Home / Deep Research / Collagenous Sprue

Collagenous Sprue

Pathophysiology description

2026-01-19
Falcon MONDO:0044092 Model: Edison Scientific Literature 30 citations

Pathophysiology description Collagenous sprue (CS) is a rare enteropathy of the small intestine defined by villous atrophy with a thickened, irregular subepithelial collagen band (>10 μm) that may entrap capillaries and stromal cells, accompanied by intraepithelial lymphocytosis and lamina propria inflammation; endoscopically, diffuse villous blunting and scalloping may be seen, but diagnosis requires histology (trichrome) (mirakhor2021collagenousenteritis–analternative pages 1-3, moreno2024spruecolágenogastritis pages 1-2, moreno2024spruecolágenogastritis pages 4-5). Clinically, patients present with chronic watery diarrhea, profound weight loss, malabsorption, protein‑losing enteropathy, anemia, and hypoalbuminemia; CS often mimics celiac disease but typically shows negative celiac serology and poor response to a gluten‑free diet (mirakhor2021collagenousenteritis–analternative pages 1-3, moreno2024spruecolágenogastritis pages 1-2, mirakhor2021collagenousenteritis–analternative pages 3-4).

Core Pathophysiology - Primary mechanisms: (1) mucosal immune activation with increased intraepithelial lymphocytes (IELs) and lamina propria inflammation; (2) epithelial barrier injury with crypt apoptosis and tight‑junction perturbation; and (3) fibroblast/myofibroblast activation leading to excessive extracellular matrix (ECM) deposition and a diagnostic subepithelial collagen band, plausibly due to TGF‑β–driven profibrotic signaling together with an imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, zabana2022pathogenesisofmicroscopic pages 10-11, valatas2017stromalandimmune pages 3-4, xiao2009collagenousspruea pages 3-4). - Dysregulated pathways: Evidence (largely inferential and by analogy to collagenous colitis and intestinal fibrosis) supports roles for TGFB1 signaling, increased TIMP1 with relative reductions/restrictions in MMP1/9 activity, IL‑15/TNF‑α–associated IEL activation and epithelial apoptosis, and barrier protein disruption (ZO‑1/TJP1) (zabana2022pathogenesisofmicroscopic pages 10-11, burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, valatas2017stromalandimmune pages 3-4, xiao2009collagenousspruea pages 3-4). - Affected cellular processes: epithelial apoptosis and tight‑junction impairment; fibroblast→myofibroblast differentiation with α‑SMA expression and increased collagen I production; impaired fibrolysis due to MMP/TIMP imbalance; immune cell infiltration (IELs, plasma cells, eosinophils) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, valatas2017stromalandimmune pages 3-4, xiao2009collagenousspruea pages 3-4, moreno2024spruecolágenogastritis pages 4-5).

Recent developments and latest research (prioritize 2023–2024) - 2024 case‑based review emphasizes CS’s association with collagenous gastritis/colitis, autoimmune comorbidities, and severe complications (ulceration, perforation, lymphoma), while also noting some recent reports of favorable responses to immunosuppression (Spanish; full text with diagnostic details including the >10 μm band cutoff and entrapped capillaries) (Sep 2024, Acta Gastroenterológica Latinoamericana; https://doi.org/10.52787/agl.v54i3.383) (moreno2024spruecolágenogastritis pages 1-2, moreno2024spruecolágenogastritis pages 4-5, moreno2024spruecolágenogastritis pages 2-4). - 2024 case report of olmesartan‑induced collagenous sprue underscores medication‑triggered disease and rapid clinical improvement after drug withdrawal, reinforcing drug‑induced immune/injury mechanisms (Oct 2024, Cureus; https://doi.org/10.7759/cureus.72571) (goshgarian2024pathognomonicfeaturesof pages 1-2). - Ongoing synthesis from foundational studies continues to support immune‑mediated mechanisms including IEL activation, crypt apoptosis, and epithelial barrier protein alterations (ZO‑1/TJP1) in ARB enteropathy overlapping with CS (Human Pathology 2016; https://doi.org/10.1016/j.humpath.2015.12.001) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5).

