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Received date: 05/10/2022 Published date: 31/10/2022 Case Report

Celiac patient with new episodes of Diahrrea:What could it be?

Joana Dias Antunes¹, Ivo Barreiro¹, Luísa Loureiro², Abílio Gonçalves²

¹Internal Medicine Resident at Department of Internal Medicina, Hospital Distrital da Figueira da Foz
²Medical specialist in Internal Medicine at Department of Internal Medicina, Hospital Distrital da Figueira da Foz

*Corresponding author

*Joana Antunes, MD, Internal Medicine Resident at Department of Internal Medicina, Hospital Distrital
da Figueira da Foz, Portugal

DOI: 10.55920/JCRMHS.2022.02.001072

SUMMARY

Celiac disease is a common autoimmune disease that affects the gut's ability to process gluten and is often associated with other autoimmune diseases.

The authors describe the clinical case of a 65-year-old woman with a history of celiac disease and autoimmune hypothyroidism, who came to the emergency department due to generalized edema, unexplained weight loss and chronic diarrhea with mucus. Fecal study was requested, with the fecal calprotectin test being positive. The endoscopic study showed flattening of the intestinal villi, with a biopsy being performed, the result of which revealed overlapping criteria for celiac disease and lymphocytic colitis.

For Celiac patients on a previously controlled gluten-free diet, but with an onset of chronic diarrhea, microscopic colitis should be suspected. Symptoms can be debilitating, so early diagnosis and treatment are critical.

Key-words: celiac disease, lymphocytic colitis, chronic diarrhea, autoimmune diseases

INTRODUCTION

Celiac Disease (CD) is a frequent autoimmune disease, with an overall prevalence of 1%. The prevalence is twice as high in females¹. Early recognition of CD is increasing, especially in Europe, North America and Oceania. It appears to be relatively uncommon in Southeast Asia and Sub-Saharan Africa.

CD is an immune-mediated enteropathy, precipitated by gluten in the diet, which primarily affects the small intestine and induces a chronic inflammatory state, with a consequent decrease in nutrient absorption and secretion of water and solutes².

The classic presentation is characterized by abdominal pain, chronic watery diarrhea, steatorrhea and nutritional deficits. Extraintestinal manifestations are common and include chronic fatigue and anemia¹.

The gold standard method for its diagnosis is the proximal small bowel mucosal biopsy. The demonstration of the presence of enteropathy in the small bowel biopsy, such as villous atrophy, cryptic hyperplasia and intraepithelial lymphocytosis confirms the diagnosis. Testing the presence of circulating antibodies (anti-transglutaminase, anti-gliadin and anti-endomysium) is recommended in CD screening, as these antibodies have high sensitivity and specificity. However, if such antibody testing is negative but clinical suspicion is high, then a biopsy should be performed¹.

The mainstay of treatment is a gluten-free diet, which improves symptoms and prevents complications. Most patients experience reversal of the disease by excluding gluten from their diets. However, untreated symptomatic disease is associated both with high morbidity and mortality.

CD is associated with other autoimmune diseases, namely Hashimoto's Thyroiditis, Graves' disease and Type 1 Diabetes mellitus². A strong association with microscopic colitis has also been described.

CASE REPORT

A 65-year-old female patient came to the Emergency Department due to generalized edema, unexplained weight loss and chronic diarrhea with mucus. She reported complaints of watery diarrhea, stool with mucus and unexplained weight loss (19%) with 2 months of evolution.

She had a personal history of celiac disease, arterial hypertension and autoimmune thyroiditis. She was medicated with furosemide 40mg once a day (qd) and cloxazolam 2mg qd. The patient denied tobacco consumption, introduction of new drugs and recent long-haul trips. She reported sporadic alcohol consumption in a social context.

On objective examination, she was oriented and cooperative, hemodynamically stable, apyretic and emaciated. She presented marked abdominal distension, pain on superficial and deep palpation, in all quadrants, without peritoneal irritation, and had a sign of an ascitic wave present.

The analytical study revealed anemia, thrombocytosis, severe hypoalbuminemia, increased transaminases, alkaline phosphatase, gamma glutamyl transpeptidase and increased international normalized ratio. There were no changes in renal function or inflammatory parameters (Table 1). She was admitted to study chronic diarrhea and unexplained weight loss. Several diagnostic hypotheses were put forward, such as non-compliance with therapy (gluten-free diet), alcoholism and lymphoma/colon neoplasm.

Albumin replacement was started, with progressive improvement of edema. A stool study was requested and fecal calprotectin was positive (Table 1). Thoraco-abdomino-pelvic computed tomography revealed “marked ascites (…). Diffuse interstitial edema of the subcutaneous plane that suggests anasarca. Diffuse parietal thickening of the small intestine with signs of wall edema”.

