Celiac disease is an autoimmune enteropathy — a disorder in which the immune system, in genetically susceptible individuals, transforms the act of eating into an attack on the self. Ingestion of gluten, the storage-protein complex of wheat, barley and rye, triggers an inflammatory cascade that flattens the villi, the finger-like projections of the small intestinal lining that absorb nutrients, producing diarrhea and malabsorption. But the disease has never confined itself to the gut. Dermatologists recognize its blistering skin manifestation, dermatitis herpetiformis; hematologists its iron deficiency anemia; neurologists its peripheral neuropathy; endocrinologists its contributions to weight loss, osteomalacia, rickets and childhood growth failure; psychiatrists its associations with mood disorders. Pulmonary involvement, however, has long occupied a strange liminal space in the medical literature — described sporadically since the 1970s, yet so uncommon that most pulmonologists will encounter it once in a career, if at all. That rarity is precisely what makes the new report so arresting.

The patient at the center of the case had been diagnosed with celiac disease 19 years earlier, after weight loss and gastrointestinal symptoms prompted serologic testing and a duodenal biopsy that revealed the disorder’s hallmark villous atrophy. His condition was managed with an intermittent gluten-free diet, and his digestive complaints were considered well controlled. His history, however, held a second set of clues: a small sliding hiatal hernia, longstanding gastroesophageal reflux extending up to the thoracic inlet, and episodes of throat clearing and coughing after meals that raised concern for micro-aspiration, the silent inhalation of tiny amounts of gastric contents into the airways. He also carried diagnoses of obstructive sleep apnea with inconsistent use of continuous positive airway pressure therapy, hypothyroidism and migraines, along with a remote cerebrovascular accident from which he had fully recovered. A bout of COVID-19 had been mild and brief, managed conservatively in the outpatient setting. Then, three years before his transplant evaluation, a gradually worsening dry cough and progressive shortness of breath began — and refused to relent.

High-resolution computed tomography of the chest painted an ambiguous picture. Images acquired during inspiration showed patchy ground-glass opacities, mosaic attenuation, reticulations and traction bronchiectasis — airways irreversibly widened by the traction of surrounding scar tissue — distributed predominantly through the mid and lower lung zones in a peribronchial and perilobular pattern. Mild dilation of the lower esophagus was also noted. Critically, there were no pulmonary nodules, no cysts and no honeycombing, the clustered cystic destruction considered a radiologic fingerprint of established usual interstitial pneumonia. End-expiratory images showed no significant air trapping, arguing against small-airway disease. Radiologists accordingly classified the findings as “indeterminate for UIP” or “alternate diagnosis,” with fibrotic autoimmune or connective tissue disease-associated interstitial lung disease, fibrotic organizing pneumonia and fibrotic hypersensitivity pneumonitis listed among the possibilities. Serial comparative imaging over the following two years revealed the grimmer truth: the chronic fibrosing interstitial process, whatever its origin, was steadily progressing.

Then came the tissue. A surgical lung biopsy obtained before the patient’s referral demonstrated a pattern of usual interstitial pneumonia: peripheral and paraseptal fibrosis studded with fibroblast foci — the whorled clusters of proliferating fibroblasts and myofibroblasts that mark the active advancing edge of pulmonary fibrosis — together with mild chronic interstitial inflammation and only rare multinucleated giant cells associated with inspissated mucus. There was no honeycombing, no hemosiderosis and no alveolar hemorrhage. A mismatch between indeterminate imaging and definitive histopathology is a recognized feature of interstitial lung disease diagnostics, which is why such cases are routed through multidisciplinary discussions. Here, clinicians, radiologists and pathologists weighed the patient’s never-smoker status, an age younger than typical for idiopathic pulmonary fibrosis, the absence of meaningful environmental exposures, unrevealing inflammatory and extensive autoimmune testing, no features of telomeropathy — the inherited telomere-biology disorders that can masquerade as pulmonary fibrosis — and a negative family history. Their verdict: a secondary UIP pattern rather than idiopathic pulmonary fibrosis, with celiac-associated pulmonary involvement a leading consideration.

