The elevated ferritin level can be attributed to the patient’s excessive alcohol consumption, as the typical transferrin saturation rules out iron overload as a potential cause.

Understanding Ferritin Levels in the Body

Ferritin is a protein found inside cells that binds to iron and stores it for later use. When ferritin levels are increased, it is usually defined as being above 300 µg/L in men and postmenopausal women, and above 200 µg/L in premenopausal women. However, it is important to note that ferritin is an acute phase protein, meaning that it can be synthesized in larger quantities during times of inflammation. This can lead to falsely elevated results, which must be interpreted in the context of the patient’s clinical picture and other blood test results.

There are two main categories of causes for increased ferritin levels: those without iron overload (which account for around 90% of patients) and those with iron overload (which account for around 10% of patients). Causes of increased ferritin levels without iron overload include inflammation, alcohol excess, liver disease, chronic kidney disease, and malignancy. Causes of increased ferritin levels with iron overload include primary iron overload (hereditary hemochromatosis) and secondary iron overload (which can occur after repeated transfusions).

On the other hand, reduced ferritin levels can be an indication of iron deficiency anemia. Since iron and ferritin are bound together, a decrease in ferritin levels can suggest a decrease in iron levels as well. Measuring serum ferritin levels can be helpful in determining whether a low hemoglobin level and microcytosis are truly caused by an iron deficiency state. It is important to note that the best test for determining iron overload is transferrin saturation, with normal values being less than 45% in females and less than 50% in males.

An urgent full blood count is required to evaluate for leukaemia in children and young adults (0-24 years) who exhibit symptoms suggestive of the disease. These symptoms may include persistent fatigue, unexplained infections, and pallor. The primary concern is to rule out leukaemia, and a full blood count should be conducted within 48 hours. While a lymph node biopsy and bone marrow biopsy may be necessary in the future, they are not currently required.

Identifying Haematological Malignancy in Young People

Young people aged 0-24 years who exhibit any of the following symptoms should undergo a full blood count within 48 hours to investigate for leukaemia: pallor, persistent fatigue, unexplained fever, unexplained persistent infections, generalised lymphadenopathy, persistent or unexplained bone pain, unexplained bruising, and unexplained bleeding. These symptoms may indicate the presence of haematological malignancy, which requires prompt diagnosis and management. It is important to identify these symptoms early to ensure timely treatment and improve outcomes for young people with suspected haematological malignancy. Therefore, healthcare professionals should be vigilant in recognising these symptoms and referring patients for urgent investigation. Proper management of haematological malignancy in young people can significantly improve their quality of life and long-term prognosis.

Sulphur-containing drugs such as sulphonamides, sulphasalazine, and sulfonylureas can cause haemolysis in individuals with G6PD deficiency. On the other hand, penicillins, cephalosporins, macrolides, and tetracyclines are considered safe for use in individuals with G6PD deficiency.

Understanding G6PD Deficiency

G6PD deficiency is a common red blood cell enzyme defect that is inherited in an X-linked recessive fashion and is more prevalent in people from the Mediterranean and Africa. The deficiency can be triggered by many drugs, infections, and broad (fava) beans, leading to a crisis. G6PD is the first step in the pentose phosphate pathway, which converts glucose-6-phosphate to 6-phosphogluconolactone and results in the production of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is essential for converting oxidized glutathione back to its reduced form, which protects red blood cells from oxidative damage by oxidants such as superoxide anion (O2-) and hydrogen peroxide. Reduced G6PD activity leads to decreased reduced glutathione and increased red cell susceptibility to oxidative stress, resulting in neonatal jaundice, intravascular hemolysis, gallstones, splenomegaly, and the presence of Heinz bodies on blood films. Diagnosis is made by using a G6PD enzyme assay, and some drugs are known to cause hemolysis, while others are considered safe.

Compared to hereditary spherocytosis, G6PD deficiency is more common in males of African and Mediterranean descent and is characterized by neonatal jaundice, infection/drug-induced hemolysis, and gallstones. On the other hand, hereditary spherocytosis affects both males and females of Northern European descent and is associated with chronic symptoms, spherocytes on blood films, and the presence of erythrocyte membrane protein band 4.2 (EMA) binding.

Thrombocytopenia can be caused by heparin, including the low molecular weight heparin enoxaparin. Prosthetic joints are not a common cause of thrombocytopenia, while the other drugs listed are not typically associated with this condition. If heparin-induced thrombocytopenia is suspected or confirmed, it is important to discontinue heparin and switch to an alternative anticoagulant like danaparoid. Platelet counts should be monitored and normalized before administering warfarin.

