Polymyositis is specifically associated with anti-synthetase antibodies. In this case, the diagnosis is aspiration pneumonia caused by dysphagia resulting from polymyositis. Polymyositis is an inflammatory myopathy of unknown origin that is characterized by symmetrical, proximal muscle weakness and elevated levels of skeletal muscle enzymes (creatine kinase). Although several autoantibodies are associated with polymyositis, many of them are not specific to the disease.

Polymyositis is an inflammatory condition that causes weakness in the muscles, particularly in the proximal areas. It is believed to be caused by T-cell mediated cytotoxic processes that target muscle fibers. This condition can be idiopathic or associated with connective tissue disorders and is often linked to malignancy. Dermatomyositis is a variant of this disease that is characterized by prominent skin manifestations, such as a purple rash on the cheeks and eyelids. It typically affects middle-aged individuals, with a female to male ratio of 3:1.

The symptoms of polymyositis include proximal muscle weakness, which may be accompanied by tenderness. Other symptoms may include Raynaud’s phenomenon, respiratory muscle weakness, and dysphagia or dysphonia. Interstitial lung disease, such as fibrosing alveolitis or organizing pneumonia, may also occur in around 20% of patients, which is a poor prognostic indicator.

To diagnose polymyositis, doctors may perform various tests, including measuring elevated creatine kinase levels and other muscle enzymes, such as lactate dehydrogenase, aldolase, AST, and ALT. An EMG and muscle biopsy may also be performed. Additionally, anti-synthetase antibodies and anti-Jo-1 antibodies may be present in patients with lung involvement, Raynaud’s, and fever.

The management of polymyositis typically involves high-dose corticosteroids, which are tapered as symptoms improve. Azathioprine may also be used as a steroid-sparing agent.

Drug Induced Lupus: Causes and Symptoms

Drug induced lupus (DIL) is a condition that occurs as a result of taking certain medications. These drugs include Procainamide, Hydralazine, Sulfasalazine, Carbamazepine, Phenytoin, Minocycline, Isoniazid, Interferons, and Anti-TNFα drugs. The good news is that DIL resolves after stopping treatment with the offending drug.

Symptoms of DIL include a purpuric, erythematous, papular rash. However, patients do not have a malar or discoid rash. They also have antinuclear antibody (homogeneous pattern), are positive for anti-ssDNA antibody, antihistone antibody, and typically are negative for anti-dsDNA antibody. It is important to note that drug induced lupus due to interferon and due to anti-TNF α agents may present with a malar or discoid rash and may be anti-dsDNA antibody positive.

Understanding the Role of HLA B27 in the Diagnosis of Axial Spondyloarthropathies

HLA B27 is a genetic marker that is often used in the diagnosis of axial spondyloarthropathies (AS). However, its sensitivity and specificity depend on the racial and ethnic background of the patient. For example, Inuits have the highest frequency of the gene, while people from Holland and Germany have a lower frequency. While HLA B27 may be helpful in diagnosis, it cannot be used as a screening test as 10% of the healthy population may test positive. Additionally, most AS patients do not need HLA B27 testing if they have certain clinical and radiological features. It is important to note that acute anterior uveitis is more common in B27-positive patients. Overall, while HLA B27 is essential in some cases, it is not a definitive test for AS and should be used in conjunction with other diagnostic tools.

Differential Diagnosis for Spinal Pain

When a patient presents with spinal pain, it is important to consider various differential diagnoses. In the case of discitis, Staphylococcus aureus is the most common bacterial cause in adults. Unlike discitis, epidural abscess typically presents with neurological symptoms in the lower limbs. The absence of urinary symptoms and a normal urinary dipstick test makes pyelonephritis unlikely. Osteoporotic spinal fractures may also cause acute pain, but these patients will have evidence of vertebral collapse on plain x-ray films. Finally, acutely painful spinal metastases are unlikely without accompanying changes on plain x-ray films. By considering these differential diagnoses, healthcare providers can more accurately diagnose and treat spinal pain.