Usual interstitial pneumonia represents the histopathological pattern of a severe, chronic and irreversibly progressive pulmonary fibrosis. It is the tissue signature of idiopathic pulmonary fibrosis, but the same pattern can arise secondary to autoimmune rheumatic diseases, medication exposures, fibrotic hypersensitivity pneumonitis and other environmental insults — which is why the multidisciplinary team worked so systematically to exclude the alternatives. The patient’s only occupational exposure, three months of cement dust during a renovation project, was undertaken with an appropriate respirator, and the biopsy showed none of the features of pneumoconiosis such as silicosis. He had no exposure to organic antigens typical of hypersensitivity pneumonitis, no systemic autoimmune features and negative serologies ruling out connective tissue disease-associated interstitial lung disease. Even his episodic pain in the knees, hips and knuckles, attributed to degenerative joint disease, carried no clinical or serologic evidence of a rheumatologic disorder. Management proceeded with nintedanib, an antifibrotic tyrosine kinase inhibitor that blocks platelet-derived growth factor, fibroblast growth factor and vascular endothelial growth factor receptors, slowing the loss of lung function in fibrosing disease. In this patient, it was not enough.

Serial pulmonary function tests charted the decline with unforgiving precision. At baseline in August 2023, his forced vital capacity — the volume of air exhaled after a maximal breath — measured 2.70 liters, or 61.7 percent of predicted. By April 2024, at his transplant evaluation, it had fallen to 2.35 liters, 53.9 percent of predicted, with total lung capacity at 48.7 percent and the diffusing capacity for carbon monoxide — a measure of how efficiently gas crosses from the alveoli into the blood — at just 37.2 percent. By February 2025, on the eve of transplant listing, forced vital capacity had collapsed to 1.79 liters, 41.2 percent of predicted, and diffusion capacity to 34.9 percent. The physiology was unmistakable: a progressively restrictive ventilatory defect with persistently reduced diffusion capacity, the signature of lungs shrinking, stiffening and losing their exchange surface. He slid into progressive hypoxic respiratory failure requiring continuous supplemental oxygen at four liters per minute, then underwent successful bilateral lung transplantation.

To contextualize the observation, the authors conducted a systematic review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, searching PubMed and Scopus from 1970 through 2026 for adult, English-language case reports of pulmonary involvement in celiac disease, deduplicating records by DOI and title. The one pulmonary association most clinicians do know is Lane–Hamilton syndrome: the co-occurrence of idiopathic pulmonary hemosiderosis — recurrent bleeding into the alveolar spaces that leaves behind hemosiderin-laden macrophages — with celiac disease, usually in children. Affected patients develop recurrent hemoptysis, dyspnea, cough and iron-deficiency anemia, sometimes progressing to hypoxemia and respiratory failure, and the pairing of hemoptysis with diarrhea is a recognized telltale. Remarkably, most reported cases improved on a gluten-free diet alone or combined with corticosteroids and immunosuppressants such as azathioprine and mycophenolate mofetil. Across nineteen published case reports spanning 1971 to 2025, seventeen involved pulmonary hemosiderosis, one documented UIP — in a patient with childhood celiac disease complicated by polyglandular autoimmune syndrome IIIA, who died of an acute exacerbation — and one described bronchiectasis with chronic rhinosinusitis. The new patient fit none of those molds: no hemoptysis, no anemia, no hemorrhage, no overlapping autoimmunity.

How a disease of the intestinal lining might scar the lung remains unresolved. The authors point to the gut–lung axis — the bidirectional immunological and microbial dialogue linking the gastrointestinal tract to the respiratory system — as the most promising framework. Candidate mechanisms include a shared immunologic susceptibility to gluten-derived peptides, proinflammatory cytokines spilling into the systemic circulation, broader immune dysregulation and epithelial injury at both mucosal barriers. The patient’s longstanding reflux and suspected micro-aspiration add a further wrinkle, since chronic aspiration is itself a recognized driver of fibrosing lung injury, although the biopsy lacked the giant-cell-rich features classically attributed to it. Celiac disease has also been linked to obstructive airway phenomena, including asthma and chronic cough, hinting that the airways may be an underappreciated target of gluten-sensitive inflammation. What the case makes plain is that the pathophysiology connecting celiac disease to pulmonary manifestations is incompletely understood — and that the lung may be a far more vulnerable downstream target than the scarcity of reports implies.

The clinical lessons cut in both directions. Because celiac disease can be subtle or even clinically silent — many patients with pulmonary hemosiderosis show little or no gastrointestinal disease — the authors stress that routine screening for celiac disease is warranted whenever idiopathic pulmonary hemosiderosis appears, a step that has repeatedly led to diagnosis and to improvement on a gluten-free diet. Conversely, an unexplained, progressive fibrosing interstitial lung disease in a patient with celiac disease may deserve scrutiny as a possible manifestation of the enteropathy rather than coincidence, even when the digestive disorder appears well controlled. The report stops short of claiming causation: it is a single case, of uncertain aetiology, its confounders narrowed but not eliminated. Yet it joins a small but growing literature suggesting that the pulmonary spectrum of celiac disease extends beyond hemorrhagic syndromes to bronchiectasis, lymphocytic bronchoalveolitis, chronic sinusitis — and now, perhaps, usual interstitial pneumonia. For a condition estimated to affect roughly one in a hundred people, that is a possibility clinicians can no longer comfortably ignore.