Current applications and real‑world implementations - Diagnostic criteria and practice: Recognition that the collagen band threshold >10 μm with trichrome positivity and entrapped capillaries, paired with villous atrophy and intraepithelial lymphocytosis, is key for diagnosis; multi‑segment evaluation (stomach, colon) is advocated when CS is suspected (moreno2024spruecolágenogastritis pages 4-5, sharma2018collagenousgastritisa pages 1-2, mirakhor2021collagenousenteritis–analternative pages 3-4). - Medication review and withdrawal: Systematic collection of medication history, particularly ARBs such as olmesartan, PPIs, and NSAIDs, and prompt withdrawal in suspected drug‑induced cases; many patients exhibit clinical and histologic reversal within months (Mayo Clinic Proc 2012; Hum Pathol 2016) (rubiotapia2012severespruelikeenteropathy pages 5-7, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5). - Immunosuppression: Corticosteroids (including budesonide) remain first‑line in many reports; refractory cases may respond to thiopurines or TNF‑α inhibitors, though evidence derives from case series and case reports (mirakhor2021collagenousenteritis–analternative pages 3-4, xiao2009collagenousspruea pages 5-6).

Expert opinions and analysis from authoritative sources - Mayo Clinic series: Olmesartan‑associated sprue‑like enteropathy likely reflects a delayed cell‑mediated immune reaction in genetically predisposed patients (frequent HLA‑DQ2), with histologic overlap with CS (villous atrophy, IELs, collagen band); clinical and histologic recovery follows drug cessation (Aug 2012, Mayo Clinic Proceedings; https://doi.org/10.1016/j.mayocp.2012.06.003) (rubiotapia2012severespruelikeenteropathy pages 5-7, rubiotapia2012severespruelikeenteropathy pages 3-4). - Systematic review emphasis: Immune‑mediated injury plus epithelial barrier disruption (including reports of ZO‑1/TJP1 alterations) underlie ARB enteropathy; frequent collagen deposition links drug‑induced enteropathy to CS phenotype (Apr 2016, Human Pathology; https://doi.org/10.1016/j.humpath.2015.12.001) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 5-7, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5). - Intestinal fibrosis frameworks: In gut fibrosis, TGF‑β–driven myofibroblast activation, TIMP1 upregulation, and reduced MMP activity drive ECM accumulation—mechanisms broadly consistent with the collagen band in CS (Apr 2017, Annals of Gastroenterology; https://doi.org/10.20524/aog.2017.0146) (valatas2017stromalandimmune pages 3-4, valatas2017stromalandimmune pages 2-3).

Relevant statistics and data from recent studies - Demographics: Reported across ages 2–85 years with ~2:1 female predominance; many cases severe with marked weight loss and malnutrition (2021 summary; 2024 case review) (mirakhor2021collagenousenteritis–analternative pages 1-3, moreno2024spruecolágenogastritis pages 2-4). - Histologic thresholds: Normal subepithelial collagen band ~5–7 μm; cutoff >10 μm used to define CS; bands of 10–20 μm or more with entrapped capillaries and stromal cells are typical (2024 case review) (moreno2024spruecolágenogastritis pages 4-5). - Drug association prevalence: In early cohorts of olmesartan enteropathy, approximately one‑third of a CS cohort was exposed to olmesartan at or near diagnosis, and most improved after discontinuation (2012 Mayo Clinic Proceedings) (rubiotapia2012severespruelikeenteropathy pages 5-7).

