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Hepatitis A

Hepatitis A (Hep A) is an inflammation of the liver caused by the Hepatitis A Virus (HAV). It causes an acute infection only — unlike Hepatitis B and C, HAV does not lead to chronic liver disease. The incubation period (the period of time you can have the infection before developing symptoms) is typically about 28 days, with a range of 15 to 50 days between exposure and the onset of symptoms.

Transmission

The virus is primarily spread when an uninfected (and unvaccinated) person ingests food or water contaminated with an infected person's faeces.

Signs and Symptoms

• Jaundice

• Itchy skin

• Fever

• Flu-like symptoms

• Fatigue

• Nausea

• Vomiting

• Abdominal pain

• Dark brown coloured urine

• Pale grey or yellow stools

• Headache

• Muscle pains

Diagnostic test

The diagnosis of Hepatitis A is made by detecting Hepatitis A Virus-specific Immunoglobulin M antibodies (IgM anti-HAV) in the blood.

IgM anti-HAV (Hepatitis A Virus IgM antibody): IgM anti-HAV is the antibody produced early in the immune response to HAV infection. Its presence indicates acute or recent infection and is the test of choice for diagnosing symptomatic patients. IgM anti-HAV typically becomes detectable around the onset of symptoms and remains positive for several months before declining.

IgG anti-HAV (Hepatitis A Virus IgG antibody): IgG anti-HAV is produced later in the immune response and persists long-term. Its presence indicates immunity, either from previous infection or from vaccination. Because IgG anti-HAV remains positive indefinitely, it cannot be used to diagnose acute illness.

Total anti-HAV (Total Hepatitis A Virus antibody): Total anti-HAV measures combined IgM and IgG antibodies. Like isolated IgG anti-HAV, it remains positive long after infection has resolved and therefore does not help diagnose acute illness.

HAV RNA (Hepatitis A Virus RNA): HAV RNA is the genetic material of the virus. HAV RNA can appear in blood or stool before IgM antibodies develop, so it is occasionally used to confirm infection early or in outbreak investigations and research settings — it is not part of routine diagnostic testing.

Treatment

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Symptoms

Symptoms of serotonin syndrome can be categorised into three categories: neuromuscular, autonomic and affecting mental state.

Neuromuscular symptoms include tremors, hyperreflexia and clonus. Autonomic includes dilated pupils, sweating, increased heart rate and increased breathing rate. Alterations in mental state include agitation, excitement, restlessness, confusion and delirium.

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Causes

Serotonin syndrome (serotonin toxicity) is caused by excess serotonergic activity in the central nervous system. This most commonly occurs when multiple serotonergic drugs are combined, but it can also occur with a single agent at high doses or in overdose.

Examples of some drugs that can cause serotonin toxicity include:

• Amphetamines and derivatives, such as dextroamphetamine and methamphetamine

• Antidepressants, such as MAOIs, SSRIs, SNRIs, and TCAs

• Lithium

• Opioids with serotonergic activity, such as tramadol, fentanyl, and pethidine

• Other agents, such as linezolid (a weak MAOI), cocaine, 5-hydroxytryptophan (a serotonin precursor), triptans, dextromethorphan, and St John’s Wort

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Diagnosis

Diagnosis is made using the Hunter Serotonin Toxicity Criteria (HSTC).

A patient must have the presence of a serotonergic agent and meet one of the following conditions:

• Spontaneous clonus

• Inducible clonus plus agitation or diaphoresis (sweating)

• Ocular clonus plus agitation or diaphoresis (sweating)

• Tremor plus hyperreflexia

• Hypertonia plus temperature above 38°C PLUS ocular clonus or inducible clonus

- UpToDate: Serotonin syndrome (serotonin toxicity) (2026)

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Treatment

Treatment is based on the severity of symptoms.

Mild serotonin toxicity

Treatment is not usually required beyond ceasing or reducing the dose of the offending drug(s), if appropriate.

Symptoms of mild serotonin toxicity include: hyperreflexia, inducible clonus, tremor, myoclonic jerks, sweating, mild hypertension, tachycardia, mydriasis, and shivering. More non-specific symptoms, such as headache or restlessness, may also occur. Hyperreflexia and clonus are most prominent in the lower limbs.

Moderate serotonin toxicity

As with mild toxicity, the priority in management is identifying and stopping or dose-reducing the offending drug(s).

