Differential Diagnosis of Polymyositis: A Comparison with Other Connective Tissue Diseases

Polymyositis is a systemic connective tissue disease that causes inflammation of the striated muscle and skin in the case of dermatomyositis. Patients typically present with muscle weakness, pain in the small joints of the fingers, and dermatitis. The disease is associated with HLA-B8 and HLA-DR3, and underlying malignancy is present in at least 5-8% of cases. Here, we compare polymyositis with other connective tissue diseases to aid in differential diagnosis.

Rheumatoid arthritis (RA) is another systemic inflammatory disease that affects mainly the joints, in particular, the proximal interphalangeal joints, in a symmetrical fashion. Pulmonary fibrosis is a known complication of RA, and muscular weakness is also a possible feature. However, in RA, joint-related symptoms are typically more prominent than muscle weakness, making polymyositis a more likely diagnosis in cases of predominant muscle weakness.

Cryptogenic fibrosing alveolitis, also known as idiopathic pulmonary fibrosis, presents with diffuse reticular infiltrates on chest radiographs and a restrictive pattern on lung function tests. However, the history of proximal muscle weakness and pain in the small joints of the hands does not fit with this diagnosis and suggests polymyositis instead.

Systemic lupus erythematosus (SLE) is an autoimmune disorder that affects multiple systems in the body. While SLE would be in the differential diagnosis for polymyositis, the prominent proximal muscle weakness and the fact that the patient is a man (SLE affects women in 90% of cases) make polymyositis a more likely diagnosis.

Ankylosing spondylitis (AS) is an inflammatory rheumatic disease that primarily affects the axial joints and entheses. AS can be associated with pulmonary fibrosis and produces a restrictive pattern on spirometry. However, the more prominent complaint of proximal muscle weakness and the involvement of the small joints of the hands make AS a less likely diagnosis in cases of predominant muscle weakness.

To prevent neural tube defects in the foetus, it is crucial to consume folic acid. It is advised that women who are planning to conceive should take a supplement of 400 micrograms of folic acid daily. This dose should be continued until the 12th week of pregnancy. If there is a family history or a previous pregnancy affected by neural tube defects, the recommended dose should be increased.

Folic Acid: Importance, Deficiency, and Prevention

Folic acid is a vital nutrient that is converted to tetrahydrofolate (THF) in the body. It is found in green, leafy vegetables and plays a crucial role in the transfer of 1-carbon units to essential substrates involved in the synthesis of DNA and RNA. However, certain factors such as phenytoin, methotrexate, pregnancy, and alcohol excess can cause a deficiency in folic acid. This deficiency can lead to macrocytic, megaloblastic anemia and neural tube defects.

To prevent neural tube defects during pregnancy, it is recommended that all women take 400mcg of folic acid until the 12th week of pregnancy. Women at higher risk of conceiving a child with a neural tube defect should take 5mg of folic acid from before conception until the 12th week of pregnancy. Women are considered higher risk if they or their partner has a neural tube defect, they have had a previous pregnancy affected by a neural tube defect, or they have a family history of a neural tube defect. Additionally, women with certain medical conditions such as coeliac disease, diabetes, or thalassaemia trait, or those taking antiepileptic drugs, or who are obese (BMI of 30 kg/m2 or more) are also considered higher risk.

In summary, folic acid is an essential nutrient that plays a crucial role in DNA and RNA synthesis. Deficiency in folic acid can lead to serious health consequences, including neural tube defects. However, taking folic acid supplements during pregnancy can prevent these defects and ensure a healthy pregnancy.

Before diagnosing chronic fatigue syndrome, other potential causes of fatigue must be ruled out through a comprehensive tiredness screen. This should include blood tests such as FBC, ESR/CRP, U&E, Cr, and eGFR, LFTs and Ca2+, TFTs, random blood glucose, anti-endomysial antibody test (to exclude coeliac disease), CK, and ferritin.

Understanding Chronic Fatigue Syndrome

Chronic fatigue syndrome is a condition that is diagnosed after at least four months of disabling fatigue that affects mental and physical function more than 50% of the time, in the absence of other diseases that may explain the symptoms. It is more common in females, and past psychiatric history has not been shown to be a risk factor. The central feature of chronic fatigue syndrome is fatigue, but other recognized features include sleep problems, muscle and joint pains, headaches, painful lymph nodes without enlargement, sore throat, cognitive dysfunction, physical or mental exertion that makes symptoms worse, general malaise or ‘flu-like’ symptoms, dizziness, nausea, and palpitations.

