Polymorphonuclear neutrophil

Where it participates (unsigned role)

1. At the end of infusion free serum antibody levels decreased, circulating immune complex levels increased and complement activation was observed, at approximately 1 to 4 hours after end of infusion increased expression of cytokines and chemokines, a 1.5 to 4-fold increase in neutrophil and monocyte counts and a broad activation of innate immune genes were observed, low-antibody subjects with levels below 20 micrograms per millilitre typically showed minimal changes except when their levels rose above 20 micrograms per millilitre after repeated dosing, mild-to-moderate infusion-related reactions occurred in subjects with antibody at or above 20 micrograms per millilitre, and premedications alleviated some of the infusion-related reactions but also inhibited cytokine responses.

   Naturally occurring anti-beta-glucan IgG antibodies → Imprime PGG / BTH1677, a soluble yeast beta-(1->3)/(1->6)-glucan source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   biomarker_context Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/glucan-research/30988115.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d", "start_char": 0, "end_char": 1787, "text_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d"}

   experimental_model

   Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication

   exposure

   Imprime PGG 4 milligrams per kilogram intravenously, with antihistamine and corticosteroid premedication in some subjects

   limitations

   Healthy volunteers and pharmacodynamic endpoints only. Nothing here measures a tumour outcome, so the antibody strata are not validated treatment-selection thresholds.

   nutrient_topic

   Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

   organism

   Human

   plain_language

   Below a certain antibody level almost nothing happened; above it, the drug worked and also caused the infusion reactions.

   primary_references

   [bg-p30988115] Immune Pharmacodynamic Responses of the Novel Cancer Immunotherapeutic Imprime PGG in Healthy Volunteers. (2019). https://pubmed.ncbi.nlm.nih.gov/30988115/ DOI: 10.4049/jimmunol.1801533

   tissue_or_cell_type

   Peripheral blood

   trigger_kind

   biomarker_context Imported condition classification; unverified.

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 281–292

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication · source_derived_draft · unverified_draft

   ### bg-antibody-level-gates-the-response At the end of infusion free serum antibody levels decreased, circulating immune complex levels increased and complement activation was observed, at approximately 1 to 4 hours after end of infusion increased expression of cytokines and chemokines, a 1.5 to 4-fold increase in neutrophil and monocyte counts and a broad activation of innate immune genes were observed, low-antibody subjects with levels below 20 micrograms per millilitre typically showed minimal changes except when their levels rose above 20 micrograms per millilitre after repeated dosing, mild-to-moderate infusion-related reactions occurred in subjects with antibody at or above 20 micrograms per millilitre, and premedications alleviated some of the infusion-related reactions but also inhibited cytokine responses. Condition category: biomarker_context nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Below a certain antibody level almost nothing happened; above it, the drug worked and also caused the infusion reactions. organism: Human tissue_or_cell_type: Peripheral blood experimental_model: Single and multiple intravenous infusions in healthy volunteers stratified by pre-treatment antibody level, with and without premedication limitations: Healthy volunteers and pharmacodynamic endpoints only. Nothing here measures a tumour outcome, so the antibody strata are not validated treatment-selection thresholds. exposure: Imprime PGG 4 milligrams per kilogram intravenously, with antihistamine and corticosteroid premedication in some subjects evidence_span: {"source_cache": "artifacts/glucan-research/30988115.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d", "start_char": 0, "end_char": 1787, "text_sha256": "bd9bd1b314472b30b2e3513ecb5e048178de145217473fa87379e0977d21f90d"} [bg-p30988115] Immune Pharmacodynamic Responses of the Novel Cancer Immunotherapeutic Imprime PGG in Healthy Volunteers. (2019). https://pubmed.ncbi.nlm.nih.gov/30988115/ DOI: 10.4049/jimmunol.1801533

   Complete structured claim and evidence

2. In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans.

   Beta-glucan → Ex vivo cytokine production by stimulated leukocytes source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"}

   experimental_model

   Randomised open-label intervention pilot study in 15 healthy male volunteers

   exposure

   Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling

   limitations

   Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive.

