Agranulocytosis is a very severe form of neutropenia. Neutrophils are a type of white blood cell that fight germs. In agranulocytosis, the number of neutrophils becomes extremely low. Doctors measure this with the absolute neutrophil count (ANC). In agranulocytosis, the ANC is usually below 100 cells per microliter of blood. This level means your body has almost no neutrophils to stop bacteria or fungi. The risk of serious infection is very high, and infection can spread fast. Quick diagnosis and treatment are important to prevent sepsis and death. NCBICleveland ClinicMedscape
Agranulocytosis means a person has a very low number of a specific group of white blood cells called granulocytes (mainly neutrophils). Neutrophils are the body’s fast “first responders” that fight bacteria and fungi. When neutrophils fall to dangerously low levels (usually an absolute neutrophil count, ANC, below 500 cells/µL), the body cannot contain routine germs. Minor infections can become severe within hours. Fever may be the only early sign, and it is a medical emergency in this condition. Agranulocytosis can happen suddenly after a drug side effect, or it can develop from diseases that damage the bone marrow. It can also be inherited. Doctors confirm it with a complete blood count (CBC) and differential, look for the cause, and treat urgently with antibiotics and often G-CSF (filgrastim) to raise neutrophils. Quick action prevents sepsis and saves life.
In simple words: agranulocytosis is when your body loses its main germ-fighting cells. Even small infections can become dangerous. Fever or a sore throat in this condition is an emergency. NCBI
Other names
Agranulocytosis may also be called “agranulosis,” “granulopenia,” or “severe neutropenia.” Some articles use “granulocytopenia” to mean a very low number of granulocytes (neutrophils, eosinophils, and basophils). In day-to-day care, doctors usually focus on neutrophils, because neutrophils are the main defenders against bacteria. So, when people say “agranulocytosis,” they almost always mean near-absence of neutrophils (ANC ~0–100/µL) and a very high risk of infection. NCBIMedscapeWikipedia
Types
1) By cause
Acquired agranulocytosis. This is the most common type. It happens after exposure to a drug, chemical, radiation, infection, autoimmune disease, or bone-marrow failure. The drop in neutrophils can be sudden. The risk of severe infection is high until the count recovers. Frontiers
Congenital (inherited) agranulocytosis / severe chronic neutropenia. Caused by gene changes that affect neutrophil production (for example, ELANE mutations in “Kostmann syndrome”). It often starts in infancy or childhood and may require long-term support. (This is rare compared with acquired forms.)
2) By mechanism
Drug-induced, idiosyncratic. An unpredictable reaction to a medicine. It is not dose-related. It may be immune-mediated or due to toxic metabolites that kill marrow cells. It often appears weeks after starting a new drug and stops after the drug is removed. PMCBMJ Decision Trees
Drug-induced, dose-related/toxic. Seen with cytotoxic chemotherapy and high-dose radiation where marrow cells are directly suppressed.
Immune-mediated (autoimmune). The body makes antibodies that destroy neutrophils or their precursors. This can happen alone or with diseases like lupus or rheumatoid arthritis (Felty syndrome includes RA, neutropenia, and splenomegaly). NCBI
3) By duration
Acute/transient. Lasts days to weeks and then improves when the trigger is removed (for example, stopping a drug).
Chronic/persistent. Lasts months or longer. Often needs ongoing monitoring and sometimes growth factor support.
Causes
Antithyroid drugs (methimazole, carbimazole, propylthiouracil). These can rarely cause sudden marrow suppression with very low neutrophils. Fever or sore throat while on these drugs needs an urgent blood count. BMJ Decision TreesPMC
Clozapine. An effective antipsychotic that has a known risk of agranulocytosis, especially in the first months. Regular blood tests are required to keep patients safe. MDPI
Sulfasalazine and other sulfa antibiotics (for example, trimethoprim-sulfamethoxazole). These can trigger idiosyncratic immune reactions leading to agranulocytosis. Stop the drug and check counts if infection symptoms appear. PMCBMJ Decision Trees
Ticlopidine (older antiplatelet) and, rarely, clopidogrel. Ticlopidine has a well-described risk; clopidogrel very rarely. Monitoring is needed if symptoms arise. PMC
Dipyrone (metamizole). Linked to agranulocytosis in some countries; not used in many places for safety reasons. PMC
Carbamazepine and other antiseizure drugs. Rare marrow toxicity can cause severe neutropenia. Any fever warrants a CBC. PMC
Chloramphenicol and linezolid. Some antibiotics can suppress marrow with prolonged use, leading to neutropenia or agranulocytosis. PMC
Penicillins/cephalosporins (high dose or prolonged). Rare immune-mediated neutropenia has been reported; watch for fever and mouth sores. PMC
Dapsone. Used for certain skin and infectious diseases; can cause severe neutropenia in rare cases. PMC
Chemotherapy. Many cancer drugs reduce marrow production of all blood cells; neutrophils fall first and lowest, raising infection risk. (This is dose-dependent marrow suppression.)
