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Lane Hamilton Syndrome

Pathophysiology description

2026-01-19
Falcon MONDO:0800124 Model: Edison Scientific Literature 15 citations

Pathophysiology description Lane-Hamilton syndrome is the coexistence of celiac disease (CD) and idiopathic pulmonary hemosiderosis (IPH), presenting as diffuse alveolar hemorrhage (DAH) with iron-deficiency anemia and pulmonary infiltrates. Histopathology in IPH shows recent/prior alveolar hemorrhage, abundant hemosiderin-laden macrophages (HLM), type II pneumocyte hyperplasia, and classically lacks capillaritis, immune complex deposition, or frank vasculitis (suggesting a non-vasculitic, immune-mediated permeability mechanism) (saha2022comparativeanalysisof pages 1-2). Proposed mechanisms for LHS emphasize an immune-mediated link between gluten-triggered small-intestinal autoimmunity and pulmonary microvascular leak: mediators such as histamine, eosinophil cationic protein, and VEGF may increase pulmonary capillary endothelial gaps, permitting erythrocyte extravasation into alveoli without structural vascular damage (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). Recurrent alveolar bleeding results in local iron/heme overload with oxidative injury and may drive fibrotic remodeling and progressive respiratory compromise over time (saha2022comparativeanalysisof pages 1-2).

A key clinical hallmark is that gastrointestinal symptoms may be absent in adult LHS, so a high index of suspicion and active screening for CD in IPH are recommended. As summarized, “Less than 20% of patients complained of any significant GI symptoms,” and serologic testing with anti‑tTG/endomysial antibodies (with IgG-based assays if IgA deficient) followed by small-bowel biopsy if positive is advised (saha2022comparativeanalysisof pages 10-11). Clinical improvement with strict gluten-free diet (GFD) is frequent; relapses often follow dietary nonadherence, underscoring a mechanistic celiac–lung link (saha2022comparativeanalysisof pages 9-10, aksu2024diettreatablecauseof pages 1-2).

Recent developments (2023–2024) - 2023 adult case: LHS in a patient with Down syndrome (increased baseline CD risk) required corticosteroids when GFD alone was insufficient; BAL demonstrated numerous macrophages, and duodenal biopsy confirmed Marsh IIIb CD lesions (Cureus, Jan 2023; DOI: https://doi.org/10.7759/cureus.33385) (fontes2023lanehamiltonsyndromein pages 3-5, fontes2023lanehamiltonsyndromein pages 5-6). - 2024 case: “Diet-treatable cause of hemoptysis” highlights remission on GFD with fatal relapse after noncompliance, reinforcing causality and the centrality of dietary intervention (Respiratory Case Reports, Jan 2024; DOI: https://doi.org/10.5505/respircase.2024.73604) (aksu2024diettreatablecauseof pages 1-2). - Recent systematic review (1971–2022) provides quantitative adult data and mechanistic synthesis, now informing current practice, including screening recommendations and relative outcomes with GFD versus steroids (Cureus, Mar 2022; DOI: https://doi.org/10.7759/cureus.23482) (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11).

Core Pathophysiology - Primary mechanisms: immune-mediated increase in pulmonary microvascular permeability (endothelial gap formation) leading to DAH; absence of vasculitis on histology typical of IPH; recurrent hemorrhage produces iron/heme-driven oxidative injury and subsequent epithelial repair with type II pneumocyte hyperplasia (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Dysregulated molecular pathways: mediator-driven vascular permeability (histamine, eosinophil cationic protein, VEGF); failure of vascular barrier function without immune complex deposition; oxidative stress pathways from heme/iron overload in alveolar space (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10). - Affected cellular processes: erythrocyte extravasation into alveoli; macrophage phagocytosis of RBC/heme and conversion to HLM; epithelial injury/repair (type II pneumocyte hyperplasia); chronic iron deposition and potential fibrogenic remodeling (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 7-8).

