Grade neutrophil deficiency, recognise infection despite muted signs, identify drug, immune, nutritional, infective and marrow causes, and stop culpable exposure while supporting safe recovery.
Neutrophils provide rapid phagocytic defence at damaged mucosa and sites of bacterial and fungal invasion. Infection risk rises as the count falls, the duration lengthens and mucosal, line or immune barriers are damaged. Profound deficiency can remove pus, focal inflammation and a large CRP response, so sore throat, oral ulcer, perianal discomfort or fever may be the only clue. Steroids can mask fever, while recent G-CSF can change the count rapidly; always interpret the current number within treatment timing.
Causes divide into reduced production, immune destruction, redistribution and sequestration. Chemotherapy and marrow failure reduce production; idiosyncratic drug agranulocytosis may be immune or toxic; autoimmune neutropenia increases destruction; sepsis consumes and redistributes cells; splenomegaly sequesters them. A time course and prior counts are high-value. Acute isolated neutropenia after a new medicine differs from months of stable mild neutropenia, and pancytopenia demands a wider marrow investigation.
Dose-related cytotoxic suppression or unpredictable immune and toxic reactions can sharply reduce granulopoiesis, sometimes after a medicine has already been stopped.
Aplastic anaemia, myelodysplasia, leukaemia, infiltration, B12, folate and copper deficiency impair production, often affecting additional blood-cell lines.
Autoimmune neutropenia, systemic lupus, HIV and acute viral infections can increase destruction or suppress production, with duration and accompanying features guiding tests.
Duffy-null genotype can produce a stable lower neutrophil count without increased infection, requiring recognition to prevent unnecessary restriction or invasive investigation.
Stem-cell or myeloid precursor injury limits marrow release, so the count remains low until surviving progenitors recover or growth-factor support takes effect.
Drug-dependent or autoimmune antibodies and splenic macrophages can remove circulating neutrophils faster than marrow replacement, sometimes preserving other lineages.
Loss of neutrophils combines with oral, intestinal, skin or line disruption, allowing endogenous organisms to invade without a robust local inflammatory response.
Fever, rigors or malaise may occur without pus, erythema or focal consolidation because neutrophil recruitment is absent.
Sore throat, fever and oral ulcers after carbimazole, clozapine or another implicated medicine demands an urgent count and medicine hold.
Anaemia, thrombocytopenia, macrocytosis, dysplasia or blasts alongside neutropenia raises global marrow failure or clonal disease.
Hypotension, confusion, raised lactate or hypoxia with neutropenia needs immediate antibiotics and organ support regardless of temperature.
Longstanding isolated mild neutropenia without infections or other abnormalities may reflect Duffy-null or another benign constitutional state.
Sample delay, analyser flags or rare EDTA-dependent cell aggregation can produce a misleading result; repeat count and film verify an unexpected stable finding.
Leukaemia can present with neutropenia, anaemia or thrombocytopenia despite no automated blast flag, requiring film and marrow assessment when clinical features persist.
Overwhelming infection may consume and redistribute neutrophils, so a low count can be consequence rather than pre-existing cause and indicates severe physiology.
Splenomegaly from liver, infective or haematological disease can sequester neutrophils with platelets and red cells, producing a multilineage peripheral cytopenia.
Gut, oral, skin and line organisms can invade rapidly, producing shock with minimal local signs when the absolute neutrophil count is profoundly reduced.
Prolonged profound neutropenia predisposes to mould and yeast disease, often presenting as persistent fever, pulmonary nodules or sinus findings despite antibiotics.
Painful oral ulceration, periodontal infection and perianal inflammation can impair nutrition and provide portals for bloodstream infection while examination signs remain subtle.
Stopping antipsychotic, antithyroid, cancer or immune therapy may destabilise the underlying illness, requiring coordinated substitution rather than an isolated laboratory instruction.
Profound neutropenia removes the cells that create local inflammation, so a deceptively quiet examination can coexist with invasive infection.
A count below 0.5 for weeks after chemotherapy carries different fungal risk from a brief post-viral nadir.
Immune agranulocytosis can present after exposure stops, making the preceding weeks as important as today's prescription chart.
A healthy genetically determined reference range should prevent inequitable exclusion from treatment while retaining normal clinical vigilance.
Waiting for fever when septic physiology is present.
Looking only at today's medicine list.
Rechallenging a suspected agranulocytosis drug casually.
Equating ancestry with benign neutropenia without assessment.
Sending every stable mild case straight to marrow biopsy.
Using G-CSF instead of antibiotics during sepsis.
Your practice draft is saved in this browser.
A patient taking carbimazole for Graves' disease develops fever, a severe sore throat and several painful mouth ulcers over one day. Which immediate advice is appropriate?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Bone pain, splenic enlargement or rupture, leucocytosis, lung injury and sickle crisis are recognised; it does not replace antibiotics or source control in infection.
Coordinate clozapine, antithyroid or seizure treatment alternatives urgently; document the reaction and avoid inadvertent exposure to the same or cross-reactive agent.