Mechanistic model of disease progression - Initiation: Environmental/drug triggers (notably ARBs) or autoimmune milieu initiate mucosal immune activation; many patients lack celiac serology and fail gluten‑free diet, implicating alternative triggers (rubiotapia2012severespruelikeenteropathy pages 5-7, mirakhor2021collagenousenteritis–analternative pages 1-3). - Epithelial insult and immune activation: Increased IELs and cytokine signaling (e.g., IL‑15, TNF‑α, IL‑6) drive crypt epithelial apoptosis; barrier dysfunction is supported by reports of ZO‑1/TJP1 disruption (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5). - Stromal remodeling: TGF‑β–driven fibroblast→myofibroblast differentiation increases COL1A1 and TIMP1 with relatively reduced MMP1/9 activity, favoring ECM accumulation and subepithelial collagen band formation (zabana2022pathogenesisofmicroscopic pages 10-11, valatas2017stromalandimmune pages 3-4, xiao2009collagenousspruea pages 3-4). - Tissue architecture and clinical phenotype: Collagen band (>10 μm) entrapping capillaries/cells and villous atrophy produce severe malabsorption, protein‑losing enteropathy, and weight loss; multi‑segment involvement (gastritis/colitis) and complications (ulceration, perforation, lymphoma) may ensue (moreno2024spruecolágenogastritis pages 4-5, moreno2024spruecolágenogastritis pages 1-2, rubiotapia2012severespruelikeenteropathy pages 3-4).

Key Molecular Players - Genes/Proteins (HGNC): TGFB1 (TGF‑β1), MMP1, MMP9, TIMP1, COL1A1, TJP1 (ZO‑1), TNF (TNF‑α), IL15, IL6; HLA‑DQA1/DQB1 (HLA‑DQ2/8 susceptibility in drug‑induced SLE) (zabana2022pathogenesisofmicroscopic pages 10-11, burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, rubiotapia2012severespruelikeenteropathy pages 5-7, xiao2009collagenousspruea pages 3-4). - Chemical entities (CHEBI): glucocorticoids (budesonide), thiopurines (azathioprine/6‑thioguanine), anti‑TNF agents; olmesartan (ARB), NSAIDs and PPIs as potential modifiers/triggers (mirakhor2021collagenousenteritis–analternative pages 3-4, rubiotapia2012severespruelikeenteropathy pages 5-7, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5, moreno2024spruecolágenogastritis pages 4-5). - Cell types (CL): Intraepithelial lymphocytes (CD8+ IELs), enterocytes, lamina propria plasma cells/eosinophils, subepithelial myofibroblasts (α‑SMA+), fibroblasts (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, valatas2017stromalandimmune pages 3-4, moreno2024spruecolágenogastritis pages 4-5). - Anatomical locations (UBERON): Small intestinal mucosa (duodenum, jejunum), lamina propria (subepithelial region), with possible involvement of gastric and colonic mucosa (moreno2024spruecolágenogastritis pages 4-5, sharma2018collagenousgastritisa pages 1-2, moreno2024spruecolágenogastritis pages 1-2).

Biological Processes (GO annotation candidates) - ECM organization and collagen fibril organization; regulation of collagen biosynthetic process (TGFB1‑mediated) (valatas2017stromalandimmune pages 3-4, zabana2022pathogenesisofmicroscopic pages 10-11). - Regulation of proteolysis and extracellular matrix disassembly (MMP/TIMP balance) (zabana2022pathogenesisofmicroscopic pages 10-11, valatas2017stromalandimmune pages 2-3). - Epithelial cell apoptotic process and regulation of cell‑cell junction organization (TJP1/ZO‑1 alteration) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5). - T cell–mediated immune response; response to cytokines (IL‑15, TNF‑α, IL‑6) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5).

Cellular Components - Subepithelial lamina propria (site of collagen band); epithelial tight junctions (ZO‑1/TJP1); extracellular space/ECM; fibroblast stress fibers (α‑SMA cytoskeleton) (moreno2024spruecolágenogastritis pages 4-5, burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, valatas2017stromalandimmune pages 3-4).

