. It is critical to remain vigilant for multiple concurrent conditions, especially in patients with severe electrolyte abnormalities and functional decline.

DISCLOSURES

Author contributions: K. Forest and M. Pham wrote large portions of the manuscript, reviewed it in its entirety, made edits, and approved final version. J. Schowalter contributed to the analysis and interpretation of data, drafting and reviewing the manuscript, and approving the final version. K. Forest is the article guarantor.

Financial disclosure: None to report.

Previous presentation: This case was previously presented at the South Dakota American College of Physicians state conference on October 2nd, 2025 in Keystone, SD.

Informed consent was obtained for this case report.

ABBREVIATIONS:

CD

celiac diseaset

EMA

endomysial antibody

TG IgA

antitissue transglutaminase IgA antibody