   nutrient_topic

   Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

   organism

   Human

   plain_language

   Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed.

   primary_references

   [bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794

   tissue_or_cell_type

   Serum and peripheral leukocytes

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 385–396

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomised open-label intervention pilot study in 15 healthy male volunteers · source_derived_draft · unverified_draft

   ### bg-in-people-nothing-was-detectable In a randomised open-label intervention pilot study in 15 healthy male volunteers, subjects in the beta-glucan group ingested beta-glucan 1000 milligrams once daily for 7 days, beta-glucan was barely detectable in serum of volunteers at all time-points, and neither cytokine production nor microbicidal activity of leukocytes were affected by orally administered beta-glucan, so the present study does not support the use of oral beta-glucan to enhance innate immune responses in humans. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Ten healthy men took a gram a day for a week; almost none of it showed up in the blood and nothing measurable changed. organism: Human tissue_or_cell_type: Serum and peripheral leukocytes experimental_model: Randomised open-label intervention pilot study in 15 healthy male volunteers limitations: Ten treated and five control subjects, one product, one dose, seven days, and ex vivo readouts. A negative pilot of this size does not establish that all oral preparations are inactive. exposure: Oral beta-glucan 1000 milligrams once daily for 7 days against no treatment, with serial sampling evidence_span: {"source_cache": "artifacts/glucan-research/25268806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b", "start_char": 0, "end_char": 1307, "text_sha256": "b5a583c465284aae8e7d3e6dd9996fafe3b6ef389c61ee2a54f066fb4701e51b"} [bg-p25268806] The effects of orally administered Beta-glucan on innate immune responses in humans, a randomized open-label intervention pilot-study. (2014). https://pubmed.ncbi.nlm.nih.gov/25268806/ DOI: 10.1371/journal.pone.0108794

   Complete structured claim and evidence

3. When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state.

   Beta-glucan → The primed state of complement receptor 3 source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"}

   experimental_model

   Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets

   exposure

   Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar

   limitations

   An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient.

   nutrient_topic

   Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan

   organism

   Human

   plain_language

   The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill.

   primary_references

   [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777

   tissue_or_cell_type

   Neutrophil and natural killer cell

   Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 216–227

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets · source_derived_draft · unverified_draft

   ### bg-soluble-glucan-primes-cr3 When phagocyte or natural killer cell CR3 adheres to iC3b on erythrocytes or tumour cells that lack CR3-binding membrane polysaccharides neither lysis nor cytotoxicity are stimulated, but soluble CR3-specific polysaccharides such as beta-glucan induced a primed state of CR3 that could trigger killing of iC3b-target cells that were otherwise resistant to cytotoxicity, priming required tyrosine kinases and a magnesium-dependent conformational change of the I-domain that exposed the CBRM1/5 activation epitope, and unlike LPS or cytokines polysaccharides did not up-regulate neutrophil CR3 expression nor expose the high affinity ICAM-1-binding state. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: The sugar does not make the killer cell find the tumour; it changes the receptor so that a target it was already touching becomes one it will kill. organism: Human tissue_or_cell_type: Neutrophil and natural killer cell experimental_model: Priming of neutrophil and natural killer cell CR3 with soluble polysaccharide, then challenge with iC3b-coated targets limitations: An in vitro cytotoxicity mechanism. It establishes how priming works and what it requires, not that the same sequence occurs in a treated patient. exposure: Soluble CR3-specific polysaccharides including beta-glucan, with antibody blockade before or after the sugar evidence_span: {"source_cache": "artifacts/glucan-research/8690804.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e", "start_char": 0, "end_char": 1478, "text_sha256": "e6e6ce1cbb7d4a4d3170e4b86ac33d4b3220d59645c53d757fe3a2681397287e"} [bg-p8690804] Soluble beta-glucan polysaccharide binding to the lectin site of neutrophil or natural killer cell complement receptor type 3 (CD11b/CD18) generates a primed state of the receptor capable of mediating cytotoxicity of iC3b-opsonized target cells. (1996). https://pubmed.ncbi.nlm.nih.gov/8690804/ DOI: 10.1172/jci118777

   Complete structured claim and evidence

4. Hyperbaric oxygen did not inhibit the initial interaction of leukocytes with brain microvasculature, but persistent adherence, which is due to beta-2 integrins, did not occur; in vitro the leukocytes showed absent beta-2 integrin function while surface expression, elastase release and superoxide production on stimulation remained normal.