Disease Progression - Sequence: trigger (often medication) → IEL‑driven/immune activation and epithelial apoptosis with barrier loss → TGF‑β–driven myofibroblast activation with net ECM accumulation (↑TIMP1/↓MMP) → subepithelial collagen band and villous atrophy → malabsorption/protein loss → complications (ulceration/perforation; occasional lymphoma) (rubiotapia2012severespruelikeenteropathy pages 5-7, zabana2022pathogenesisofmicroscopic pages 10-11, rubiotapia2012severespruelikeenteropathy pages 3-4, moreno2024spruecolágenogastritis pages 1-2). - Phases: (i) inflammatory/immune injury; (ii) fibrogenic remodeling; (iii) established collagen band with severe malabsorption; (iv) potential regression if drug withdrawn and/or immunosuppression, although course is heterogeneous (rubiotapia2012severespruelikeenteropathy pages 5-7, mirakhor2021collagenousenteritis–analternative pages 3-4, freeman2010updateoncollagenous pages 1-2).

Phenotypic Manifestations (HP terms) - Chronic diarrhea (HP:0002028), Weight loss (HP:0001824), Malabsorption (HP:0002242), Protein‑losing enteropathy (HP:0005226), Anemia (HP:0001903), Hypoalbuminemia (HP:0003073), Villous atrophy on small intestinal biopsy (HP:0011472) (mirakhor2021collagenousenteritis–analternative pages 1-3, moreno2024spruecolágenogastritis pages 4-5, mirakhor2021collagenousenteritis–analternative pages 3-4).

Cell type involvement (CL terms) - Intraepithelial lymphocyte, small intestine (CL:0009101); Intestinal epithelial cell (CL:0002563); Subepithelial myofibroblast (often annotated as intestinal myofibroblast; related: CL:0000186 fibroblast, with α‑SMA+ phenotype) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, valatas2017stromalandimmune pages 3-4).

Anatomical locations (UBERON terms) - Duodenum (UBERON:0002114), Jejunum (UBERON:0002115), Intestinal lamina propria (UBERON:0001982), Gastric mucosa (UBERON:0001275), Colonic mucosa (UBERON:0001155) (moreno2024spruecolágenogastritis pages 4-5, moreno2024spruecolágenogastritis pages 1-2, sharma2018collagenousgastritisa pages 1-2).

Chemical entities (CHEBI) - Olmesartan (CHEBI:7791), Nonsteroidal anti‑inflammatory drug (CHEBI:35475), Proton pump inhibitor (CHEBI:50784), Budesonide (CHEBI:3160), Azathioprine (CHEBI:2955), 6‑Thioguanine (CHEBI:9565), Infliximab/adalimumab (anti‑TNF biologics; protein therapeutics) (rubiotapia2012severespruelikeenteropathy pages 5-7, mirakhor2021collagenousenteritis–analternative pages 3-4, moreno2024spruecolágenogastritis pages 4-5).

Evidence items with PMIDs/DOIs/URLs and quotes - “Collagenous sprue … characterized by … villous atrophy and a thick subepithelial collagen band … diagnosis requires endoscopy with biopsy.” (2021; source includes endoscopic and histologic description) (mirakhor2021collagenousenteritis–analternative pages 1-3). - “A normal subepithelial collagen band is 5–7 μm … a diagnostic cutoff … >10 μm … with entrapped capillaries and stromal cells … Masson trichrome positive.” (Sep 2024; Acta Gastroenterol Latinoam; https://doi.org/10.52787/agl.v54i3.383) (moreno2024spruecolágenogastritis pages 4-5). - “Olmesartan‑associated sprue‑like enteropathy … mediated primarily by a delayed, cell‑mediated immune mechanism … TGF‑β perturbation hypothesized … high prevalence of HLA‑DQ2 among cases … histology shows villous atrophy … in some cases collagen deposition … recovery after stopping olmesartan.” (Aug 2012; Mayo Clin Proc; https://doi.org/10.1016/j.mayocp.2012.06.003) (rubiotapia2012severespruelikeenteropathy pages 5-7, rubiotapia2012severespruelikeenteropathy pages 3-4). - “Proposed roles for IL‑15 signaling and disruption of tight junction protein ZO‑1, implying both immune activation and epithelial barrier dysfunction … frequent increase in subepithelial collagen … overlap with autoimmune enteropathy … reverses after cessation of olmesartan.” (Apr 2016; Hum Pathol; https://doi.org/10.1016/j.humpath.2015.12.001) (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5). - “ECM accumulation in collagenous enteropathy likely reflects increased collagen I synthesis and impaired degradation via MMP/TIMP imbalance; TGFB1, TIMP1 upregulated with restricted MMP1/9 activity.” (Jul 2022; J Crohn’s & Colitis; https://doi.org/10.1093/ecco-jcc/jjab123) (zabana2022pathogenesisofmicroscopic pages 10-11); supported by gut fibrosis frameworks (Apr 2017; Ann Gastroenterol; https://doi.org/10.20524/aog.2017.0146) (valatas2017stromalandimmune pages 3-4). - Complications: reports of ulceration, perforation, and lymphoma associations in CS (Sep 2009; WJG; https://doi.org/10.3748/wjg.15.4446) and 2024 review (rubiotapia2012severespruelikeenteropathy pages 3-4, moreno2024spruecolágenogastritis pages 1-2).