An endoscopic study was requested, which showed “duodenal mucosa with apparently flattening of the intestinal villi” (Figures 1 and 2) and biopsies were performed. The results revealed overlapping criteria for celiac disease and lymphocytic colitis.

The patient was discharged with a medication indication of budesonide 9 mg qd, as well as an indication of a reinforced gluten-free diet. She was oriented for Internal Medicine and Gastroenterology consultation. She started progressive weaning from budesonide 2 months after discharge and it was suspended after 5 months, without complications. There was also control of celiac disease, with a gluten-free diet, and recovery of the initial weight. She is currently no longer in therapy and is being observed every 6 months in a gastroenterology consultation.

Figure 1: Subtotal villous atrophy with crypt hyperplasia and intra-epithelial lymphocytosis.

Figure 2: Colonic mucosa shows infiltration of the epithelium by multiple lymphocytes.

Table 1: Analytical study carried out on admission

DISCUSSION

Microscopic colitis is a chronic inflammatory disease of the colon and includes two entities: lymphocytic colitis and collagenous colitis. The colon looks normal in a colonoscopy, so the diagnosis depends on a biopsy of the colonic mucosa^1,2. Histologically, lymphocytic colitis is characterized by enlargement of the lamina propria, infiltration of chronic inflammatory cells and recruitment of intraepithelial lymphocytes, with damage to the surface of the lamina propria. In the case of collagenous colitis, there is also a thickening of the subepithelial collagen layer³.

Microscopic colitis is characterized by chronic, watery and non-bloody diarrhea, urgency and fecal incontinence. Half of the patients complain of abdominal pain, weight loss and extra-intestinal complaints such as arthralgia, arthritis or uveitis². Laboratory findings include anemia, high sedimentation rate and in 50% of cases positive autoantibodies, namely rheumatoid factor, antinuclear, antimitochondrial and antineutrophilic cytoplasmic antibodies.²

Treatment is based on the use of antidiarrheal agents and corticotherapy. Budesonide is recommended in patients with persistent diarrhea, despite therapy with antidiarrheal agents, at a dose of 9mg daily, for 6 to 8 weeks⁴. After clinical stabilization, gradual discontinuation is indicated. In uncontrolled patients, therapy should be continued for 12 or more weeks. Prednisone is reserved for patients who do not respond to budesonide².

Patients with CD are at increased risk of microscopic colitis (approximately 70 times higher than in the general population)³. Approximately 15% of patients with microscopic colitis have CD. However, only 4% of celiac patients have a concomitant diagnosis of lymphocytic or collagenous colitis³. Middle-aged women have a higher risk of developing microscopic colitis, with an average age at diagnosis of 65 years².

The relationship between the two pathologies seems to be in part genetic - it is known that HLA-DR3-DQ2 predisposes to celiac disease and is also associated with microscopic colitis⁴.

Therefore, in celiac patients previously controlled on a gluten-free diet and with an onset of chronic diarrhea, it is essential to consider the concomitant diagnosis of microscopic colitis. If clinical suspicion is high, colonoscopy with biopsy should be performed to confirm the diagnosis⁵.

The clinical follow-up of this patient, in particular, is important, as she has a very significant autoimmune background. It brings together, in addition to autoimmune thyroiditis, celiac disease and lymphocytic colitis, all immune-mediated pathologies. The appearance of other autoimmune diseases is a possibility to be taken into account, so the follow-up of this patient in consultation is essential.

Conclusion

The importance of this clinical case lies in the fact that the appearance of microscopic colitis in celiac patients is uncommon. However, this differential diagnosis should not be forgotten when new episodes of diarrhea appear in previously well-controlled patients on gluten-free diet. Early diagnosis and treatment are essential to improve the prognosis.

Conflict of Interests: All authors declare no conflicts of interest.

REFERENCES

Arasaradnam RP, Brown S, Forbes A, Fox MR, Hungin P, Kelman L et al. Guidelines for the investigation of chronic diarrhoea in adults: British Society of Gastroenterology, 3rd edition. Gut. 2018; 67:1380–1399.
Villanueva MS, Alimi Y. Microscopic colitis (lymphocytic and collagenous), eosinophilic colitis, and celiac disease. Clin Colon Rectal Surg. 2015; 28(2):118-126.
Lauret E, Rodrigo L. Celiac disease and autoimmune-associated conditions. Biomed Res Int. 2013; 2013:127589.
Barta Z, Zold E, Nagy A, Zeher M, Csipo I. Celiac disease and microscopic colitis: a report of 4 cases. World J Gastroenterol. 2011; 17(16):2150-2154.
Stewart M, Andrews CN, Urbanski S, Beck PL, Storr M. The association of coeliac disease and microscopic colitis: a large population-based study. Aliment Pharmacol Ther. 2011; 33(12):1340-9.

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