Radiation exposure. Radiation injures marrow stem cells, lowering neutrophil production and causing severe neutropenia.
Autoimmune diseases (e.g., systemic lupus erythematosus). The immune system may destroy neutrophils or their marrow precursors.
Felty syndrome (rheumatoid arthritis + neutropenia + splenomegaly). The spleen may sequester neutrophils and autoimmunity can reduce counts. NCBI
Aplastic anemia. Bone marrow fails to make enough blood cells of all lines, including neutrophils.
Myelodysplastic syndromes and leukemia. Abnormal marrow cells crowd out normal cell production, lowering neutrophils.
Hypersplenism. An enlarged spleen traps and destroys blood cells, which can worsen neutropenia.
Severe infections (sepsis). Neutrophils may be consumed or production may be suppressed during overwhelming infection; counts can drop very low. NCBI
Viral infections (HIV, hepatitis, EBV, CMV, parvovirus). Viruses can reduce marrow output or increase destruction of neutrophils.
Nutritional deficiencies (vitamin B12, folate, copper). Lack of these nutrients impairs marrow cell formation and can cause marked neutropenia.
Toxins/chemicals (for example, benzene) and adulterants (e.g., levamisole-adulterated cocaine). These can directly damage marrow or trigger immune destruction of neutrophils. Wikipedia
Symptoms
Fever. Even a low fever can be the first sign of a serious infection. In neutropenia, fever is an emergency because the body cannot fight germs well. NCBI
Sore throat. The throat and tonsils get infected easily when neutrophils are absent. Pain or swelling can appear quickly.
Mouth ulcers and gum pain. The mouth lining breaks down and germs grow fast, causing ulcers, gingivitis, and bad breath.
Pain with swallowing. Swollen, sore tissues in the throat make swallowing painful, especially with fungal or bacterial infections.
Cough or shortness of breath. Lung infections (pneumonia) can develop quickly. Breathing trouble or chest pain needs urgent care.
Sinus pain or runny nose with pressure. Sinus infections are common and may progress to serious disease without strong early signs.
Skin infections. Red, warm, tender spots or boils may appear. They can spread fast because neutrophils are missing.
Perianal pain. Pain around the rectum may point to a deep infection or abscess. Exams in this area must be careful to avoid injury.
Abdominal pain. Can indicate gut infection, liver or spleen problems, or a hidden abscess.
Burning urine or pelvic pain. Urinary infections may spread to the blood if not treated fast.
Chills or shaking (rigors). Suggests the body is fighting a bloodstream infection. Seek help immediately.
Extreme tiredness and weakness. Infection and inflammation cause overall fatigue.
Headache or confusion. May be due to high fever, dehydration, or severe sepsis.
Non-healing sores or wounds. Cuts or dental problems heal slowly and can get worse without neutrophils.
Low blood pressure, fast heart rate, or dizziness. These are late and dangerous signs of sepsis and shock. Call emergency services. NCBI
Diagnostic tests
Physical exam
Vital signs and sepsis screen. The doctor checks temperature, heart rate, breathing rate, blood pressure, and oxygen level. Fever with suspected neutropenia is treated as an emergency because infection can progress very fast. NCBI
Mouth and throat exam. The doctor looks for ulcers, red or swollen tonsils, white patches from fungal infection, or pus. These signs suggest infection in a common entry site.
Skin and soft tissue exam. The doctor looks for redness, warmth, pain, swelling, or drainage. Small skin infections can spread quickly in agranulocytosis.
Lung exam. Listening to the chest can reveal crackles or reduced sounds that suggest pneumonia. Cough and chest pain guide further tests.