Type 1 diabetes is well-known for its autoimmune origins, where the body’s immune system mistakenly attacks insulin-producing beta cells in the pancreas. Celiac disease, on the other hand, is characterized by an inappropriate immune response to gluten, resulting in damage to the small intestine. The intersection of these two chronic conditions can lead to a cascade of symptoms that complicate clinical management and patient quality of life. In the case discussed by the authors, the interplay between these diseases presents unique challenges that warrant in-depth investigation.

The case in question involved a female patient already diagnosed with Type 1 diabetes who began to exhibit signs concerning for pseudoascites. This condition presents as an accumulation of fluid in the abdominal cavity but lacks the typical underlying causes such as liver cirrhosis or malignancy. Instead, pseudoascites in this patient was linked to the malabsorption issues commonly associated with celiac disease. Malabsorption can result in an imbalance of fluid dynamics in the body, leading to the misleading signs typically associated with genuine ascites. This distinction highlights the importance of accurate diagnosis in patients with complex autoimmune conditions.

In the clinical setting, the differentiation between pseudoascites and true ascites is crucial. Diagnostic imaging, such as ultrasound, often reveals fluid in the abdomen, but further evaluation is necessary to assess the underlying etiology. In this case, further investigation showed no signs of malignancy or liver dysfunction, steering the clinicians towards alternative diagnoses related to the patient’s existing celiac disease. This aspect of diagnostics emphasizes how a comprehensive understanding of a patient’s medical history can influence clinical decisions and treatment pathways.

One intriguing facet of this research is the implications it raises for clinical practice. It is not merely the presence of diabetes or celiac disease that warrants attention; rather, it is the understanding of how these conditions can interplay in unexpected ways, manifesting in symptoms that can baffle even experienced healthcare professionals. The need for heightened awareness of such complications reflects broader themes in chronic disease management, urging clinicians to maintain a holistic view of their patients’ health.

Treatment options for pseudoascites, particularly when caused by celiac disease, largely focus on dietary management. The cornerstone of therapy involves the strict adherence to a gluten-free diet, which serves to reduce inflammation in the intestines and allow for proper nutrient absorption. As the patient improves and malabsorption issues resolve, symptoms associated with pseudoascites can diminish significantly. This approach underscores the pivotal role nutrition plays in managing autoimmune conditions and the importance of multidisciplinary care models that integrate dietitians alongside medical professionals.

The authors also highlight the need for ongoing research in this area to better understand the mechanisms that drive the development of such atypical manifestations of celiac disease. Current literature primarily focuses on gastrointestinal symptoms; however, this study opens the door to a wider array of complications that may arise in the context of coexisting conditions. As the medical community advances its understanding of disease interactions, future studies should aim to unravel the complex web of pathophysiology that links diabetes and celiac disease.

In conclusion, this case study provides significant insight into the complexities of managing coexisting autoimmune disorders. It serves as a reminder that even experienced clinicians must constantly evolve their understanding of disease interaction and be alert to the myriad ways in which symptoms can present. For patients with Type 1 diabetes and celiac disease, recognizing and appropriately diagnosing pseudoascites could lead to more effective management strategies and improved quality of life. With continuing research, we can hope for more refined approaches that address the unique challenges posed by these overlapping health issues.

Understanding the intricate relationship between autoimmune diseases is essential for advancing medical knowledge and improving patient outcomes. As healthcare evolves, the importance of accurate diagnosis and personalized treatment plans continues to gain recognition within the broader medical context.

Ultimately, case reports such as this play a critical role in the medical literature, fueling discussions about patient care, diagnostics, and treatment protocols. The story of this patient encapsulates not only the difficulties faced by those with chronic illnesses but also the promising pathways that can emerge when research and clinical expertise align.

Subject of Research: Pseudoascites due to Celiac Disease in Type 1 Diabetes

Article Title: Pseudoascites Due to Celiac Disease in a Patient with Type 1 Diabetes

Article References:

Bell, D.S.H., Jerkins, T. Pseudoascites Due to Celiac Disease in a Patient with Type 1 Diabetes.
Diabetes Ther 16, 1525–1528 (2025). https://doi.org/10.1007/s13300-025-01744-5

Image Credits: AI Generated

DOI: https://doi.org/10.1007/s13300-025-01744-5

Keywords: Type 1 Diabetes, Celiac Disease, Pseudoascites, Autoimmune Disorders, Malabsorption, Diet Management, Chronic Illness, Patient Care, Gastrointestinal Disorders.