Key Molecular Players - Genes/Proteins (HGNC): - TGM2 (tissue transglutaminase, TG2): autoantigen in CD; anti‑tTG antibody serology recommended in IPH screening (saha2022comparativeanalysisof pages 10-11). - VEGFA (VEGF): permeability mediator implicated in proposed LHS pathogenesis (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Chemical Entities (CHEBI): - Gluten: environmental trigger of CD; GFD frequently induces pulmonary remission; relapse with nonadherence (aksu2024diettreatablecauseof pages 1-2, saha2022comparativeanalysisof pages 9-10). - Histamine and eosinophil cationic protein: mediators increasing endothelial permeability (saha2022comparativeanalysisof pages 9-10). - Iron, heme, hemosiderin: drivers and markers of oxidative injury; HLM indicate prior hemorrhage (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 7-8). - Cell Types (CL): - Alveolar macrophages (HLM in BAL/biopsy) (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2). - Pulmonary capillary endothelial cells (site of increased permeability) (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Eosinophils/basophils and T lymphocytes (immune effectors implicated in mediator release and systemic autoimmunity in CD) (saha2022comparativeanalysisof pages 10-11, fontes2023lanehamiltonsyndromein pages 3-5). - Type II pneumocytes (hyperplasia in repair) (saha2022comparativeanalysisof pages 1-2). - Anatomical Locations (UBERON): - Alveolar lumen/epithelium and pulmonary capillaries: hemorrhage and permeability sites (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10). - Small intestine/duodenum: CD histology (villous atrophy, crypt hyperplasia, intraepithelial lymphocytosis) (fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 7-8).

Biological Processes (GO annotations; evidence-linked) - Regulation of vascular permeability (GO:0043114): mediator-induced endothelial gap formation enabling DAH (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Inflammatory response (GO:0006954) and leukocyte activation (GO:0002367): immune effector involvement (eosinophils, T cells) (saha2022comparativeanalysisof pages 10-11, fontes2023lanehamiltonsyndromein pages 3-5). - Heme catabolic process (GO:0006785) and iron ion homeostasis (GO:0055072): handling of alveolar heme/iron in hemorrhage (saha2022comparativeanalysisof pages 1-2). - Response to oxidative stress (GO:0006979) and reactive oxygen species metabolic process (GO:0072593): iron/heme-induced oxidative injury (saha2022comparativeanalysisof pages 1-2). - Epithelium regeneration (GO:0060574)/epithelial cell proliferation (GO:0050673): type II pneumocyte hyperplasia after injury (saha2022comparativeanalysisof pages 1-2).

Cellular Components (GO components) - Extracellular space (GO:0005615) and alveolar lumen (UBERON): RBCs and mediators accumulate during DAH (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2). - Plasma membrane of capillary endothelial cells (GO:0005901) and endothelial cell–cell junction (GO:0005911): increased permeability sites (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Basement membrane (GO:0005604) adjacent to alveolar epithelium: typically no immune-complex–mediated damage reported in IPH histology (saha2022comparativeanalysisof pages 1-2).

Disease Progression - Trigger: gluten ingestion drives CD autoimmunity in a genetically predisposed host; systemic immune activation and mediators hypothesized to act on pulmonary microvasculature (saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 9-10). - Early pulmonary events: increased endothelial permeability with RBC extravasation → DAH; radiologic ground-glass opacities; anemia may precede overt hemoptysis (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 10-11). - Chronic stage: recurrent hemorrhage → alveolar iron/heme overload → oxidative injury; type II pneumocyte hyperplasia; potential fibrosis and respiratory impairment (saha2022comparativeanalysisof pages 1-2). - Modifiers: absence of GI symptoms common; relapse with GFD nonadherence; steroids/immunosuppressants may be required if GFD alone insufficient (saha2022comparativeanalysisof pages 10-11, aksu2024diettreatablecauseof pages 1-2, fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 7-8).

Phenotypic Manifestations (HPO) - Diffuse alveolar hemorrhage (HP:0032443): core pulmonary process (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2). - Hemoptysis (HP:0002105) and dyspnea (HP:0002094): pulmonary symptoms; hemoptysis may be absent in children (aksu2024diettreatablecauseof pages 1-2, saha2022comparativeanalysisof pages 7-8). - Iron-deficiency anemia (HP:0001892): near-universal in LHS adult series; “All patients with LHS in our study suffered from anemia” (saha2022comparativeanalysisof pages 10-11). - Ground-glass opacities on chest imaging (HP:0025179): typical radiologic correlate of DAH (saha2022comparativeanalysisof pages 7-8). - Malabsorption/diarrhea/weight loss (HP:0002242/HP:0002014/HP:0004325): variable; GI symptoms often absent in adult LHS (fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 10-11).