Abdomen and spleen exam. The doctor checks for tenderness, organ enlargement, or perianal pain. A large spleen may point toward autoimmune or hypersplenic causes.
“Manual” tests
Capillary refill time. Pressing on a fingernail or skin and watching color return helps judge blood flow. Slow refill can be a sign of shock from infection.
Manual ANC calculation. The absolute neutrophil count is calculated from the white blood cell count and the percent of neutrophils and bands. This number guides risk and urgency. (ANC ≈ WBC × [% neutrophils + % bands] / 100.)
Manual peripheral smear review. A lab professional or doctor looks at blood under a microscope. They confirm very low or absent neutrophils and look for abnormal precursors or blasts that may suggest leukemia.
Rapid bedside antigen tests (e.g., strep, influenza, COVID as indicated). These simple kit tests can quickly identify a source of fever while formal cultures are pending.
Lab and pathological tests
Complete blood count (CBC) with differential. This confirms neutropenia and shows if other blood cells are also low. In agranulocytosis, ANC is usually <100/µL. Cleveland Clinic
Blood cultures (multiple sets). Drawn before antibiotics, they look for bacteria or fungi in the blood. Positive results guide targeted treatment. NCBI
Urine culture. Detects urinary infections that may cause fever and can spread to the blood if untreated.
Throat or sputum culture (and wound cultures if needed). Finds the specific germ in the mouth, throat, lungs, or skin so the right antibiotic can be chosen.
Inflammation markers (CRP, procalcitonin). These rise with infection and help track response to treatment while awaiting culture results. NCBI
Bone marrow aspiration and biopsy. Shows how the marrow is working. It can reveal poor neutrophil production, marrow failure, leukemia, or myelodysplasia. Microscopy often shows very few granulocyte precursors in agranulocytosis. PMC
Flow cytometry and cytogenetic/molecular tests. These tests look for abnormal cell markers or chromosome changes to rule out leukemia or myelodysplastic syndromes.
Nutritional and infection panels. Vitamin B12, folate, copper levels, and viral tests (HIV, hepatitis, EBV/CMV) help find reversible causes or co-infections.
Electrodiagnostic tests
Electrocardiogram (ECG) and continuous monitoring (as needed). There is no special nerve-or-muscle “electrodiagnostic” test for agranulocytosis itself. But ECG and telemetry help watch for sepsis-related heart strain, shock, and drug side effects while the patient is acutely ill. NCBI
Imaging tests
Chest X-ray. Looks for pneumonia or other lung problems, which are common and dangerous sources of fever in severe neutropenia. NCBI
Targeted CT scan (for example, sinuses, chest, abdomen, pelvis). CT helps find hidden abscesses, deep tissue infections, or sinus/lung problems when the source of fever is not clear. It is useful when the patient is not improving or has localizing pain. NCBI
Non-pharmacological treatments
Safety first: Non-drug care never replaces urgent antibiotics in febrile neutropenia. These measures support recovery and reduce infection risk.
Physiotherapy
Early, gentle mobilization
Description (≈150 words): Short, frequent walks in the room or corridor once clinically stable keep the lungs expanding, maintain blood flow, and prevent deconditioning. Start with sitting at the edge of bed, marching in place, and 2–5-minute strolls, progressing as tolerated. Avoid crowded spaces. Coordinate sessions after antibiotics and when fever is controlled.
Purpose: Preserve strength, reduce pneumonia and blood clots.
Mechanism: Improves ventilation-perfusion, limb muscle pump, microcirculation.
Benefits: Less weakness, better mood and appetite, fewer atelectasis-related fevers.Breathing exercises (diaphragmatic + incentive spirometry)
Description: Practice slow belly breathing and regular incentive spirometer sets (10 breaths/hour while awake). Add “stacked” breaths and gentle huff coughs if sputum present.
Purpose: Prevent pneumonia/atelectasis.
Mechanism: Increases lung volume, recruits alveoli, improves mucociliary clearance.
Benefits: Better oxygenation, less shortness of breath, fewer chest infections.Airway clearance with huff coughing
Description: Teach relaxed “huff” (forced expiratory technique) instead of harsh coughing that can fatigue or cause pain. Use sessions after nebulized saline if prescribed.
Purpose: Move secretions safely.