To diagnose chronic fatigue syndrome, a large number of screening blood tests are carried out to exclude other pathology, such as FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening, and urinalysis. The management of chronic fatigue syndrome includes cognitive behavior therapy, graded exercise therapy, pacing, low-dose amitriptyline for poor sleep, and referral to a pain management clinic if pain is a predominant feature. Cognitive behavior therapy is very effective, with a number needed to treat of 2. Graded exercise therapy is a formal supervised program, not advice to go to the gym. Pacing involves organizing activities to avoid tiring. Children and young people have a better prognosis than adults.

In summary, chronic fatigue syndrome is a debilitating condition that affects both mental and physical function. It is more common in females and is diagnosed after at least four months of disabling fatigue. The management of chronic fatigue syndrome includes cognitive behavior therapy, graded exercise therapy, pacing, low-dose amitriptyline for poor sleep, and referral to a pain management clinic if pain is a predominant feature. Children and young people have a better prognosis than adults.

Understanding Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic lung condition that causes progressive fibrosis of the interstitium of the lungs. Unlike other causes of lung fibrosis, IPF has no underlying cause. It is typically seen in patients aged 50-70 years and is more common in men.

The symptoms of IPF include progressive exertional dyspnoea, dry cough, clubbing, and bibasal fine end-inspiratory crepitations on auscultation. Diagnosis is made through spirometry, impaired gas exchange tests, and imaging such as chest x-rays and high-resolution CT scans.

Management of IPF includes pulmonary rehabilitation, but very few medications have been shown to be effective. Some evidence suggests that pirfenidone, an antifibrotic agent, may be useful in selected patients. Many patients will eventually require supplementary oxygen and a lung transplant.

The prognosis for IPF is poor, with an average life expectancy of around 3-4 years. CT scans can show advanced pulmonary fibrosis, including honeycombing. While there is no cure for IPF, early diagnosis and management can help improve quality of life and potentially prolong survival.

Investigating Hyperprolactinaemia: Tests and Imaging

Hyperprolactinaemia is a condition characterized by elevated levels of prolactin, often caused by a microadenoma in the pituitary gland. While no single test can determine the cause of hyperprolactinaemia, a prolactinoma is likely if the prolactin level is above 250 ng/ml. Inhibitory effects of raised prolactin may result in low levels of follicle-stimulating hormone (FSH), but this is not diagnostic. Magnetic resonance imaging (MRI) is the preferred imaging technique for investigating the cause of hyperprolactinaemia, rather than a skull computed tomography (CT) or X-ray, which may only show enlarged pituitary fossa with large adenomas. Additionally, thyroid function tests may be necessary to investigate mildly raised prolactin levels in the absence of pituitary pathology.

Understanding Dehydration in Children: Symptoms and Management

Dehydration is a common concern in children, especially when they are suffering from illnesses like gastroenteritis. It is important to recognize the different levels of dehydration and manage them accordingly.

Clinical dehydration is characterized by symptoms such as restlessness and decreased urine output. Signs of clinical dehydration include irritability, sunken eyes, dry mucous membranes, tachycardia, and normal capillary refill time (CRT).

Children with no clinically detectable dehydration do not show any signs or symptoms of dehydration and can be managed with oral fluids until the illness subsides.

Clinical shock is a severe form of dehydration that requires immediate medical attention. Symptoms of clinical shock include a decreased level of consciousness, pale or mottled skin, cold extremities, tachycardia, tachypnea, hypotension, weak peripheral pulses, and a prolonged CRT. Children with clinical shock require admission and rehydration with intravenous fluids and electrolyte supplementation.

A euvolemic child, on the other hand, has a normal general appearance, normal eyes, a moist tongue, and present tears. They have a normal CRT and are not tachycardic.

It is important to recognize the signs and symptoms of dehydration in children and manage it accordingly to prevent further complications. Fluid overload is also a concern, but in cases of gastroenteritis-induced dehydration, rehydration is necessary.