Additional measures include:

• Benzodiazepines for anxiety, agitation, and sedation

• Cyproheptadine (a non-specific 5-HT₂ antagonist with antihistaminic and sedative properties) as a single higher dose for distressing neuromuscular excitation or agitation

• For long half-life serotonergic agents (e.g., fluoxetine), repeated lower doses of cyproheptadine may be preferred over a single large dose

Symptoms of moderate serotonin toxicity include: all mild features, plus temperature up to 38°C, hyperactive bowel sounds, ocular clonus, agitation, and hypervigilance. Clonus is often still inducible but may be spontaneous.

Severe serotonin toxicity

This is a medical emergency, usually managed in a critical care setting.

Management includes:

• Early sedation, with intubation and ventilation if required, to control agitation, hyperthermia, and muscle rigidity

• Cyproheptadine (oral or via NG tube) is used first-line in serious cases. In severe cases, chlorpromazine (IV, with fluid loading first to reduce the risk of hypotension) may be used; if IV chlorpromazine is unavailable, olanzapine (IM/SC) may be considered as an alternative. Neither cyproheptadine nor chlorpromazine is supported by controlled trial evidence, though both have been used successfully in case reports of serotonin toxicity following overdose

• Aggressive cooling for hyperthermia

• Once stabilised, all serotonergic drugs should remain stopped and reassessed

Symptoms of severe serotonin toxicity include: all mild and moderate features, plus a temperature of more than 38.5°C, dramatic swings in pulse rate and blood pressure, delirium, muscle rigidity, and spontaneous (sustained) clonus.

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Restarting serotonergic medication

Depending on the cause of the serotonin toxicity (e.g., a drug interaction versus a single agent at high dose), a serotonergic medication may be cautiously restarted at a lower dose once all symptoms have fully resolved, with close monitoring during reintroduction. If an MAOI was involved, an extended washout period is required before restarting other serotonergic agents. Patients should be educated about the signs and symptoms of serotonin toxicity and advised on what to do if symptoms recur.

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References

• American Family Physician: Prevention, Diagnosis, and Management of Serotonin Syndrome (https://www.aafp.org/afp/2010/0501/p1139)

• BMJ Best Practice: Serotonin Syndrome (https://bestpractice.bmj.com/topics/en-gb/991)

• BNF: Antidepressant drugs (https://bnf.nice.org.uk/treatment-summaries/antidepressant-drugs/)

• BNF: Appendix 1 Interactions (https://bnf.nice.org.uk/interactions/appendix-1-interactions/)

• Geeky Medics: Serotonin Syndrome (https://geekymedics.com/serotonin-syndrome/)

• International Journal of Molecular Sciences: The Serotonin Syndrome: From Molecular Mechanisms to Clinical Practice (https://doi.org/10.3390/ijms20092288)

• NHS HEE: Serotonin Syndrome (https://www.hee.nhs.uk/sites/default/files/documents/Serotonin_Syndrome.pdf)

• Osmosis: Serotonin Syndrome (https://www.osmosis.org/answers/serotonin-syndrome)

• Patient: Serotonin Syndrome (https://patient.info/doctor/drug-therapy/serotonin-syndrome)

• Right Decision Service: supporting decisions for Scotland’s health and care: Serotonin Syndrome (https://www.rightdecisions.scot.nhs.uk/mypsych-app/working-in-greater-glasgow-clyde/medicines-companion/emergencies-2222/serotonin-syndrome/)

• TOXBASE: Serotonin Syndrome (https://www.toxbase.org/poisons-index-a-z/s-products/serotonin-syndrome/)

• UpToDate: Serotonin syndrome (serotonin toxicity) (https://www.uptodate.com/contents/serotonin-syndrome-serotonin-toxicity)

Hyperkalaemia is a medical condition in which the potassium level in the blood is raised. It can be classified as mild (potassium between 5.5 – 5.9 mmol/L), moderate (potassium between 6.0 – 6.4 mmol/L), and severe (potassium more than 6.5 mmol/L). Symptoms can include muscle weakness and paralysis, fatigue, respiratory depression, and cardiac arrhythmias, including sinus bradycardia, ventricular tachycardia, ventricular fibrillation, and asystole.