Mechanism: Keeps small airways open, shifts mucus proximally.
Benefits: Lower risk of mucus plugging and secondary infection.Energy-conservation pacing
Description: Break tasks into steps, rest before tired, sit for grooming, use a shower chair; prioritize essentials.
Purpose: Prevent over-fatigue that can worsen recovery.
Mechanism: Matches activity to current mitochondrial and cardiovascular capacity.
Benefits: More stable energy, faster functional gains.Progressive resistance with light bands
Description: 5–10 minutes, major muscle groups, alternate days once afebrile. Stop if HR, BP, or O2 worsen.
Purpose: Preserve muscle mass.
Mechanism: Stimulates muscle protein synthesis.
Benefits: Better mobility and independence.Balance and gait drills
Description: Heel-to-toe, side steps, sit-to-stand practice with supervision.
Purpose: Reduce falls during illness.
Mechanism: Trains vestibular/proprioceptive systems.
Benefits: Safer ambulation.Gentle stretching & joint range
Description: Daily neck, shoulder, hip, calf stretches.
Purpose: Prevent stiffness from bed rest.
Mechanism: Maintains tendon/soft tissue length.
Benefits: Comfort, easier mobility.Postural training
Description: Seated posture checks, scapular setting, thoracic extension against a towel roll.
Purpose: Improve breathing mechanics.
Mechanism: Optimizes diaphragm and rib motion.
Benefits: Less fatigue, clearer breathing.Cough-splinting and chest wall protection
Description: Hug a pillow to chest/abdomen when coughing.
Purpose: Reduce pain and protect wounds if any.
Mechanism: Stabilizes chest wall.
Benefits: More effective cough with less pain.Safe stair practice (if going home)
Description: Supervised trial before discharge, emphasizing slow pace and rest at landings.
Purpose: Ensure home safety.
Mechanism: Task-specific training.
Benefits: Fewer near-falls after discharge.Circulation boosters (ankle pumps, calf raises)
Description: 10–20 repetitions hourly while awake.
Purpose: Reduce clot risk.
Mechanism: Enhances venous return.
Benefits: Less swelling, comfort.Pelvic floor and core activation
Description: Low-intensity holds and breathing-linked activation.
Purpose: Support coughing and posture.
Mechanism: Coordinates diaphragm–core unit.
Benefits: Reduced back strain.Gentle yoga-style poses (non-crowded, supervised)
Description: Cat-cow, child’s pose, supported forward fold—avoid group studios during neutropenia.
Purpose: Flexibility and calm.
Mechanism: Parasympathetic activation.
Benefits: Pain relief, better sleep.Therapeutic positioning
Description: Head-of-bed 30–45°, change positions every 2 hours.
Purpose: Prevent aspiration and pressure injury.
Mechanism: Improves drainage & perfusion.
Benefits: Fewer respiratory issues.Home exercise plan with symptom thresholds
Description: Clear stop rules (fever, chest pain, dizziness); log sessions; tele-check if available.
Purpose: Safe continuity.
Mechanism: Self-monitoring reduces risk.
Benefits: Sustainable recovery.
Mind-body and educational therapies
Fever emergency plan education
Description (≈150 words): Teach that any fever ≥38.0°C (100.4°F) during neutropenia is an emergency. The patient practices saying: “I am neutropenic and febrile.” They keep a written plan with the nearest emergency department, transport options, and medication list.
Purpose: Cut time to antibiotics.
Mechanism: Pre-commitment and rehearsal.
Benefits: Faster care, lower sepsis risk.Infection-control coaching (hand hygiene, mask, oral care)
Description: Structured teaching on 20-second handwashing, alcohol rub use, surgical mask in clinics, twice-daily soft toothbrush, alcohol-free mouthwash, saline/bicarbonate rinses.
Purpose: Reduce germ exposure and mouth sources.
Mechanism: Lowers inoculum and mucosal injury.
Benefits: Fewer infections, less mucositis pain.Food safety & “neutropenic diet” counseling
Description: Emphasize safe food handling (clean, separate, cook, chill). Prefer fully cooked meats/eggs, pasteurized dairy/juices, washed/peeled produce; avoid salad bars, sushi, raw sprouts, unpasteurized items. Note: strict “sterile” diets add little benefit; focus on evidence-based handling.
Purpose: Reduce food-borne infection.