Embedded artifact | Mechanism / Process | Key molecules / genes (HGNC) | Cell types (CL) | Tissue / Anatomy (UBERON) | Evidence summary (1–2 sentences) | Strongest recent/landmark sources (year, journal, URL) with context IDs | |---|---|---|---|---|---| | Subepithelial collagen band formation: MMP/TIMP imbalance & TGF-β signaling | TGFB1, MMP1, MMP9, TIMP1, COL1A1 | Myofibroblasts (α-SMA+), fibroblasts, fibrocytes | Small intestinal mucosa (duodenum/jejunum) lamina propria | Reports show increased collagen I synthesis with upregulated TGFB1 and TIMP1 and relatively reduced MMP activity, producing diagnostic >10 μm subepithelial collagen bands and steroid-responsive fibrosis. | Zabana Y et al., 2022, J Crohn's & Colitis; https://doi.org/10.1093/ecco-jcc/jjab123 (zabana2022pathogenesisofmicroscopic pages 10-11); Valatas V et al., 2017, Ann Gastroenterol; https://doi.org/10.20524/aog.2017.0146 (valatas2017stromalandimmune pages 3-4); Xiao Z et al., 2009 (xiao2009collagenousspruea pages 3-4) | | Intraepithelial lymphocytosis & mucosal immune activation; IL-15 / TNF-α with epithelial apoptosis & barrier (ZO-1/TJP1) disruption | IL15, TNF (TNF), IFNG, IL6, TJP1 (ZO-1) | Intraepithelial lymphocytes (IELs; CD8+), enterocytes, antigen-presenting cells | Small intestinal epithelium (duodenal mucosa) | Many cases show increased IELs and cytokine-driven epithelial injury (crypt apoptosis) and reports of tight-junction (ZO-1/TJP1) disruption, linking immune activation to barrier loss and enteropathy. | Rubio-Tapia A et al., 2012, Mayo Clin Proc; https://doi.org/10.1016/j.mayocp.2012.06.003 (rubiotapia2012severespruelikeenteropathy pages 5-7); Burbure N et al., 2016, Hum Pathol; https://doi.org/10.1016/j.humpath.2015.12.001 (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3); Mirakhor E et al., 2021 (mirakhor2021collagenousenteritis–analternative pages 1-3) | | Drug-induced (olmesartan) immune-mediated sprue-like enteropathy progressing to collagenous sprue | AGTR1, TGFB1, HLA-DQA1 / HLA-DQB1 (HLA-DQ2/8 associated) | CD4+ / CD8+ T cells, IELs, myofibroblasts | Small intestine (duodenum/jejunum); possible multi-segment involvement (stomach, colon) | Case series link olmesartan exposure to severe villous atrophy with IELs and frequent subepithelial collagen; clinical and histologic reversal after drug cessation supports a drug-triggered immune/injury mechanism with fibrotic remodeling in susceptible patients. | Rubio-Tapia A et al., 2012, Mayo Clin Proc; https://doi.org/10.1016/j.mayocp.2012.06.003 (rubiotapia2012severespruelikeenteropathy pages 5-7); Burbure N et al., 2016, Hum Pathol; https://doi.org/10.1016/j.humpath.2015.12.001 (burbure2016olmesartanassociatedspruelikeenteropathy pages 7-8); Goshgarian MA et al., 2024, Cureus; https://doi.org/10.7759/cureus.72571 (goshgarian2024pathognomonicfeaturesof pages 1-2) | | Myofibroblast activation (α-SMA+) and ECM overproduction in gut fibrosis | ACTA2 (α-SMA), TGFB1, PDGFA/PDGFR, CTGF, IL17A | Subepithelial myofibroblasts (α-SMA+), fibroblasts, recruited circulating fibrocytes | Lamina propria of small intestine (jejunal/duodenal mucosa) | TGF-β and proinflammatory cytokines drive fibroblast-to-myofibroblast differentiation, upregulate collagen/fibronectin and TIMP1, and reduce fibrolysis, producing persistent ECM accumulation in fibrotic/ collagenous lesions. | Valatas V et al., 2017, Ann Gastroenterol; https://doi.org/10.20524/aog.2017.0146 (valatas2017stromalandimmune pages 3-4); related experimental/ECM studies summarized in systematic reviews (valatas2017stromalandimmune pages 2-3) | | Multisegment collagenous gastroenteritides (gastritis/colitis associations) and complications (ulceration, perforation, lymphoma) | COL1A1, COL3A1, COL5A1, MMP/TIMP axes, TGFB1; IgG4 (plasma cell phenotype reported) | Plasma cells (IgG4+ in some series), IELs, lamina propria inflammatory cells | Stomach (gastric mucosa), small intestine, colon | Case series document collagen deposition across gastric, small-bowel and colonic sites (collagenous gastritis/enteritis/colitis) with clinical complications including ulceration, perforation, and reported associations with intestinal lymphoma in select cohorts. | Moreno ML et al., 2024, Acta Gastroenterol Lat Am; https://doi.org/10.52787/agl.v54i3.383 (moreno2024spruecolágenogastritis pages 1-2); Freeman HJ, 2010, World J Gastroenterol; https://doi.org/10.3748/wjg.v16.i3.296 (freeman2010updateoncollagenous pages 1-2); Freeman & Webber, 2009 (free perforation) (rubiotapia2012severespruelikeenteropathy pages 3-4) |