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Causes

Hyperkalemia is caused by three main mechanisms. First, impaired renal potassium excretion, as seen in acute or chronic renal failure, inhibition of the renin-angiotensin-aldosterone system (RAAS) caused by medications such as ACE inhibitors (Angiotensin-Converting Enzyme inhibitors), ARBs (Angiotensin II Receptor Blockers), and aldosterone antagonists. Secondly, transcellular shifts of potassium out of cells, such as in tumour lysis syndrome, rhabdomyolysis, metabolic acidosis, insulin deficiency, and beta-blocker use, which impairs β₂-adrenergic-mediated potassium uptake into cells. Finally, increased potassium intake, such as from a high-potassium diet or salt substitutes containing potassium chloride, though this rarely causes hyperkalemia on its own unless renal excretion is also impaired.

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Potassium and the heart

Cardiomyocyte action potential

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“Hepatorenal syndrome (HRS) is defined as the occurrence of renal failure in a patient with advanced liver disease in the absence of an identifiable cause of renal failure. Thus, the diagnosis is essentially one of exclusion of other causes of renal failure” — EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis (2010).

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Classification and diagnosis

There are two different types of hepatorenal syndrome (HRS). HRS-AKI (HRS-Acute Kidney Injury), previously known as Type 1 HRS, which is defined as an increase in serum creatinine of ≥26.5 micromol/L within 48 hours, or ≥1.5 times baseline. HRS-NAKI (HRS-Non-Acute Kidney Injury), previously known as Type 2 HRS, encompasses kidney dysfunction not meeting HRS-AKI criteria. HRS-NAKI is further divided into HRS-AKD (HRS-Acute Kidney Disease) and HRS-CKD (HRS-Chronic Kidney Disease). HRS-AKD is characterised by an eGFR below 60 mL/min for less than three months, while HRS-CKD is defined by an eGFR below 60 mL/min for more than three months.

Diagnosis of HRS-AKI requires all of the following International Club of Ascites (ICA) criteria to be met:

• Cirrhosis with ascites.

• Serum creatinine meeting HRS-AKI criteria.

• No response to diuretic withdrawal and 2 day fluid challenge with 1g/kg/day of Human Albumin Solution (HAS) 20%.

• Absence of shock.

• No current or recent nephrotoxic medication use e.g. NSAIDs, contrast dye, etc.

• No structural kidney disease:

  • normal ultrasound.

  • absence of proteinuria <500 mg/day.

  • absence of haematuria <50 red cells per high power field.

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Pathophysiology

Advanced liver cirrhosis leads to portal hypertension due to scarring of the liver. Portal hypertension promotes bacterial translocation across the gut wall and increased stress on splanchnic vessels, which upregulates endothelial nitric oxide synthase and drives splanchnic nitric oxide production. This causes splanchnic vasodilation and increased blood flow to the splanchnic organs, reducing the effective arterial blood volume (EABV).

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The precise causes of IBD are not fully understood, but current evidence supports a multifactorial aetiology involving a complex interplay between genetic susceptibility and environmental triggers. Environmental factors implicated in the development or exacerbation of IBD include diet, smoking, infection, gut microbiota dysbiosis, certain drugs and appendectomy.

The immunological basis of IBD remains an area of active research. One prevailing hypothesis is that chronic intestinal inflammation results from increased activity of effector lymphocytes and proinflammatory cytokines that override normal mucosal immune control mechanisms. An alternative, though not mutually exclusive, hypothesis proposes that IBD arises from a primary failure of regulatory lymphocytes and cytokines, such as IL-10 and TGF-β, to suppress effector immune pathways adequately. In Crohn’s disease specifically, there is evidence that T-cells exhibit resistance to apoptosis following inactivation, contributing to the persistence of mucosal inflammation.

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Crohn’s disease

Crohn’s disease is a chronic inflammatory condition characterised by inflammation that can affect any part of the gastrointestinal tract from the mouth to the anus. Unlike ulcerative colitis, inflammation in Crohn’s disease is discontinuous, with affected segments separated by areas of healthy mucosa, known as skip lesions. Rectal sparing is a feature that helps distinguish Crohn’s disease from ulcerative colitis, though rectal involvement can occasionally occur. Inflammation is characterised by deep ulceration, which extends through the full thickness of the bowel wall. Fistulas, which are channels that can form between the bowel and the skin or between the bowel and another organ, are common in Crohn’s disease, and so are strictures, which are caused by chronic inflammation and subsequent fibrosis, leading to narrowing of the gut walls and potentially causing obstructive symptoms.