Mechanism: Limits exposure to high-risk bacteria/fungi.
Benefits: Safer nutrition without unnecessary restriction.Catheter care education
Description: Daily check of redness, tenderness, or discharge; keep dressings dry; never immerse lines; report fevers immediately.
Purpose: Prevent line sepsis.
Mechanism: Barrier integrity and early detection.
Benefits: Fewer bloodstream infections.Sleep hygiene & stress reduction
Description: Fixed sleep/wake times, limit screens at night, quiet pre-bed routine; add brief mindfulness or breathing sets.
Purpose: Support immune recovery and mood.
Mechanism: Lowers cortisol and sympathetic tone.
Benefits: Better energy, pain tolerance.Guided imagery / relaxation training
Description: Short audio-guided sessions visualizing safe recovery and calm breathing.
Purpose: Ease anxiety, improve adherence.
Mechanism: Activates parasympathetic pathways.
Benefits: Lower heart rate, improved sleep.Return-to-activity and work planning
Description: Set phased goals aligned with ANC recovery and clinician advice.
Purpose: Safe reintegration.
Mechanism: Graded exposure and pacing.
Benefits: Less relapse, better quality of life.Vaccination literacy (non-live vaccines when counts recover, per clinician)
Description: Teach which vaccines are safe/timed (influenza, pneumococcal, COVID-19 inactivated/approved forms) and which live vaccines to avoid until cleared.
Purpose: Prevent future infections.
Mechanism: Builds adaptive immunity safely.
Benefits: Fewer severe infections long-term.Household hygiene coaching
Description: Family handwashing, avoid sharing razors/brushes, clean high-touch surfaces, pet litter handled by others, garden/soil avoided during severe neutropenia.
Purpose: Lower home exposure.
Mechanism: Reduces pathogen load.
Benefits: Fewer breakthrough infections.Medication safety education (drug list review)
Description: Provide a wallet card listing the offending drug (if known) and high-risk drugs to avoid (e.g., future antithyroid if it caused the event).
Purpose: Prevent recurrence.
Mechanism: Informs all future prescribers.
Benefits: Safer lifelong care.
Drug treatments
*Doses here are typical adult ranges; exact dosing depends on kidney/liver function, local protocols, cultures, and clinician judgment.
Piperacillin–tazobactam (IV anti-pseudomonal β-lactam)
Dose: 4.5 g IV every 6–8 h. Time: Start immediately for febrile neutropenia.
Purpose: Broad empiric coverage including Pseudomonas.
Mechanism: Cell-wall inhibition + β-lactamase block.
Side effects: Allergy, diarrhea, rare kidney injury, sodium load.Cefepime (IV fourth-gen cephalosporin)
Dose: 2 g IV every 8–12 h.
Purpose: Alternative first-line anti-pseudomonal.
Mechanism: Cell-wall synthesis inhibition.
Side effects: Allergy, encephalopathy in renal impairment—dose adjust.Meropenem (IV carbapenem)
Dose: 1 g IV every 8 h.
Purpose: Escalation or ESBL risk.
Mechanism: Broad cell-wall inhibition; very stable to β-lactamases.
Side effects: Seizure risk (high doses/renal failure), diarrhea.Vancomycin (IV glycopeptide)
Dose: Weight/trough-guided (e.g., 15–20 mg/kg IV every 8–12 h).
Purpose: Add if catheter infection, MRSA risk, skin/line infection, hypotension.
Mechanism: Binds D-Ala-D-Ala; blocks cell-wall assembly.
Side effects: Kidney injury, “red man” infusion reaction; monitor levels.Filgrastim (G-CSF, granulocyte colony-stimulating factor)
Dose: 5 µg/kg SC daily until ANC recovery.
Time: Start in severe/prolonged neutropenia, chemotherapy-related cases, or high-risk febrile neutropenia.
Purpose: Speed neutrophil recovery.
Mechanism: Stimulates marrow neutrophil production and release.
Side effects: Bone pain, leukocytosis, rare splenic enlargement.Pegfilgrastim (long-acting G-CSF)
Dose: 6 mg SC once per chemo cycle (timed 24 h after chemo; not for active febrile treatment).
Purpose: Prophylaxis to prevent severe neutropenia after chemo.
Mechanism: Sustained G-CSF signaling.