Current applications and real-world implementations - Diagnostic implementation: For any IPH/DAH of unclear cause, screen for CD with anti‑tTG/endomysial antibodies (with IgG-based testing if IgA deficient). Proceed to small-intestinal biopsy if positive. BAL for HLM supports IPH; lung biopsy rarely required but remains gold standard when diagnosis uncertain (saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 7-8, fontes2023lanehamiltonsyndromein pages 5-6). - Treatment: Strict, lifelong GFD is foundational; many LHS cases remit on GFD alone. Systemic corticosteroids are commonly used during acute DAH or when GFD alone is insufficient; steroid-sparing agents (e.g., azathioprine) have been used in selected cases (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 7-8, fontes2023lanehamiltonsyndromein pages 3-5, aksu2024diettreatablecauseof pages 1-2). Nonadherence to GFD is a common cause of relapse and can be fatal (aksu2024diettreatablecauseof pages 1-2).

Expert opinions and analysis from authoritative sources - Systematic review recommendation: given frequent absence of GI symptoms and a substantial co-prevalence, “serologic testing for CD in all patients diagnosed with IPH” is recommended (Cureus, 2022; https://doi.org/10.7759/cureus.23482) (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 10-11). - Mechanistic stance: IPH/LHS likely represents an “immune-mediated pulmonary hemosiderosis,” with permeability increase mediated by inflammatory mediators rather than classic vasculitis (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11).

Relevant statistics and data - Adult LHS proportion among reported IPH: ~25% (16/65 adults) overall in the 1971–2022 literature; among those specifically tested, up to 59% seropositive for CD antibodies (Cureus, 2022; https://doi.org/10.7759/cureus.23482) (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10). - Treatment patterns and outcomes: corticosteroids used in ~95% of IPH/LHS as first-line for acute management, but 60% of LHS patients could be discharged on GFD alone without steroids; recurrence lower in LHS cohort vs IPH-only, with multiple relapses occurring off GFD; mortality 21.3% in IPH-only cohort vs 0% in LHS at follow-up in the reviewed adult literature (Cureus, 2022; https://doi.org/10.7759/cureus.23482) (saha2022comparativeanalysisof pages 9-10). - Case-level evidence of GFD dependence: remission with GFD and relapse (including fatal outcome) with noncompliance (Respiratory Case Reports, 2024; https://doi.org/10.5505/respircase.2024.73604) (aksu2024diettreatablecauseof pages 1-2).

Gene/protein annotations with ontology terms (HGNC, GO) - TGM2 (HGNC:11777; tissue transglutaminase): autoantigen targeted by anti‑tTG antibodies used for CD screening in IPH/LHS evaluation (processes: antigen processing/presentation; GO:0019882; immune response GO:0006955) (saha2022comparativeanalysisof pages 10-11). - VEGFA (HGNC:12680): mediator of vascular permeability (GO:0043114) implicated in proposed LHS mechanisms (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - Processes linked: inflammatory response (GO:0006954), regulation of vascular permeability (GO:0043114), heme catabolic process (GO:0006785), response to oxidative stress (GO:0006979), iron ion homeostasis (GO:0055072) (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10).

Cell type involvement (CL terms) - CL: alveolar macrophage (HLM): sentinel of prior hemorrhage (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2). - CL: endothelial cell (pulmonary capillary): permeability changes (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11). - CL: eosinophil/basophil; CL: T cell: inflammatory mediator sources/immune effectors (saha2022comparativeanalysisof pages 10-11, fontes2023lanehamiltonsyndromein pages 3-5). - CL: alveolar type 2 cell: hyperplasia after injury (saha2022comparativeanalysisof pages 1-2).