Predominant symptoms of active disease include diarrhoea, urgency and frequency of bowel movements, abdominal pain and cramping, and weight loss. Blood in the stool may occur, but it is less consistent than in ulcerative colitis and is more likely in patients with colonic involvement. Weight loss in Crohn’s disease is multifactorial, resulting from malabsorption (particularly in small bowel disease), reduced oral intake due to pain and nausea, and increased metabolic demand from chronic inflammation, and can lead to significant nutritional deficiency.

Treatment aims to induce remission, maintain remission and prevent relapse.

Inducing Remission

Disease severity is classified as mild, moderate or severe using validated scoring tools such as the Harvey-Bradshaw Index (HBI) or the Crohn’s Disease Activity Index (CDAI), and treatment is guided by both disease severity and location.

In mild-to-moderate disease, corticosteroids are the mainstay of induction therapy. Oral budesonide is preferred for Crohn’s disease affecting the ileum and/or ascending colon due to its high first-pass metabolism and more favourable systemic side-effect profile compared to conventional corticosteroids. Oral prednisolone is used for more severe or extensive disease.

In moderate-to-severe or corticosteroid-refractory disease, advanced therapies are indicated. Biological therapies include Tumour Necrosis Factor-alpha (TNF-α) inhibitors such as infliximab and adalimumab; the gut-selective α₄β₇ integrin inhibitor vedolizumab; Interleukin-12/23 (IL-12/23) inhibitor such as ustekinumab; and Interleukin-23 (IL-23) inhibitors such as risankizumab, mirikizumab and guselkumab. The Janus kinase (JAK) inhibitor upadacitinib is also licensed for moderately to severely active Crohn’s disease in the UK. Combination therapy with an immunomodulator such as azathioprine or mercaptopurine is recommended with TNF-α inhibitors to reduce immunogenicity. Surgery, including bowel resection, remains an important treatment option for patients with stricturing or fistulating disease or those who are refractory to medical therapy.

Maintaining Remission

Once remission has been achieved, ongoing therapy is required to prevent relapse. Options for maintenance include azathioprine, mercaptopurine and methotrexate, which are used as immunomodulators. Biological therapies and JAK inhibitors used to induce remission are generally continued for maintenance in patients with moderate-to-severe disease. Mesalazine is not recommended for the maintenance of remission in Crohn’s disease by major guidelines, including the British Society of Gastroenterology (BSG) and the European Crohn’s and Colitis Organisation (ECCO), owing to a lack of robust supporting evidence, regardless of disease distribution.

Preventing Relapse

The most evidence-based strategy for preventing relapse is adherence to maintenance medication. Smoking cessation is particularly important in Crohn’s disease, as smoking is a well-established risk factor for disease activity. This should be done slowly to prevent the risk of flaring. Patients should also be advised to identify and, where possible, avoid personal trigger factors, which may include dietary factors and psychological stress.

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Ulcerative colitis

Ulcerative colitis (UC) is a long-term inflammatory condition affecting the large intestine (colon) and rectum. Inflammation begins at the rectum and extends proximally in a continuous and diffuse pattern, potentially involving the entire colon (extensive colitis/pancolitis). The extent of disease is classified by the Montreal Classification as proctitis (E1), left-sided colitis (E2) or extensive colitis (E3).

Predominant symptoms of active disease include bloody diarrhoea with mucus and/or pus, urgency and frequency in passing faeces, and abdominal pain. If inadequately managed, UC can be associated with extraintestinal manifestations (EIMs). UC is also associated with life-threatening acute gastrointestinal complications, including toxic megacolon and bowel perforation. In addition, chronic, longstanding inflammation is associated with an increased risk of colorectal cancer, particularly in patients with extensive disease and prolonged disease duration.

As with Crohn’s disease, the aims of treatment include inducing remission, maintaining remission and preventing relapse.

Inducing Remission

Disease severity is classified as mild, moderate or severe using validated scoring tools such as the Truelove and Witts Severity Index or the Mayo Score, and treatment is guided by both severity and the extent of inflammation.

In mild-to-moderate disease, treatment is determined by disease extent. Proctitis is treated with topical mesalazine as first-line therapy, with topical corticosteroids or oral mesalazine used as adjuncts if needed. In left-sided and extensive disease, the combination of oral and topical mesalazine is more effective than either alone and is recommended by the BSG and the National Institute for Health and Care Excellence (NICE) as first-line therapy. In patients who fail to respond to aminosalicylate therapy, corticosteroids can be added to induce remission.

