The patient is likely septic and has already received antibiotics and fluids as mentioned in the question. It is important to hold her immunosuppression, which means methotrexate should not be administered. As she is on long-term steroid therapy, doubling the dose is necessary to prevent Addisonian crisis.

Once the patient has been adequately resuscitated and treated, a referral to rheumatology can be considered. However, at present, the focus should be on managing her sepsis rather than her rheumatoid arthritis.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.

Differential Diagnosis for Hypophosphatemia

Hypophosphatemia, or low levels of phosphate in the blood, can be caused by various conditions. Two possible causes are oncogenic osteomalacia and hypoparathyroidism. However, based on the given information, hypoparathyroidism is unlikely as there has been no surgery that could have led to secondary hypoparathyroidism.

Oncogenic osteomalacia is associated with certain tumors, including mesenchymal tumors, adenocarcinomas, and hematological malignancies. These tumors produce a phosphaturic substance, such as fibroblast growth factor 23 (FGF23), which decreases reabsorption of phosphate and production of 1,25-dihydroxy vitamin D by the kidney. This results in hypophosphatemia, causing symptoms such as rickets, osteomalacia, bone pain, muscle weakness, and fractures. Treatment involves vitamin D metabolites and phosphate supplements, and removal of the primary tumor can also improve symptoms.

Another possible cause of hypophosphatemia is X-linked hypophosphatemia, which presents with symptoms of rickets in childhood and is treated with calcitriol and phosphate supplementation. Tumour lysis syndrome, associated with induction chemotherapy, and hyperparathyroidism, associated with hypercalcemia and renal impairment, are other differential diagnoses that can be ruled out based on the given information.

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.

Previously, scleroderma patients were most likely to die from renal crisis. However, the use of ACE inhibitors as a form of intensive treatment has been effective in decreasing this danger. While anti-dsDNA and Rh factor are signs of SLE, RA/Sjogrens, or other conditions, there are no indications of arthritis or skin rashes.

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.

The condition known as macrophage activation syndrome is identified by an overactive immune response and cytokine storm in a patient with a rheumatological condition who also has an EBV infection. There is no indication of a parvovirus infection in the scenario presented.

Understanding Macrophage Activation Syndrome

Macrophage activation syndrome is a rare condition that is linked to rheumatological disorders like rheumatoid arthritis, systemic lupus erythematosus, and juvenile idiopathic arthritis. It is characterized by a decrease in the number of blood cells and an intercurrent infection, particularly the Epstein-Barr virus. If left untreated, the disease can be fatal within two months.

To diagnose the condition, doctors may perform a bone marrow aspiration to check for haemophagocytosis, which is the key feature of the disease. Other symptoms include excessive hyperferritinemia, elevated triglycerides, deranged liver function tests, and hypofibrinogenemia.

The treatment for macrophage activation syndrome involves immunosuppression. It is important to recognize the symptoms of this rare condition and seek medical attention promptly to prevent serious complications. Proper diagnosis and treatment can help improve the prognosis for those affected by this disorder.

The renal manifestations of systemic lupus erythematosus (SLE) are highly variable and difficult to classify. Lupus nephritis affects a third of patients early in the disease, but is frequently unrecognised until nephritic and/or nephrotic syndrome with renal failure occur. Histologically, a number of different types of renal disease are recognised in SLE, with immune-complex mediated glomerular disease being the most common. The up to date International Society of Nephrology/Renal Pathology Society 2003 classification divides these into six different patterns. Treatment with immunosuppressive therapy is required in cases of diffuse glomerulonephritis to prevent progression to end-stage renal failure. A biopsy is indicated in those patients with abnormal urinalysis and/or reduced renal function to provide a histological classification as well as information regarding activity, chronicity and prognosis.

Antiphospholipid Antibody Syndrome and Thrombotic Thrombocytopenic Purpura

Antiphospholipid antibody syndrome is a condition characterized by a prothrombotic state in the body, despite laboratory tests indicating an anticoagulant state. This is caused by the presence of antiphospholipid antibodies, such as anticardiolipin and lupus anticoagulant, which lead to coagulation defects in vitro. However, in vivo, these antibodies can cause arterial and venous thromboses, as well as thrombocytopenia.

On the other hand, thrombotic thrombocytopenic purpura is a severe systemic illness that presents with a classic pentad of symptoms, including microangiopathic hemolytic anemia, thrombocytopenia, renal dysfunction, neurologic abnormalities, and fever. While it is rare to find all five symptoms in a patient, the presence of any combination of these symptoms should raise suspicion for TTP.