Understanding Drug-Induced Thrombocytopenia

Drug-induced thrombocytopenia is a condition where a person’s platelet count drops due to the use of certain medications. This condition is believed to be immune-mediated, meaning that the body’s immune system mistakenly attacks and destroys platelets. Some of the drugs that have been associated with drug-induced thrombocytopenia include quinine, abciximab, NSAIDs, diuretics like furosemide, antibiotics such as penicillins, sulphonamides, and rifampicin, and anticonvulsants like carbamazepine and valproate. Heparin, a commonly used blood thinner, is also known to cause drug-induced thrombocytopenia. It is important to be aware of the potential side effects of medications and to consult with a healthcare provider if any concerning symptoms arise. Proper management and monitoring of drug-induced thrombocytopenia can help prevent serious complications.

Patients who are taking bone marrow suppression drugs, particularly methotrexate, should steer clear of using chloramphenicol eye drops for treating bacterial conjunctivitis. Co-trimoxazole and trimethoprim should also be avoided as they can increase the risk of methotrexate toxicity and pancytopenia. Aspirin and lisinopril are unlikely to interact seriously with methotrexate. However, caution should be exercised when using gliclazide and metformin in patients with a history of CKD 3, although the concurrent use of chloramphenicol is not expected to pose any problems.

Aplastic anaemia is a condition characterized by a decrease in the number of blood cells due to a poorly functioning bone marrow. It is most commonly seen in individuals around the age of 30 and is marked by a reduction in red blood cells, white blood cells, and platelets. While lymphocytes may be relatively spared, the overall effect is a condition known as pancytopenia. In some cases, aplastic anaemia may be the first sign of acute lymphoblastic or myeloid leukaemia. A small number of patients may later develop paroxysmal nocturnal haemoglobinuria or myelodysplasia.

The causes of aplastic anaemia can be idiopathic, meaning that they are unknown, or they can be linked to congenital conditions such as Fanconi anaemia or dyskeratosis congenita. Certain drugs, such as cytotoxics, chloramphenicol, sulphonamides, phenytoin, and gold, as well as toxins like benzene, can also cause aplastic anaemia. Infections such as parvovirus and hepatitis, as well as exposure to radiation, can also contribute to the development of this condition.

To prevent subacute combined degeneration of the cord, it is crucial to address the B12 deficiency before treating the folic acid deficiency in a patient who is deficient in both. Additionally, referral to secondary care may be necessary to determine the root cause of the deficiency.

Understanding Macrocytic Anaemia

Macrocytic anaemia is a type of anaemia that can be classified into two categories: megaloblastic and normoblastic. Megaloblastic anaemia is caused by a deficiency in vitamin B12 or folate, which leads to the production of abnormally large red blood cells in the bone marrow. This type of anaemia can also be caused by certain medications, alcohol, liver disease, hypothyroidism, pregnancy, and myelodysplasia.

On the other hand, normoblastic anaemia is caused by an increase in the number of immature red blood cells, known as reticulocytes, in the bone marrow. This can occur as a result of certain medications, such as methotrexate, or in response to other underlying medical conditions.

It is important to identify the underlying cause of macrocytic anaemia in order to provide appropriate treatment. This may involve addressing any nutritional deficiencies, managing underlying medical conditions, or adjusting medications. With proper management, most cases of macrocytic anaemia can be successfully treated.

Managing Low Vitamin B12 Levels: Recommendations and Considerations

When a patient presents with a vitamin B12 level at the lower end of the normal range, it is important to determine whether they are deficient or not. This can be complicated by the fact that people within the normal range can still experience symptoms of deficiency. In this case, the patient may have latent pernicious anaemia, dietary deficiency or food malabsorption, or be taking medications that affect gastric acid production.

To determine the cause of the low B12 levels, the serum vitamin B12 test should be repeated after 4-8 weeks. If levels remain unchanged or have fallen further, blood should be taken for intrinsic factor antibodies and a short trial of empirical therapy (oral cyanocobalamin 50 micrograms daily for four weeks) should be given. If the antibody test is positive, lifelong therapy with hydroxocobalamin is recommended. If it is negative, a further vitamin B12 check is recommended after 3-4 months. If this is well within the reference range, food malabsorption as the cause is a strong possibility and long-term low dose cobalamin therapy should be considered.

It is important to provide patients with strict instructions to seek immediate medical attention if symptoms of neuropathy develop. Additionally, failure of the B12 level to rise after oral treatment is an indication for lifelong treatment as for pernicious anaemia. Further investigations (plasma methylmalonic acid or holotranscobalamin) may help confirm biochemical deficiency.