Side effects: Bone pain, rare splenic rupture; timing is crucial.Sargramostim (GM-CSF)
Dose: 250 µg/m² SC/IV daily.
Purpose: Alternate growth factor (post-transplant, refractory cases).
Mechanism: Stimulates granulocytes and monocytes.
Side effects: Fever, fluid retention, bone pain.Antifungal therapy (e.g., Voriconazole)
Dose: 6 mg/kg IV/PO q12h × 2 doses then 4 mg/kg q12h.
Purpose: Add if persistent fever >4–5 days or fungal imaging signs.
Mechanism: Inhibits fungal ergosterol synthesis.
Side effects: Visual changes, liver enzyme elevation, many drug interactions.Echinocandin (e.g., Caspofungin)
Dose: 70 mg IV load then 50 mg daily.
Purpose: Candidemia coverage in unstable patients.
Mechanism: Inhibits fungal β-(1,3)-D-glucan synthesis.
Side effects: Liver enzyme rise, histamine reaction.Acyclovir (antiviral for HSV/VZV)
Dose: 5–10 mg/kg IV q8h for severe; or 400 mg PO TID prophylaxis in select settings.
Purpose: Treat mucocutaneous HSV or prophylax if high risk.
Mechanism: Inhibits viral DNA polymerase.
Side effects: Kidney crystal nephropathy—hydrate; dose adjust in renal disease.Levofloxacin (oral fluoroquinolone prophylaxis in high-risk chemo per protocol)
Dose: 500 mg PO daily (selected patients).
Purpose: Prevent bacterial infections during expected prolonged neutropenia.
Mechanism: Inhibits bacterial DNA gyrase/topoisomerase.
Side effects: Tendon injury, QT prolongation, CNS effects; use only when indicated.Amphotericin B liposomal
Dose: 3–5 mg/kg IV daily.
Purpose: Broad antifungal for unstable or resistant infections.
Mechanism: Binds ergosterol, forms membrane pores.
Side effects: Nephrotoxicity (less with liposomal), electrolyte loss, infusion reactions.Prednisone (for autoimmune neutropenia, short course)
Dose: 0.5–1 mg/kg/day then taper per response.
Purpose: Suppress immune destruction of neutrophils.
Mechanism: Decreases autoantibody-mediated clearance.
Side effects: Hyperglycemia, mood changes, infection risk—use judiciously.IVIG (intravenous immunoglobulin)
Dose: 0.4 g/kg/day × 3–5 days (regimens vary).
Purpose: Severe immune-mediated or refractory drug-induced neutropenia.
Mechanism: Fc-receptor blockade and immune modulation.
Side effects: Headache, thrombosis risk, aseptic meningitis (rare).Lithium (select drug-induced cases such as clozapine-related, specialist use)
Dose: Serum-level–guided (e.g., 300–600 mg PO BID/TID); only under specialist care.
Purpose: Can raise neutrophil counts by marrow stimulation.
Mechanism: Increases G-CSF and demargination.
Side effects: Narrow therapeutic window—renal/thyroid effects, tremor; monitor levels.
Stop the offending drug immediately when identified (e.g., antithyroid, clozapine, TMP-SMX). This is one of the most effective “treatments.”
Dietary molecular “supplements” or nutrients
Important: Supplements do not treat febrile neutropenia and can interact with medicines. Always coordinate with your clinician.
Vitamin B12
Dose: 1000 µg/day orally (or IM if malabsorption).
Function/Mechanism: Corrects megaloblastic changes that impair marrow production; cofactor for DNA synthesis (methionine synthase).
Note: Only helpful if deficient.Folate (vitamin B9)
Dose: 1 mg PO daily.
Function: DNA synthesis support for rapidly dividing marrow cells.
Mechanism: Restores thymidylate synthesis pathway.
Note: Treat B12 first if both are low.Copper
Dose: As prescribed (e.g., 2–8 mg elemental/day) if deficiency proven.
Function: Essential for hematopoiesis.
Mechanism: Enzyme cofactor (cytochrome c oxidase, ceruloplasmin).
Note: Copper deficiency can cause neutropenia; repletion reverses it.Vitamin C
Dose: 200–500 mg/day (diet first).
Function: Collagen synthesis, wound healing; antioxidant.