The leading cause of death in systemic sclerosis is respiratory involvement, specifically interstitial lung disease and pulmonary arterial hypertension. In this case, the patient’s positive Scl-70 antibody suggests an increased risk for interstitial lung disease. While cardiac arrhythmias can occur in systemic sclerosis, they are not a significant cause of mortality. While primary biliary cirrhosis and autoimmune hepatitis can occur in this condition, they are relatively rare complications and not associated with the same mortality as interstitial lung disease. Although patients with systemic sclerosis are at higher risk of infectious complications, interstitial lung disease remains the most common cause of mortality in this condition.

Understanding Systemic Sclerosis

Systemic sclerosis is a condition that affects the skin and other connective tissues, but its cause is still unknown. It is more common in females than males, with three patterns of the disease. The first pattern is limited cutaneous systemic sclerosis, which is characterised by Raynaud’s as the first sign, scleroderma affecting the face and distal limbs, and associated with anti-centromere antibodies. A subtype of this pattern is CREST syndrome, which includes Calcinosis, Raynaud’s phenomenon, Oesophageal dysmotility, Sclerodactyly, and Telangiectasia.

The second pattern is diffuse cutaneous systemic sclerosis, which affects the trunk and proximal limbs, and is associated with scl-70 antibodies. This pattern has a poor prognosis, with respiratory involvement being the most common cause of death, including interstitial lung disease and pulmonary arterial hypertension. Other complications include renal disease and hypertension, and patients with renal disease should be started on an ACE inhibitor.

The third pattern is scleroderma without internal organ involvement, which is characterised by tightening and fibrosis of the skin, manifesting as plaques or linear. Antibodies play a significant role in systemic sclerosis, with ANA positive in 90% of cases, RF positive in 30%, anti-scl-70 antibodies associated with diffuse cutaneous systemic sclerosis, and anti-centromere antibodies associated with limited cutaneous systemic sclerosis.

It is important to note that a negative temporal artery biopsy does not rule out GCA, and shorter biopsy specimens are more likely to produce falsely reassuring results. To address this, the BSR recommends that biopsy specimens should be at least 1 cm in length.

If a patient experiences transient visual loss, it may indicate the onset of permanent blindness. In such cases, the BSR recommends administering IV methylprednisolone at a dosage of 500-1000 mg daily for 3 days.

For patients with uncomplicated GCA or established visual loss, the recommended treatment is 60 mg prednisolone daily.

It should be noted that prednisolone 15mg daily is only appropriate for isolated PMR and is not recommended in this case. The other treatment options listed are for fibromyalgia and are therefore not applicable.

Temporal arteritis is a type of large vessel vasculitis that often occurs in patients over the age of 60 and is commonly associated with polymyalgia rheumatica. This condition is characterized by changes in the affected artery that skip certain sections while damaging others. Symptoms of temporal arteritis include headache, jaw claudication, and visual disturbances, with anterior ischemic optic neuropathy being the most common ocular complication. A tender, palpable temporal artery is also often present, and around 50% of patients may experience symptoms of PMR, such as muscle aches and morning stiffness.

To diagnose temporal arteritis, doctors will typically look for elevated inflammatory markers, such as an ESR greater than 50 mm/hr or elevated CRP levels. A temporal artery biopsy may also be performed to confirm the diagnosis, with skip lesions often being present. Treatment for temporal arteritis involves urgent high-dose glucocorticoids, which should be given as soon as the diagnosis is suspected and before the temporal artery biopsy. If there is no visual loss, high-dose prednisolone is typically used, while IV methylprednisolone is usually given if there is evolving visual loss. Patients with visual symptoms should be seen by an ophthalmologist on the same day, as visual damage is often irreversible. Other treatments may include bone protection with bisphosphonates and low-dose aspirin, although the evidence supporting the latter is weak.