In moderate-to-severe disease, oral corticosteroids are typically used. In acute severe ulcerative colitis (ASUC), patients require hospital admission and treatment with intravenous corticosteroids as first-line therapy. In those who fail to respond within 72 hours, rescue therapy with either intravenous ciclosporin (off-label) or infliximab should be considered. In refractory or frequently relapsing moderate-to-severe disease, a range of advanced therapies may be used, including biological therapies such as infliximab, adalimumab, golimumab, vedolizumab, ustekinumab, risankizumab, mirikizumab and guselkumab; JAK inhibitors such as tofacitinib, filgotinib and upadacitinib; and Sphingosine-1-phosphate (S1P) receptor modulators such as ozanimod and etrasimod. Surgery in the form of colectomy remains an important option in patients with refractory disease or those who develop life-threatening complications.

Maintaining Remission

Once remission has been achieved, ongoing treatment is required to maintain it. Options include mesalazine, azathioprine or mercaptopurine, and advanced therapies – including biological agents, JAK inhibitors and S1P receptor modulators – in patients with more complex or refractory disease. The choice of maintenance therapy is guided by the treatment used to induce remission, disease severity and patient factors.

Preventing Relapse

The most evidence-based strategy for preventing relapse is adherence to maintenance medication, particularly mesalazine in patients with mild-to-moderate disease. Patients should also be advised to identify and, where possible, avoid personal trigger factors, which may include dietary factors and psychological stress, though the evidence for these as modifiable relapse triggers is less robust than for medication adherence.

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Mesalazine

Mesalazine is an aminosalicylate used primarily in the management of ulcerative colitis. Major guidelines, including those from BSG and ECCO, do not recommend mesalazine for either the induction or maintenance of remission in Crohn's disease, owing to a lack of robust supporting evidence.

Different preparations are released at different parts of the gastrointestinal tract. Pentasa^® is time-dependent and starts releasing the active drug from the duodenum to the colon. Mezavant XL^®, Octasa^® and Asacol^® are pH-dependent and start releasing at pH≥7 in the terminal ileum to the entire colon. Salofalk^® is also pH dependent and releases at pH≥6 from the mid-ileum to the colon. Therefore, it is recommended that mesalazine should be prescribed by brand.

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Azathioprine

Azathioprine is an immunomodulator used to maintain remission in IBD. It can also be used alongside TNF-α inhibitors such as infliximab, adalimumab or golimumab to reduce immunogenicity and help preserve their therapeutic effects.

Azathioprine is converted to mercaptopurine via a non-enzymatic glutathione-mediated reaction. Mercaptopurine then undergoes metabolism via competing pathways. Thiopurine methyltransferase (TPMT) converts mercaptopurine to the pharmacologically inactive metabolite 6-methylmercaptopurine (MeMP), which is also hepatotoxic. Alternatively, xanthine oxidase converts mercaptopurine to the inactive metabolite 6-thiouric acid. The remaining mercaptopurine is channelled toward the production of 6-thioguanine nucleotides (TGN), the pharmacologically active metabolites responsible for immunosuppression through incorporation into DNA and inhibition of purine synthesis, leading to suppression of T-lymphocyte proliferation.

TPMT activity significantly influences the balance of these metabolites. Before initiating therapy, TPMT activity should be tested. Patients with low or absent TPMT activity are unable to efficiently methylate mercaptopurine, meaning it is almost entirely channelled toward TGN production, placing them at serious risk of profound myelosuppression and life-threatening bone marrow toxicity. Conversely, patients with high TPMT activity rapidly convert mercaptopurine to MeMP, producing subtherapeutic TGN levels. In these patients, low-dose allopurinol can be co-administered to inhibit xanthine oxidase, blocking an alternative degradation pathway and redirecting metabolism toward TGN production. However, when allopurinol is used, the azathioprine or mercaptopurine dose must be reduced by approximately 25-33% to avoid toxic TGN accumulation.

Therapeutic drug monitoring (TDM) can be performed by measuring TGN and MeMP levels, helping clinicians to guide dose optimisation, assess adherence, and identify toxicity in patients taking azathioprine or mercaptopurine.

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Extraintestinal manifestation of IBD

Approximately 25-40% of people living with IBD develop extraintestinal manifestations (EIMs), which are conditions that occur outside the gastrointestinal tract.