Mechanism: Improves neutrophil migration/oxidative burst in deficiency.
Note: High doses not proven to raise counts.Vitamin D
Dose: 800–2000 IU/day (or tailored to level).
Function: Immune modulation; supports barrier function.
Mechanism: VDR signaling affects innate/adaptive responses.
Note: Correct deficiency; avoid megadoses.Protein and calories (medical nutrition therapy)
Dose: 1.2–1.5 g/kg/day protein if ill (dietitian-guided).
Function: Substrate for immune cells, healing.
Mechanism: Prevents catabolism, supports marrow.
Note: Most impactful “supplement” is adequate food.Zinc (cautious, deficiency only)
Dose: 8–11 mg/day elemental (RDA); short course if low.
Function: Enzyme cofactor for immunity.
Mechanism: Thymic and neutrophil function.
Note: Excess zinc can worsen neutropenia via copper depletion.Selenium (if low)
Dose: 50–200 µg/day.
Function: Antioxidant enzymes (glutathione peroxidase).
Mechanism: Redox balance in immune cells.
Note: Narrow safety window.Glutamine (for mucositis support)
Dose: 10–30 g/day divided (when appropriate).
Function: Fuel for enterocytes/immune cells; may reduce mucosal injury.
Mechanism: Supports gut barrier → fewer translocation events.
Note: Mixed evidence; discuss with oncology/ID team.Omega-3 fatty acids (nutrition balance)
Dose: 1–2 g/day EPA+DHA total from food or supplement if advised.
Function: Resolve inflammation and support cardiovascular health.
Mechanism: Pro-resolving lipid mediators.
Note: May modestly increase bleeding risk with thrombocytopenia—clinician guidance needed.
Avoid probiotics/fermented supplements during severe neutropenia because of rare but reported bloodstream infections.
Immunity-booster / regenerative / stem-cell–related” therapies
Filgrastim (G-CSF) – Dose: 5 µg/kg SC daily. Function: Rapidly raises ANC. Mechanism: Stimulates marrow neutrophil production and release.
Pegfilgrastim – Dose: 6 mg SC per cycle. Function: Long-acting prophylaxis post-chemo. Mechanism: Sustained G-CSF receptor agonism.
Sargramostim (GM-CSF) – Dose: 250 µg/m² daily. Function: Broader myeloid stimulation. Mechanism: GM-CSF receptor activation.
Eltrombopag (select marrow failure) – Dose: 50–150 mg PO daily; off-label for aplastic anemia to support trilineage hematopoiesis. Mechanism: TPO receptor agonist on stem/progenitor cells. Note: Requires specialist oversight; liver and clotting monitoring.
Plerixafor (mobilization agent) – Dose: 0.24 mg/kg SC for stem-cell mobilization. Function: Helps collect stem cells for transplant. Mechanism: CXCR4 antagonist releases stem cells to blood. Note: Not a direct neutropenia fix unless used in a transplant plan.
IVIG (immune modulation) – Dose: 0.4 g/kg/day × 3–5 days. Function: Temporarily reduces autoimmune destruction. Mechanism: Fc receptor blockade; anti-idiotype effects.
True stem-cell therapy for agranulocytosis is hematopoietic stem-cell transplantation (HSCT)—a procedure, not a drug—covered below.
Procedures/surgeries
Hematopoietic stem-cell transplantation (HSCT)
Procedure: Conditioning chemotherapy ± radiation, infusion of donor stem cells, engraftment phase.
Why: Curative in congenital severe neutropenia failing G-CSF or with malignant transformation; also used in aplastic anemia or marrow failure syndromes.Central venous catheter insertion
Procedure: Ultrasound-guided line placement.
Why: Reliable access for IV antibiotics, antifungals, nutrition, and blood draws in prolonged therapy.Incision and drainage of abscess
Procedure: Surgical or interventional drainage with cultures.
Why: Source control when antibiotics alone cannot penetrate loculated pus (neutropenic patients may have “dry” collections—imaging helps).Debridement for necrotizing soft-tissue infection
Procedure: Urgent surgical removal of dead tissue.
Why: Life-saving source control in rapidly spreading infection.Splenectomy (rare, selective)
Procedure: Laparoscopic/ open removal of spleen.
Why: Refractory autoimmune neutropenia with hypersplenism when all medical options fail; risks and lifelong infection prevention needed.