In summary, managing low vitamin B12 levels requires careful consideration of the possible causes and appropriate testing and treatment. Repeat testing, testing for intrinsic factor antibodies, and a trial of oral cyanocobalamin are all important steps in determining the best course of action for each individual patient.

The image depicts bone marrow failure caused by acute myeloid leukemia, which occurs when abnormal white blood cells accumulate in the bone marrow, replacing normal blood cells. This type of leukemia is more common in individuals over the age of 45, whereas acute lymphoblastic leukemia is mostly seen in children. Unlike lymphoma, which typically presents with enlarged lymph nodes, acute myeloid leukemia can lead to bone marrow failure. Von Willebrand’s disease may cause severe cases of epistaxis and bleeding gums, but abnormalities in blood test results are rare.

Acute myeloid leukaemia is a prevalent form of acute leukaemia in adults that can occur as a primary disease or as a result of a myeloproliferative disorder. The condition is characterized by bone marrow failure, which can lead to anaemia, neutropenia, thrombocytopenia, splenomegaly, and bone pain. Poor prognostic features include being over 60 years old, having more than 20% blasts after the first course of chemotherapy, and deletions of chromosome 5 or 7.

Acute promyelocytic leukaemia M3 is a subtype of acute myeloid leukaemia that is associated with t(15;17) and the fusion of PML and RAR-alpha genes. This type of leukaemia typically presents at a younger age than other types of AML, with an average age of 25 years old. Auer rods, which are visible with myeloperoxidase stain, are often present, and patients may experience DIC or thrombocytopenia at presentation. However, the prognosis for acute promyelocytic leukaemia M3 is generally good.

The French-American-British (FAB) classification system categorizes acute myeloid leukaemia into seven subtypes based on the degree of maturation of the cells: MO (undifferentiated), M1 (without maturation), M2 (with granulocytic maturation), M3 (acute promyelocytic), M4 (granulocytic and monocytic maturation), M5 (monocytic), M6 (erythroleukaemia), and M7 (megakaryoblastic).

Splenectomy and its Management

Splenectomy is a surgical procedure that involves the removal of the spleen. After the operation, patients are at a higher risk of infections caused by pneumococcus, Haemophilus, meningococcus, and Capnocytophaga canimorsus. To prevent these infections, patients should receive vaccinations such as Hib, meningitis A & C, annual influenza, and pneumococcal vaccines. Antibiotic prophylaxis with penicillin V is also recommended for at least two years and until the patient is 16 years old, although some patients may require lifelong prophylaxis.

Splenectomy is indicated for various reasons such as trauma, spontaneous rupture, hypersplenism, malignancy, splenic cysts, hydatid cysts, and splenic abscesses. Elective splenectomy is different from emergency splenectomy, and it is usually performed laparoscopically. Complications of splenectomy include haemorrhage, pancreatic fistula, and thrombocytosis. Post-splenectomy changes include an increase in platelets, Howell-Jolly bodies, target cells, and Pappenheimer bodies. Patients are at an increased risk of post-splenectomy sepsis, which typically occurs with encapsulated organisms. Therefore, prophylactic antibiotics and pneumococcal vaccines are essential to prevent infections.

Managing High INR Levels in Patients on Warfarin: Choosing the Right Course of Action

When a patient on warfarin presents with a high international normalised ratio (INR), prompt management is crucial to prevent haemorrhage. The appropriate course of action depends on the severity of the INR elevation and whether the patient is bleeding.

If the patient has no active bleeding and their INR is between 5-8, warfarin should be withheld for 24-48 hours and restarted at a reduced dose. The INR should be rechecked 2-3 days later, and the cause investigated.

If the patient is bleeding, warfarin should be stopped and intravenous vitamin K administered. It can be restarted once the INR is below 5.

For an INR greater than 8 in a patient with no bleeding, the correct management is to stop warfarin, give vitamin K orally, and repeat the INR in 24 hours.

Dose reduction alone is not sufficient for an INR greater than 5, and warfarin should also be withheld for 1-2 days, with rechecking sooner (3-4 days).

While a confirmatory laboratory sample may be reasonable, it should not delay action being taken. Point-of-care testing is comparable in accuracy to laboratory samples, and management should reflect this.

In summary, managing high INR levels in patients on warfarin requires careful consideration of the severity of the INR elevation and whether the patient is bleeding. Prompt action and appropriate monitoring can prevent haemorrhage and ensure optimal patient outcomes.