EIMs can affect multiple organ systems, and joint disease is one of the most common manifestations. One type is pauciarticular, affecting fewer than five large joints and typically paralleling intestinal disease activity. The other is polyarticular, involving five or more small joints and following a course that is independent of bowel inflammation. Cutaneous manifestations include erythema nodosum and pyoderma gangrenosum. Ocular manifestations include episcleritis, which is the most common eye complaint, and uveitis, which is less common but more serious.

Metabolic and nutritional complications are also common. IBD is a recognised cause of secondary osteoporosis, resulting from chronic inflammation, corticosteroid use, and malabsorption. Osteomalacia can occur, particularly in patients with small bowel Crohn’s disease, where vitamin D malabsorption is more pronounced. Iron deficiency anaemia (IDA) and anaemia of chronic disease (ACD) are both frequently encountered. Deficiencies in folate and vitamin B12 can also occur, the latter being especially relevant in patients with ileal Crohn’s disease or those who have undergone ileal resection.

Hepatobiliary complications include gallstones, which are more prevalent in patients with ileal Crohn’s disease due to impaired bile acid reabsorption, and primary sclerosing cholangitis (PSC), which occurs more frequently in ulcerative colitis than Crohn’s disease. IBD is associated with a prothrombotic state due to chronic inflammation, predisposing patients to venous thromboembolic (VTE) complications such as deep vein thrombosis (DVT) and portal vein thrombosis (PVT); this risk is present in both Crohn’s disease and ulcerative colitis. The risk of VTE is estimated to be approximately 2-3 fold higher than in the general population and is further elevated during active flares and hospitalisation. VTE prophylaxis should therefore be considered in all hospitalised IBD patients with an active flare, in accordance with local and national guidelines.

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References

• British Society of Gastroenterology guidelines on inflammatory bowel disease in adults: 2025 (2025) (https://doi.org/10.1136/gutjnl-2024-334395)

• ECCO Guidelines on Extraintestinal Manifestations in Inflammatory Bowel Disease (2023) (https://doi.org/10.1093/ecco-jcc/jjad108)

• ECCO Guidelines on Therapeutics in Crohn’s Disease: Medical Treatment (2024) (https://doi.org/10.1093/ecco-jcc/jjae091)

• ECCO Guidelines on Therapeutics in Ulcerative Colitis: Medical Treatment (2021) (https://doi.org/10.1093/ecco-jcc/jjab178)

• NICE: Inflammatory bowel disease (2026) (https://www.nice.org.uk/guidance/conditions-and-diseases/digestive-tract-conditions/inflammatory-bowel-disease)

• SPS: Using mesalazine tablets appropriately (2025) (https://www.sps.nhs.uk/articles/using-mesalazine-tablets-appropriately/)

Iron is absorbed via the proximal part of the duodenum. It is transferred into the blood via ferroportin. Once in the blood, iron binds to transferrin. Transferrin levels (measured as total iron-binding capacity, TIBC) increase when iron is low, as the body tries to ‘scavenge’ more iron. Transferrin saturation (TSAT) is the percentage of transferrin binding sites actually occupied by iron. Each transferrin molecule has two iron binding sites (so in this diagram the TSAT is 50% as there are 3 molecules of iron bound to a total of 6 sites). Transferrin carries iron to the bone marrow for red blood cell production and to the liver for storage. Iron is stored inside cells within ferritin molecules. When iron levels are high, the liver produces hepcidin, which degrades ferroportin, blocking further iron export into the blood. Ferritin is the main storage complex and is present mostly in the liver, but also in the bone marrow, spleen, and muscles. Small amounts of ferritin also circulate in the blood. Low levels of serum ferritin are indicative of iron deficiency anaemia (IDA).

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References

• British Society for Haematology: Guideline for the laboratory diagnosis of iron deficiency in adults (excluding pregnancy) and children (https://doi.org/10.1111/bjh.17900)

• BSG Guidelines for the Management of Iron Deficiency Anaemia in Adults (https://doi.org/10.1136/gutjnl-2021-325210)

• NICE CKS: Anaemia - iron deficiency (https://cks.nice.org.uk/topics/anaemia-iron-deficiency/)

• LearnHaem - Anaemia (https://www.learnhaem.com/courses/anaemia/)

• LabTestOnlineUK (https://labtestsonline.org.uk/)