Prevention strategies
Keep and show a fever plan; call/attend ED for ≥38.0°C.
Avoid the offending drug permanently; wear a medical alert tag.
Hand hygiene and simple masking in clinics/crowds.
Food safety: cook meats/eggs fully; avoid unpasteurized foods and raw sprouts/sushi.
Oral care: soft brush, saline/bicarbonate rinses; dental review when counts safe.
Vaccination with non-live vaccines when cleared by your clinician.
Catheter care and site checks; avoid unnecessary lines.
Household measures: shared surface cleaning; others manage pet litter/gardening.
Regular CBC monitoring when starting any high-risk medicine (e.g., clozapine, antithyroid).
Travel readiness: antibiotics plan and clinic contacts if traveling during low counts.
When to see a doctor (red flags)
Fever ≥38.0°C (100.4°F) once—go now.
Shaking chills, confusion, dizziness, fainting.
Shortness of breath, chest pain, oxygen saturation falling.
Rapidly spreading skin redness, severe pain, or black/gray patches.
Painful mouth ulcers with trouble swallowing or inability to drink.
Burning urination or flank pain.
Abdominal pain with persistent diarrhea.
Any new line redness or discharge.
Bleeding or bruising suggesting other cell line problems.
Persistent fever >24 hours despite antibiotics.
What to eat and what to avoid
Eat: Fully cooked meats, poultry, fish; Avoid: raw/undercooked versions (sushi, runny eggs).
Eat: Pasteurized milk, yogurt, cheeses; Avoid: unpasteurized dairy or soft cheeses from unknown sources.
Eat: Well-washed and peeled fruits/vegetables; Avoid: unwashed produce, salad bars, raw sprouts.
Eat: Freshly cooked leftovers reheated thoroughly; Avoid: buffets, foods sitting at room temperature.
Eat: Well-cooked legumes and grains; Avoid: undercooked beans or rice held warm for long periods.
Drink: Safe water, sealed bottles if uncertain; Avoid: untreated well or street-vendor ice.
Include: Adequate protein (eggs fully cooked, poultry, fish, tofu) to support healing.
Include: Healthy fats (olive oil, nuts if safe and fresh); Avoid: moldy/stale nuts.
Limit/avoid: Alcohol (interacts with drugs, depresses immunity).
Be careful with herbal products and probiotics—avoid unless your clinician approves.
Frequently asked questions
Is agranulocytosis the same as neutropenia?
All agranulocytosis is severe neutropenia; neutropenia is the broader term and can be mild, moderate, or severe.What ANC is dangerous?
ANC <500/µL is dangerous; fever + ANC <500 is an emergency.Can I look “okay” and still be very sick?
Yes. With few neutrophils, classic redness or pus may be absent; fever may be the only sign.How fast do I need antibiotics?
As soon as possible—ideally within 1 hour of arrival when febrile.How long does recovery take?
Drug-induced cases may recover in days to 1–2 weeks after stopping the drug; marrow diseases take longer and need specific therapy.Will G-CSF cure me?
It accelerates neutrophil recovery but does not cure the underlying cause unless the cause was transient marrow suppression.Can vitamins fix agranulocytosis?
Only if your problem is a true deficiency (B12, folate, copper). Otherwise vitamins are supportive, not curative.Are probiotics safe?
Not during severe neutropenia—rare bloodstream infections have been reported.What about vaccines?
Non-live vaccines are generally used when your team says counts are safe. Live vaccines are avoided until cleared.Can I keep my pets?
Yes, with care: others should handle litter; avoid scratches; wash hands after contact.Will this happen again?
Avoiding the trigger drug prevents many recurrences. Some marrow disorders can relapse and need long-term plans.Is clozapine always dangerous?
Clozapine can cause agranulocytosis in a small percent; strict routine CBC monitoring allows many to use it safely when benefits outweigh risks.Do I need a special diet forever?
No. Focus on safe handling during neutropenia. When ANC recovers, diet can liberalize per your team.When is HSCT considered?
In congenital severe neutropenia failing G-CSF, in aplastic anemia, or if malignant transformation occurs—specialist decision.Can stress lower neutrophils?
Stress alone does not cause agranulocytosis, but good sleep and stress control help overall immunity and recovery.
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The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: September 10, 2025.
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