It is important to note that protein C/S deficiency and idiopathic thrombocytopenic purpura do not lead to the same symptoms as antiphospholipid antibody syndrome or TTP. Therefore, proper diagnosis and management are crucial in ensuring the best possible outcomes for patients with these conditions.

Cutaneous Lupus Erythematosus

Cutaneous lupus erythematosus (CLE) is a skin disease that may occur as part of systemic lupus erythematosus (SLE) or as a separate condition without any systemic disease. There are three types of CLE: discoid lupus erythematosus (DLE), subacute cutaneous lupus erythematosus (SACLE), and acute cutaneous lupus erythematosus (ACLE). While DLE presents as well-defined scaly plaques that heal with central scarring, ACLE presents as diffuse erythema, maculopapular rash, photosensitivity, and oral ulcers.

SACLE is a classic type of CLE that is ANA positive in 60% of patients. However, only 10-15% of patients with SACLE progress to SLE with moderate disease activity. On the other hand, 80% of SACLE patients are anti-Ro antibody positive. It is important to note that while some types of CLE may progress to SLE, others may not. ACLE, for instance, often accompanies a flare of systemic disease.

In summary, the different types of CLE and their characteristics is crucial in diagnosing and managing lupus erythematosus. While some types may progress to SLE, others may not, and it is important to monitor patients closely to ensure timely intervention and treatment.

Treatment Options for Reactive Arthritis with Keratoderma Blennorrhagica

Reactive arthritis is a type of spondyloarthritis caused by a previous gastrointestinal or urogenital infection. The possible pathogens include Chlamydia trachomatis, Yersinia, Salmonella, Shigella, Campylobacter, E. coli, Clostridium difficile, and Chlamydia pneumoniae. In this case, the patient’s social history and symptoms suggest a Chlamydia infection, which can also cause keratoderma blennorrhagica.

The treatment for reactive arthritis involves addressing the underlying infection and using NSAIDs for symptomatic relief. Doxycycline 100 mg bd is a suitable antibiotic for Chlamydia infection. Methotrexate 2.5 mg po weekly and azathioprine are not recommended for reactive arthritis and are more commonly used for other types of arthritis.

Prednisolone 40 mg po daily is not suggested for reactive arthritis, but intra-articular steroid injections can be used for those who do not respond to oral NSAIDs. Coal tar skin creams can be used to treat the psoriatic-type rash, which is more likely keratoderma blennorrhagica in this case. Topical steroids or salicylates are also effective treatments for this condition.

In summary, the treatment options for reactive arthritis with keratoderma blennorrhagica include antibiotics for the underlying infection, NSAIDs for symptomatic relief, intra-articular steroid injections for non-responsive cases, and topical creams for the skin rash.

Folinic acid is the preferred remedy for addressing the harmful effects of methotrexate.

To manage the myelosuppressive effects resulting from her methotrexate treatment, the recommended course of action is to administer folinic acid rescue therapy.

Methotrexate is an antimetabolite that hinders the activity of dihydrofolate reductase, an enzyme that is crucial for the synthesis of purines and pyrimidines. It is a significant drug that can effectively control diseases, but its side-effects can be life-threatening. Therefore, careful prescribing and close monitoring are essential. Methotrexate is commonly used to treat inflammatory arthritis, especially rheumatoid arthritis, psoriasis, and acute lymphoblastic leukaemia. However, it can cause adverse effects such as mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.

Women should avoid pregnancy for at least six months after stopping methotrexate treatment, and men using methotrexate should use effective contraception for at least six months after treatment. Prescribing methotrexate requires familiarity with guidelines relating to its use. It is taken weekly, and FBC, U&E, and LFTs need to be regularly monitored. Folic acid 5mg once weekly should be co-prescribed, taken more than 24 hours after methotrexate dose. The starting dose of methotrexate is 7.5 mg weekly, and only one strength of methotrexate tablet should be prescribed.

It is important to avoid prescribing trimethoprim or co-trimoxazole concurrently as it increases the risk of marrow aplasia. High-dose aspirin also increases the risk of methotrexate toxicity due to reduced excretion. In case of methotrexate toxicity, the treatment of choice is folinic acid. Overall, methotrexate is a potent drug that requires careful prescribing and monitoring to ensure its effectiveness and safety.