   Hyperbaric oxygen therapy → Neutrophil beta-2 integrin adhesive function source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"}

   experimental_model

   Rats poisoned with carbon monoxide, with leukocyte function assays

   exposure

   3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control

   limitations

   The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail.

   nutrient_topic

   Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

   organism

   Rat

   plain_language

   The white cells still arrive and still work, but they cannot lock on and stay.

   primary_references

   [hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

   tissue_or_cell_type

   Brain microvasculature and polymorphonuclear leukocytes

   Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 751–762

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats poisoned with carbon monoxide, with leukocyte function assays · source_derived_draft · unverified_draft

   ### hbot-b2-integrin-inhibition Hyperbaric oxygen did not inhibit the initial interaction of leukocytes with brain microvasculature, but persistent adherence, which is due to beta-2 integrins, did not occur; in vitro the leukocytes showed absent beta-2 integrin function while surface expression, elastase release and superoxide production on stimulation remained normal. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: The white cells still arrive and still work, but they cannot lock on and stay. organism: Rat tissue_or_cell_type: Brain microvasculature and polymorphonuclear leukocytes experimental_model: Rats poisoned with carbon monoxide, with leukocyte function assays limitations: The pressure-only control separates oxygen from pressure. The integrin defect is functional: surface expression was normal, which is the informative detail. exposure: 3 atmospheres absolute for 45 minutes, given 24 hours before or up to 45 minutes after poisoning; 3 ATA pressure without oxygen as a control evidence_span: {"source_cache": "artifacts/hbot-research/8248932.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f", "start_char": 0, "end_char": 1870, "text_sha256": "54ab057eb31320490d893896d8ab5b0c856a8b59489424b14b81409f01a78f7f"} [hbot-p8248932] Functional inhibition of leukocyte B2 integrins by hyperbaric oxygen in carbon monoxide-mediated brain injury in rats. (1993). https://pubmed.ncbi.nlm.nih.gov/8248932/ DOI: 10.1006/taap.1993.1243

   Complete structured claim and evidence

5. Neutrophil adhesion to endothelial cells increased 3.4-fold after hypoxia and hypoglycaemia and was reduced to control levels by hyperbaric oxygen.

   Hyperbaric oxygen therapy → Persistent neutrophil adherence to endothelium source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"}

   experimental_model

   Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model

   exposure

   Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME

   limitations

   An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route.

   nutrient_topic

   Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Hyperbaric oxygen therapy

   organism

   Human and bovine cells

   plain_language

   With the docking molecule gone, the white cells no longer stick.

   primary_references

   [hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

   tissue_or_cell_type

   Vascular endothelium

   Hyperbaric oxygen: the exposure, its reactive species, the signals they carry, and the nutrient-dependent enzymes that handle them (2026-09-19) · lines 725–736

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model · source_derived_draft · unverified_draft

   ### hbot-pmn-adhesion-drop Neutrophil adhesion to endothelial cells increased 3.4-fold after hypoxia and hypoglycaemia and was reduced to control levels by hyperbaric oxygen. Condition category: normal nutrient_topic: Hyperbaric oxygen research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: With the docking molecule gone, the white cells no longer stick. organism: Human and bovine cells tissue_or_cell_type: Vascular endothelium experimental_model: Human umbilical vein and bovine aortic endothelial cells in an in vitro ischaemia-reperfusion model limitations: An in vitro model requiring both hypoxia and hypoglycaemia to induce the adhesion molecule. The nitric oxide synthase inhibitor arm supports the proposed route. exposure: Hyperbaric oxygen after combined hypoxia and hypoglycaemia; L-NAME evidence_span: {"source_cache": "artifacts/hbot-research/10666024.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8", "start_char": 0, "end_char": 1182, "text_sha256": "9bb8781cab37af1af9f292e4611c19f273de986e86be681a357058d2cfb87ad8"} [hbot-p10666024] Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. (2000). https://pubmed.ncbi.nlm.nih.gov/10666024/ DOI: 10.1152/ajpcell.2000.278.2.c292