Management of Syphilis

Syphilis can be effectively managed with intramuscular benzathine penicillin as the first-line treatment. In cases where penicillin cannot be used, doxycycline may be used as an alternative. After treatment, nontreponemal titres such as rapid plasma reagin (RPR) or Venereal Disease Research Laboratory (VDRL) should be monitored to assess the response. A fourfold decline in titres is often considered an adequate response to treatment.

It is important to note that the Jarisch-Herxheimer reaction may occur following treatment. This reaction is characterized by fever, rash, and tachycardia after the first dose of antibiotic. Unlike anaphylaxis, there is no wheezing or hypotension. The reaction is thought to be due to the release of endotoxins following bacterial death and typically occurs within a few hours of treatment. However, no treatment is needed other than antipyretics if required.

In summary, the management of syphilis involves the use of intramuscular benzathine penicillin or doxycycline as an alternative. Nontreponemal titres should be monitored after treatment, and the Jarisch-Herxheimer reaction may occur but does not require treatment unless symptomatic.

Distinguishing Causes of Obstructive Jaundice: A Medical Overview

Obstructive jaundice is a condition characterized by the yellowing of the skin and eyes due to the blockage of the bile ducts. Ascending cholangitis is a common cause of this condition, often associated with gallstone disease. Patients with this condition may experience fever, tachycardia, and abdominal pain. Influenza, on the other hand, rarely causes localized pain in the right upper quadrant and is unlikely to result in obstructive jaundice. Pancreatic cancer typically presents with painless jaundice, while acute hepatitis is often associated with a history of travel or high-risk behaviors. Biliary colic, which is caused by gallstones, can lead to colicky pain after eating. Understanding the different causes of obstructive jaundice is crucial in determining the appropriate treatment plan for patients.

Hepatitis B Markers: Understanding Their Significance

Hepatitis B is a viral infection that affects the liver. There are several markers used to diagnose and monitor the disease, including antibody to hepatitis B surface antigen (anti-HBs), hepatitis B envelope antigen (HBeAg), anti-hepatitis B envelope antibody (anti-HBe), hepatitis B virus (HBV) DNA, and immunoglobulin M (IgM) anti-hepatitis B core antigen (anti-HBc).

Anti-HBs is produced after a resolved infection or effective vaccination and is the only HBV antibody marker present after vaccination. High-risk individuals should have their anti-HBs level checked after completing their primary course of vaccination.

HBeAg is a marker of infectivity and can serve as a marker of active replication in chronic hepatitis. It is not present following vaccination. Anti-HBe is a predictor of long-term clearance of HBV in patients undergoing antiviral therapy and indicates lower levels of HBV and, therefore, lower infectivity. Both HBeAg and anti-HBe remain negative following vaccination.

HBV DNA is used to quantify viral load in a patient with proven acute or chronic hepatitis B infection. A positive result suggests not only the likelihood of active hepatitis but also that the disease is much more infectious as the virus is actively replicating. HBV DNA remains negative following vaccination.

The presence of IgM anti-HBc is diagnostic of an acute or recently acquired infection. It remains negative following vaccination.

According to the current NICE guidelines, a patient with a reduced left ventricular ejection fraction should be prescribed an aldosterone antagonist. However, a loop diuretic should only be prescribed if there is evidence of fluid overload.

Myocardial infarction (MI) is a serious condition that requires proper management to prevent further complications. In 2013, NICE released guidelines on the secondary prevention of MI. One of the key recommendations is the use of four drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent), ACE inhibitor, beta-blocker, and statin. Patients are also advised to adopt a Mediterranean-style diet and engage in regular exercise. Sexual activity may resume four weeks after an uncomplicated MI, and PDE5 inhibitors may be used six months after the event.

Most patients with acute coronary syndrome are now given dual antiplatelet therapy, with ticagrelor and prasugrel being the preferred options. The treatment period for these drugs is 12 months, after which they should be stopped. However, this period may be adjusted for patients at high risk of bleeding or further ischaemic events. Additionally, patients with heart failure and left ventricular systolic dysfunction should be treated with an aldosterone antagonist within 3-14 days of the MI, preferably after ACE inhibitor therapy.

Overall, the NICE guidelines provide a comprehensive approach to the secondary prevention of MI. By following these recommendations, patients can reduce their risk of further complications and improve their overall health outcomes.