Villous atrophy refers to a condition where the small, finger-like projections (villi) lining the inner surface of the small intestine become flattened or damaged. Villi vastly increase the surface area for nutrient absorption from digested food. When atrophied, their ability to absorb nutrients like vitamins, minerals, fats, and carbohydrates is significantly impaired. This impairment can lead to various health issues due to malabsorption.
Underlying Causes of Villous Atrophy
Villous atrophy can arise from several distinct conditions, with celiac disease being a frequently recognized cause. Celiac disease involves an autoimmune reaction triggered by the ingestion of gluten, a protein found in wheat, barley, and rye. In individuals with celiac disease, gluten exposure prompts the immune system to mistakenly attack the villi, leading to their damage and flattening.
Beyond celiac disease, various infections can also induce villous atrophy. Parasitic infections, such as Giardiasis caused by the parasite Giardia lamblia, can inflame and damage the intestinal lining. Similarly, tropical sprue, a condition thought to be caused by an infection or overgrowth of bacteria in the small intestine, can also lead to widespread villous damage in individuals living in or visiting tropical regions.
Certain autoimmune conditions, distinct from celiac disease, may also contribute to villous atrophy. Autoimmune enteropathy, for instance, involves the immune system directly attacking the cells lining the small intestine, resulting in villous damage without a specific dietary trigger like gluten. This condition can present with persistent diarrhea and malabsorption, similar to celiac disease, but it requires different diagnostic and management approaches.
Medications represent another potential cause of villous atrophy. One notable example is olmesartan, a drug primarily used to treat high blood pressure, which has been linked to severe enteropathy resembling celiac disease. This drug-induced condition can cause significant villous flattening and malabsorption. Other less common causes include conditions such as common variable immunodeficiency (CVID), which impairs the immune system, and certain types of intestinal lymphoma, where cancerous cells infiltrate the small intestine lining.
The Diagnostic Process
Confirming villous atrophy and identifying its specific cause typically begins with a thorough evaluation of a patient’s medical history and current symptoms. Individuals often present with indicators of malabsorption, such as chronic diarrhea, unexplained weight loss, abdominal bloating, and fatigue. Anemia, often due to iron or vitamin B12 deficiency, is also a common finding that suggests impaired absorption.
Following the initial assessment, blood tests are frequently performed to help narrow down potential causes. For suspected celiac disease, serology tests measure specific antibodies in the blood, such as tissue transglutaminase IgA (tTG-IgA) and endomysial antibodies (EMA). Elevated levels of these antibodies suggest an autoimmune response to gluten, indicating a higher likelihood of celiac disease. While these blood tests are valuable screening tools, they are not definitive for diagnosing villous atrophy itself.
The definitive diagnosis of villous atrophy and its severity relies on an upper endoscopy with biopsy. During this procedure, a thin, flexible tube with a camera is guided through the esophagus and stomach into the small intestine. Small tissue samples, or biopsies, are then taken from different sections of the duodenum and jejunum. These samples are subsequently examined under a microscope by a pathologist.
Microscopic examination allows the pathologist to directly observe the villi and assess the degree of damage, confirming the presence of atrophy. The severity of villous atrophy is often classified using a system like the Marsh score, which grades the changes from mild villous blunting to complete flattening of the villi. This histological assessment confirms the diagnosis and guides further management.
Management and Villi Recovery
The management of villous atrophy centers on addressing the specific underlying cause identified during the diagnostic process. Once the root cause is managed, the intestinal lining’s regenerative capacity allows the villi to heal. This targeted approach is important for restoring proper nutrient absorption and alleviating symptoms.
For individuals diagnosed with celiac disease, the primary and most effective treatment is strict adherence to a lifelong gluten-free diet. Removing all sources of gluten—which include wheat, barley, and rye—stops the autoimmune attack on the villi. This allows the intestinal lining to begin the process of repair and regeneration. Consistent avoidance of gluten is important for sustained recovery.
In cases where infections are the cause, such as Giardiasis, treatment involves specific antimicrobial medications, like metronidazole, to eradicate the pathogen. For tropical sprue, a course of broad-spectrum antibiotics, often combined with folic acid supplementation, is typically prescribed to resolve the bacterial overgrowth and support villi recovery. If a medication like olmesartan is identified as the culprit, discontinuing the drug usually leads to a gradual but complete resolution of the villous atrophy.
The regeneration of villi after the underlying cause is addressed can vary in timeline, but significant improvement is often observed within several months. For instance, in celiac disease, histological recovery of villi can take six months to two years. The small intestine’s lining continuously renews its cells, which facilitates the rebuilding of the damaged villi.
In addition to treating the cause, addressing any nutritional deficiencies that resulted from the period of malabsorption is an important part of management. Patients may require supplementation for nutrients like iron, vitamin B12, folate, and vitamin D, which are commonly poorly absorbed when villi are damaged. Nutritional support helps correct deficiencies and supports the body’s overall healing process.