McArdle disease, also known as myophosphorylase deficiency or Glycogen storage disease V, is frequently misdiagnosed as chronic fatigue syndrome, despite presenting in adolescence with exercise intolerance, cramps, and weakness. This condition is inherited in an autosomal recessive manner. Diagnostic clues include the absence of a rise in venous blood lactate during exercise and muscle biopsy findings of elevated glycose concentration and muscle phosphorylase deficiency. Elevated CK and myoglobinuria are typically observed during investigations. Diagnosis can be confirmed through forearm muscle exercise testing or genetic testing. Management involves avoiding low carbohydrate diets and low intensity aerobic exercise.

Understanding McArdle’s Disease

McArdle’s disease is a type V glycogen storage disease that is inherited in an autosomal recessive manner. It is caused by a deficiency in myophosphorylase, which leads to a decrease in muscle glycogenolysis. This condition is characterized by several features, including muscle pain and stiffness following exercise, muscle cramps, myoglobinuria, and low lactate levels during exercise.

Individuals with McArdle’s disease often experience muscle pain and stiffness after engaging in physical activity. This is due to the inability of their muscles to break down glycogen into glucose, which is necessary for energy production during exercise. As a result, the muscles become fatigued and painful. Additionally, muscle cramps are a common symptom of this condition, as well as myoglobinuria, which is the presence of myoglobin in the urine. Finally, individuals with McArdle’s disease have low lactate levels during exercise, which is a result of the inability of their muscles to produce lactate.

In summary, McArdle’s disease is a genetic disorder that affects muscle function and energy production during exercise. It is characterized by several symptoms, including muscle pain and stiffness, muscle cramps, myoglobinuria, and low lactate levels during exercise. Understanding the features of this condition is important for proper diagnosis and management.

Hepatitis Caused by Methotrexate

When a patient develops hepatitis due to methotrexate, the first step is to discontinue the drug and closely monitor liver function tests (LFTs). If the LFTs do not return to normal, an ultrasound scan of the abdomen and hepatitis autoimmune serology should be arranged. Although rheumatoid arthritis can be associated with autoimmune hepatitis, it is much less common than methotrexate-induced hepatotoxicity. Therefore, it is important to identify the cause of hepatitis in order to provide appropriate treatment and prevent further liver damage. Proper monitoring and prompt action can help manage this condition effectively.

Importance of Checking TPMT Levels Before Starting Azathioprine

Prior to initiating treatment with azathioprine, it is crucial to check the patient’s blood for thiopurine methyltransferase (TPMT) levels. Azathioprine is metabolized into 6-mercaptopurine (6-MP) in the body, which can either be converted into inactive 6-methyl mercaptopurine or methylated into active compounds by TPMT. In Caucasians, 89% of individuals have normal or high levels of TPMT, while 11% have low levels and 0.3% are deficient in TPMT. Administering azathioprine to those who are TPMT deficiency can lead to severe side effects such as myelosuppression.

Patients with normal or high levels of TPMT can safely begin treatment with azathioprine. However, those with low levels of TPMT should be closely monitored and given low doses of azathioprine under expert supervision. Therefore, it is essential to check TPMT levels before starting azathioprine to ensure the safety and efficacy of the treatment.

Reactive Arthritis

Reactive arthritis is a medical condition that is typically characterized by a combination of three symptoms: urethritis, conjunctivitis, and seronegative arthritis. This type of arthritis usually affects the large weight-bearing joints, such as the knee and ankle, but not all three symptoms are always present in a patient. Reactive arthritis can be triggered by either a sexually transmitted infection or a dysenteric infection. One of the most notable signs of this condition is the appearance of a brown macular rash known as keratoderma blenorrhagica, which is usually seen on the palms and soles.

The main treatment for reactive arthritis involves the use of non-steroidal anti-inflammatory drugs (NSAIDs). These medications can help to alleviate the pain and inflammation associated with the condition. Additionally, antibiotics may be prescribed to individuals who have recently experienced a non-gonococcal venereal infection. This can help to reduce the likelihood of that person developing reactive arthritis. Overall, the symptoms and treatment options for reactive arthritis can help individuals to manage this condition and improve their quality of life.