Anatomical locations (UBERON) - UBERON: alveolar lumen/epithelium; UBERON: capillary (pulmonary): hemorrhage site (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10). - UBERON: small intestine/duodenum: primary CD pathology (fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 7-8).

Chemical entities (CHEBI) - CHEBI: gluten, histamine, eosinophil cationic protein, iron, heme, hemosiderin: mediators/triggers or injury products central to LHS pathophysiology (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 7-8, aksu2024diettreatablecauseof pages 1-2).

Evidence items with PMIDs/DOIs/URLs - Saha BK et al. Comparative analysis of adult patients with IPH and LHS. Cureus. Mar 2022. DOI: 10.7759/cureus.23482. URL: https://doi.org/10.7759/cureus.23482 (mechanisms, statistics, screening recommendations, outcomes) (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 13-14). - Fontes J et al. Lane-Hamilton syndrome in an adult with Down syndrome: a case report. Cureus. Jan 2023. DOI: 10.7759/cureus.33385. URL: https://doi.org/10.7759/cureus.33385 (adult case; diagnostics; need for steroids) (fontes2023lanehamiltonsyndromein pages 3-5, fontes2023lanehamiltonsyndromein pages 5-6). - Aksu EA et al. Diet-treatable cause of hemoptysis: Lane Hamilton syndrome. Respiratory Case Reports. Jan 2024. DOI: 10.5505/respircase.2024.73604. URL: https://doi.org/10.5505/respircase.2024.73604 (GFD dependence; relapse with nonadherence; clinical emphasis) (aksu2024diettreatablecauseof pages 1-2). - Chakravarty A et al. Lane-Hamilton syndrome with respiratory failure: a case report. Int J Clin Pediatr. Jul 2020. DOI: 10.14740/ijcp379. URL: https://doi.org/10.14740/ijcp379 (pediatric case; triad; diagnostic principles) (saha2022comparativeanalysisof pages 7-8).