Table: Concise mechanistic evidence mapping for collagenous sprue: lists processes, genes/proteins, cell/tissue context, short evidence summaries, and landmark citations (with URLs and context IDs) to support ontology annotation and further research.

Notes and limitations - Collagenous sprue remains rare; mechanistic evidence is drawn from case series/case reports, fibrotic gut biology, and microscopic colitis analogies. Prospective molecular profiling in CS is limited; proposed pathways (IL‑15/TJP1, TGFB1/MMP/TIMP) reflect best current evidence and related disease models (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3, zabana2022pathogenesisofmicroscopic pages 10-11, valatas2017stromalandimmune pages 3-4).

References

  1. (mirakhor2021collagenousenteritis–analternative pages 1-3): E Mirakhor, J Choe, and RI Goodman. Collagenous enteritis–an alternative cause of malabsorptive enteropathy. Unknown journal, 2021.

  2. (moreno2024spruecolágenogastritis pages 1-2): María Laura Moreno, Ezequiel Balaban, Sofía Laudanno, Ignacio Brichta, Ana Florencia Costa, Carla Wassner, Nadia Kujta, Mauricio Paternó, Mariana Rizzolo, and Mirta Kujaruk. Sprue colágeno, gastritis colágena y una asociación infrecuente con enfermedad inflamatoria intestinal. reporte de un caso. Acta Gastroenterológica Latinoamericana, 54:278-286, Sep 2024. URL: https://doi.org/10.52787/agl.v54i3.383, doi:10.52787/agl.v54i3.383. This article has 0 citations.