   Complete structured claim and evidence

6. Two patients on high-dose oral mebendazole for echinococcosis developed severe reversible neutropenia apparently due to marrow suppression, with platelets and red cells also reversibly suppressed in one, high blood levels of 239 nanograms per millilitre in one patient may have caused the neutropenia and several toxic side effects as well as a striking shrinkage of that patient’s pulmonary and liver cysts, neutropenia with high-dose therapy may occur in up to 5% of patients, and the white cell count should be monitored frequently during the first several weeks.

   Mebendazole → Neutropenia from marrow suppression source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   biomarker_context Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/mebendazole-research/6842806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031", "start_char": 0, "end_char": 755, "text_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031"}

   experimental_model

   Case reports of two patients on high-dose oral mebendazole for echinococcosis

   exposure

   High-dose oral mebendazole, with a blood level of 239 nanograms per millilitre in one patient

   limitations

   Two cases. The estimate that neutropenia may occur in up to 5% of patients is the authors’ judgement, not a measured rate from these two.

   nutrient_topic

   Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. · Mebendazole

   organism

   Human

   plain_language

   The patient whose cysts shrank most was the patient whose marrow was suppressed.

   primary_references

   [mbz-p6842806] Severe, reversible neutropenia during high-dose mebendazole therapy for echinococcosis. (1983). https://pubmed.ncbi.nlm.nih.gov/6842806/ DOI: 10.1001/jama.1983.03330450059026

   tissue_or_cell_type

   Bone marrow

   trigger_kind

   biomarker_context Imported condition classification; unverified.

   Mebendazole: the tubulin it binds, why that is selective, the crystal form that decides whether any of it works, and the off-target that became an oncology programme (2026-09-22) · lines 628–639

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Case reports of two patients on high-dose oral mebendazole for echinococcosis · source_derived_draft · unverified_draft

   ### mbz-neutropenia-with-the-benefit Two patients on high-dose oral mebendazole for echinococcosis developed severe reversible neutropenia apparently due to marrow suppression, with platelets and red cells also reversibly suppressed in one, high blood levels of 239 nanograms per millilitre in one patient may have caused the neutropenia and several toxic side effects as well as a striking shrinkage of that patient’s pulmonary and liver cysts, neutropenia with high-dose therapy may occur in up to 5% of patients, and the white cell count should be monitored frequently during the first several weeks. Condition category: biomarker_context nutrient_topic: Mebendazole research collection; topical membership is not evidence of a direct clinical effect, and mebendazole is recorded separately from albendazole, from the benzimidazole class and from its own crystal forms. plain_language: The patient whose cysts shrank most was the patient whose marrow was suppressed. organism: Human tissue_or_cell_type: Bone marrow experimental_model: Case reports of two patients on high-dose oral mebendazole for echinococcosis limitations: Two cases. The estimate that neutropenia may occur in up to 5% of patients is the authors’ judgement, not a measured rate from these two. exposure: High-dose oral mebendazole, with a blood level of 239 nanograms per millilitre in one patient evidence_span: {"source_cache": "artifacts/mebendazole-research/6842806.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031", "start_char": 0, "end_char": 755, "text_sha256": "bdad328a3c1865dc991e7d6825c6da6e68742c580b2f8e0d455635ab57e69031"} [mbz-p6842806] Severe, reversible neutropenia during high-dose mebendazole therapy for echinococcosis. (1983). https://pubmed.ncbi.nlm.nih.gov/6842806/ DOI: 10.1001/jama.1983.03330450059026

   Complete structured claim and evidence