Lane-Hamilton key annotations | Category | Entity (preferred name) | Ontology ID (HGNC/GO/CL/UBERON/CHEBI as appropriate) | Role / Mechanistic note | Evidence | |---|---|---|---|---| | Gene / Protein | Tissue transglutaminase (TG2 / TGM2) | HGNC:TGM2 | Autoantigen in celiac disease; target of anti-tTG antibodies linking intestinal autoimmunity to extraintestinal manifestations | (saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 7-8) | | Antibody / Biomarker | Endomysial / anti-tTG antibodies | Antibody:anti-tTG/EMA | Serologic markers used to screen for celiac disease in patients with IPH/LHS | (saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 9-10) | | Antibody / Biomarker | Deamidated gliadin peptide IgA (DGP IgA) | CHEBI:deamidated_gliadin_peptide | Serologic marker for celiac disease; reported positive in LHS case reports | (fontes2023lanehamiltonsyndromein pages 3-5) | | Mediator | Histamine | CHEBI:histamine | Increases capillary permeability; hypothesized to contribute to pulmonary capillary endothelial gap formation and RBC extravasation | (saha2022comparativeanalysisof pages 9-10) | | Mediator | Eosinophil cationic protein (ECP) | CHEBI:eosinophil_cationic_protein | Eosinophil-derived mediator implicated in increasing endothelial permeability in proposed LHS pathogenesis | (saha2022comparativeanalysisof pages 9-10) | | Mediator / Growth factor | Vascular endothelial growth factor (VEGF) | HGNC:VEGFA | Increases vascular permeability; proposed contributor to alveolar hemorrhage in immune-mediated models | (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11) | | Cell type | Alveolar macrophage | CL:alveolar_macrophage | Phagocytose erythrocytes/heme → become hemosiderin-laden macrophages (HLM); HLM presence indicates prior alveolar bleeding | (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2) | | Cell type | Eosinophil | CL:eosinophil | Immune effector releasing cationic proteins and mediators that may increase vascular permeability | (saha2022comparativeanalysisof pages 10-11, saha2022comparativeanalysisof pages 9-10) | | Cell type | Basophil | CL:basophil | Source of histamine and other mediators that can affect capillary permeability | (saha2022comparativeanalysisof pages 10-11) | | Cell type | T lymphocyte | CL:T_cell | Central to gluten-driven intestinal immune response; systemic T-cell–mediated autoimmunity hypothesized to link CD to lung involvement | (saha2022comparativeanalysisof pages 7-8, fontes2023lanehamiltonsyndromein pages 3-5) | | Cell type | Type II pneumocyte (alveolar type 2 cell) | CL:alveolar_type_2_cell | Hyperplasia observed in IPH histology after alveolar injury; involved in epithelial repair | (saha2022comparativeanalysisof pages 1-2) | | Cell type | Pulmonary capillary endothelial cell | CL:endothelial_cell | Site where increased endothelial gaps/permeability permit RBC extravasation into alveolar spaces in proposed mechanisms | (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 10-11) | | Anatomical site | Alveolar lumen | UBERON:alveolar_lumen | Lumenal space where RBCs accumulate and are cleared by macrophages forming HLM; radiologic ground-glass opacities reflect alveolar filling | (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2) | | Anatomical site | Alveolar epithelium | UBERON:alveolar_epithelium | Site of epithelial injury and type II pneumocyte hyperplasia in IPH histopathology | (saha2022comparativeanalysisof pages 1-2) | | Anatomical site | Pulmonary capillary | UBERON:capillary | Microvascular bed implicated in leakage/hemorrhage without frank vasculitis in LHS proposed models | (saha2022comparativeanalysisof pages 9-10) | | Anatomical site | Small intestine / Duodenum | UBERON:small_intestine; UBERON:duodenum | Primary site of gluten-triggered immune activation (villous atrophy) that defines celiac disease and is temporally linked to pulmonary manifestations in LHS | (fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 7-8) | | Chemical entity | Gluten | CHEBI:gluten | Environmental trigger of celiac disease; gluten-free diet (GFD) leads to clinical improvement or remission of pulmonary hemorrhage in many LHS reports | (saha2022comparativeanalysisof pages 7-8, aksu2024diettreatablecauseof pages 1-2) | | Chemical entity | Iron | CHEBI:iron | Local iron overload from recurrent alveolar bleeding → oxidative injury and potential progression to fibrosis | (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 7-8) | | Chemical entity | Heme | CHEBI:heme | Released from erythrocytes in alveolar hemorrhage; drives free-radical oxidative damage contributing to lung injury | (saha2022comparativeanalysisof pages 1-2) | | Chemical entity | Hemosiderin | CHEBI:hemosiderin | Iron-storage complex accumulating in alveolar macrophages; histologic/bronchoscopic marker of prior alveolar bleeding | (saha2022comparativeanalysisof pages 7-8, saha2022comparativeanalysisof pages 1-2) |

Table: A concise ontology-mapped table of the molecular players, cells, anatomical sites, and chemicals implicated in Lane-Hamilton syndrome, with mechanism notes and source citations from the gathered evidence (saha2022comparativeanalysisof pages 1-2, aksu2024diettreatablecauseof pages 1-2).

Direct quotes (supporting key statements) - “Less than 20% of patients complained of any significant GI symptoms,” supporting screening for CD in all IPH (saha2022comparativeanalysisof pages 10-11). - “A gluten-free diet (GFD) alone was effective in the majority of LHS patients,” with lower recurrence/mortality vs IPH without CD (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10). - Relapses “occurred off GFD,” reinforcing dietary adherence as a determinant of outcomes (saha2022comparativeanalysisof pages 9-10, aksu2024diettreatablecauseof pages 1-2).

Limitations - Mechanistic hypotheses (e.g., histamine/ECP/VEGF-mediated permeability) are based on clinical-pathologic correlation; direct histologic proof of immune-complex or capillaritis mechanisms is typically absent in IPH/LHS specimens (saha2022comparativeanalysisof pages 9-10, saha2022comparativeanalysisof pages 1-2). High-quality, prospective mechanistic studies remain limited.