  3. (moreno2024spruecolágenogastritis pages 4-5): María Laura Moreno, Ezequiel Balaban, Sofía Laudanno, Ignacio Brichta, Ana Florencia Costa, Carla Wassner, Nadia Kujta, Mauricio Paternó, Mariana Rizzolo, and Mirta Kujaruk. Sprue colágeno, gastritis colágena y una asociación infrecuente con enfermedad inflamatoria intestinal. reporte de un caso. Acta Gastroenterológica Latinoamericana, 54:278-286, Sep 2024. URL: https://doi.org/10.52787/agl.v54i3.383, doi:10.52787/agl.v54i3.383. This article has 0 citations.

  4. (mirakhor2021collagenousenteritis–analternative pages 3-4): E Mirakhor, J Choe, and RI Goodman. Collagenous enteritis–an alternative cause of malabsorptive enteropathy. Unknown journal, 2021.

  5. (burbure2016olmesartanassociatedspruelikeenteropathy pages 1-3): Nina Burbure, Benjamin Lebwohl, Carolina Arguelles-Grande, Peter H.R. Green, Govind Bhagat, and Stephen Lagana. Olmesartan-associated sprue-like enteropathy: a systematic review with emphasis on histopathology. Human pathology, 50:127-34, Apr 2016. URL: https://doi.org/10.1016/j.humpath.2015.12.001, doi:10.1016/j.humpath.2015.12.001. This article has 122 citations and is from a peer-reviewed journal.

  6. (zabana2022pathogenesisofmicroscopic pages 10-11): Yamile Zabana, Gian Tontini, Elisabeth Hultgren-Hörnquist, Karolina Skonieczna-Żydecka, Giovanni Latella, Ann Elisabeth Østvik, Wojciech Marlicz, Mauro D’Amato, Angel Arias, Stephan Miehlke, Andreas Münch, Fernando Fernández-Bañares, and Alfredo J Lucendo. Pathogenesis of microscopic colitis: a systematic review. Journal of Crohn's & colitis, 16:143-161, Jul 2022. URL: https://doi.org/10.1093/ecco-jcc/jjab123, doi:10.1093/ecco-jcc/jjab123. This article has 35 citations.

  7. (valatas2017stromalandimmune pages 3-4): V. Valatas, E. Filidou, I. Drygiannakis, and G. Kolios. Stromal and immune cells in gut fibrosis: the myofibroblast and the scarface. Annals of Gastroenterology, 30:393-404, Apr 2017. URL: https://doi.org/10.20524/aog.2017.0146, doi:10.20524/aog.2017.0146. This article has 80 citations.

  8. (xiao2009collagenousspruea pages 3-4): Z Xiao, VM Dasari, DF Kirby, and M Bronner. Collagenous sprue: a case report and literature review. Unknown journal, 2009.

  9. (moreno2024spruecolágenogastritis pages 2-4): María Laura Moreno, Ezequiel Balaban, Sofía Laudanno, Ignacio Brichta, Ana Florencia Costa, Carla Wassner, Nadia Kujta, Mauricio Paternó, Mariana Rizzolo, and Mirta Kujaruk. Sprue colágeno, gastritis colágena y una asociación infrecuente con enfermedad inflamatoria intestinal. reporte de un caso. Acta Gastroenterológica Latinoamericana, 54:278-286, Sep 2024. URL: https://doi.org/10.52787/agl.v54i3.383, doi:10.52787/agl.v54i3.383. This article has 0 citations.

  10. (goshgarian2024pathognomonicfeaturesof pages 1-2): McKennah A Goshgarian, Jeffrey Laczek, and Michael Lustberg. Pathognomonic features of olmesartan-induced collagenous sprue resulting in severe small bowel malabsorption. Cureus, Oct 2024. URL: https://doi.org/10.7759/cureus.72571, doi:10.7759/cureus.72571. This article has 0 citations and is from a poor quality or predatory journal.

  11. (burbure2016olmesartanassociatedspruelikeenteropathy pages 3-5): Nina Burbure, Benjamin Lebwohl, Carolina Arguelles-Grande, Peter H.R. Green, Govind Bhagat, and Stephen Lagana. Olmesartan-associated sprue-like enteropathy: a systematic review with emphasis on histopathology. Human pathology, 50:127-34, Apr 2016. URL: https://doi.org/10.1016/j.humpath.2015.12.001, doi:10.1016/j.humpath.2015.12.001. This article has 122 citations and is from a peer-reviewed journal.