Summary LHS represents an immune-mediated form of DAH linked to celiac autoimmunity, where permeability mediators rather than vasculitic injury enable recurrent alveolar hemorrhage. Diagnostic implementation hinges on routine CD screening in IPH, even without GI symptoms. Strict GFD is often disease-modifying, with steroids/immunosuppressants reserved for acute or refractory disease. Recent 2023–2024 reports affirm the centrality of GFD and document real-world relapse with nonadherence and cases requiring adjunctive immunosuppression. Continued research is needed to define definitive molecular mediators and to establish standardized management pathways (saha2022comparativeanalysisof pages 1-2, saha2022comparativeanalysisof pages 9-10, fontes2023lanehamiltonsyndromein pages 3-5, saha2022comparativeanalysisof pages 10-11, aksu2024diettreatablecauseof pages 1-2).

References

  1. (saha2022comparativeanalysisof pages 1-2): Biplab K Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T Milman. Comparative analysis of adult patients with idiopathic pulmonary hemosiderosis and lane-hamilton syndrome: a systematic review of the literature in the period 1971-2022. Cureus, Mar 2022. URL: https://doi.org/10.7759/cureus.23482, doi:10.7759/cureus.23482. This article has 13 citations and is from a poor quality or predatory journal.

  2. (saha2022comparativeanalysisof pages 9-10): Biplab K Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T Milman. Comparative analysis of adult patients with idiopathic pulmonary hemosiderosis and lane-hamilton syndrome: a systematic review of the literature in the period 1971-2022. Cureus, Mar 2022. URL: https://doi.org/10.7759/cureus.23482, doi:10.7759/cureus.23482. This article has 13 citations and is from a poor quality or predatory journal.

  3. (saha2022comparativeanalysisof pages 10-11): Biplab K Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T Milman. Comparative analysis of adult patients with idiopathic pulmonary hemosiderosis and lane-hamilton syndrome: a systematic review of the literature in the period 1971-2022. Cureus, Mar 2022. URL: https://doi.org/10.7759/cureus.23482, doi:10.7759/cureus.23482. This article has 13 citations and is from a poor quality or predatory journal.

  4. (aksu2024diettreatablecauseof pages 1-2): Esra Arslan Aksu, Oğuz Karcıoğlu, and Oğuz Uzun. Diet-treatable cause of hemoptysis: lane hamilton syndrome. Respiratory Case Reports, 13:78-81, Jan 2024. URL: https://doi.org/10.5505/respircase.2024.73604, doi:10.5505/respircase.2024.73604. This article has 0 citations.

  5. (fontes2023lanehamiltonsyndromein pages 3-5): Joana Fontes, Bárbara Sousa, Marta Moreira, Nuno Pardal, and Rafael Lopes Freitas. Lane-hamilton syndrome in an adult with down syndrome: a case report. Cureus, Jan 2023. URL: https://doi.org/10.7759/cureus.33385, doi:10.7759/cureus.33385. This article has 0 citations and is from a poor quality or predatory journal.

  6. (fontes2023lanehamiltonsyndromein pages 5-6): Joana Fontes, Bárbara Sousa, Marta Moreira, Nuno Pardal, and Rafael Lopes Freitas. Lane-hamilton syndrome in an adult with down syndrome: a case report. Cureus, Jan 2023. URL: https://doi.org/10.7759/cureus.33385, doi:10.7759/cureus.33385. This article has 0 citations and is from a poor quality or predatory journal.

  7. (saha2022comparativeanalysisof pages 7-8): Biplab K Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T Milman. Comparative analysis of adult patients with idiopathic pulmonary hemosiderosis and lane-hamilton syndrome: a systematic review of the literature in the period 1971-2022. Cureus, Mar 2022. URL: https://doi.org/10.7759/cureus.23482, doi:10.7759/cureus.23482. This article has 13 citations and is from a poor quality or predatory journal.

  8. (saha2022comparativeanalysisof pages 13-14): Biplab K Saha, Praveen Datar, Alexis Aiman, Alyssa Bonnier, Santu Saha, and Nils T Milman. Comparative analysis of adult patients with idiopathic pulmonary hemosiderosis and lane-hamilton syndrome: a systematic review of the literature in the period 1971-2022. Cureus, Mar 2022. URL: https://doi.org/10.7759/cureus.23482, doi:10.7759/cureus.23482. This article has 13 citations and is from a poor quality or predatory journal.