  12. (sharma2018collagenousgastritisa pages 1-2): Prabin Sharma, Andrea Barbieri, and Amir Masoud. Collagenous gastritis: a case report and literature review. Journal of Natural Science, Biology and Medicine, 9:285-287, Jul 2018. URL: https://doi.org/10.4103/jnsbm.jnsbm_184_17, doi:10.4103/jnsbm.jnsbm_184_17. This article has 6 citations.

  13. (rubiotapia2012severespruelikeenteropathy pages 5-7): Alberto Rubio-Tapia, Margot L. Herman, Jonas F. Ludvigsson, Darlene G. Kelly, Thomas F. Mangan, Tsung-Teh Wu, and Joseph A. Murray. Severe spruelike enteropathy associated with olmesartan. Mayo Clinic proceedings, 87 8:732-8, Aug 2012. URL: https://doi.org/10.1016/j.mayocp.2012.06.003, doi:10.1016/j.mayocp.2012.06.003. This article has 527 citations and is from a domain leading peer-reviewed journal.

  14. (xiao2009collagenousspruea pages 5-6): Z Xiao, VM Dasari, DF Kirby, and M Bronner. Collagenous sprue: a case report and literature review. Unknown journal, 2009.

  15. (rubiotapia2012severespruelikeenteropathy pages 3-4): Alberto Rubio-Tapia, Margot L. Herman, Jonas F. Ludvigsson, Darlene G. Kelly, Thomas F. Mangan, Tsung-Teh Wu, and Joseph A. Murray. Severe spruelike enteropathy associated with olmesartan. Mayo Clinic proceedings, 87 8:732-8, Aug 2012. URL: https://doi.org/10.1016/j.mayocp.2012.06.003, doi:10.1016/j.mayocp.2012.06.003. This article has 527 citations and is from a domain leading peer-reviewed journal.

  16. (burbure2016olmesartanassociatedspruelikeenteropathy pages 5-7): Nina Burbure, Benjamin Lebwohl, Carolina Arguelles-Grande, Peter H.R. Green, Govind Bhagat, and Stephen Lagana. Olmesartan-associated sprue-like enteropathy: a systematic review with emphasis on histopathology. Human pathology, 50:127-34, Apr 2016. URL: https://doi.org/10.1016/j.humpath.2015.12.001, doi:10.1016/j.humpath.2015.12.001. This article has 122 citations and is from a peer-reviewed journal.

  17. (valatas2017stromalandimmune pages 2-3): V. Valatas, E. Filidou, I. Drygiannakis, and G. Kolios. Stromal and immune cells in gut fibrosis: the myofibroblast and the scarface. Annals of Gastroenterology, 30:393-404, Apr 2017. URL: https://doi.org/10.20524/aog.2017.0146, doi:10.20524/aog.2017.0146. This article has 80 citations.

  18. (freeman2010updateoncollagenous pages 1-2): Hugh James Freeman. Update on collagenous sprue. World journal of gastroenterology, 16 3:296-8, Jan 2010. URL: https://doi.org/10.3748/wjg.v16.i3.296, doi:10.3748/wjg.v16.i3.296. This article has 15 citations and is from a poor quality or predatory journal.

  19. (burbure2016olmesartanassociatedspruelikeenteropathy pages 7-8): Nina Burbure, Benjamin Lebwohl, Carolina Arguelles-Grande, Peter H.R. Green, Govind Bhagat, and Stephen Lagana. Olmesartan-associated sprue-like enteropathy: a systematic review with emphasis on histopathology. Human pathology, 50:127-34, Apr 2016. URL: https://doi.org/10.1016/j.humpath.2015.12.001, doi:10.1016/j.humpath.2015.12.001. This article has 122 citations and is from a peer-reviewed journal.