Clinical scenario:
A 27-year-old male suddenly developed aggressiveness and violent behaviour within 24 hours while at his workplace. The patient had no insight into his illness and was brought to the local psychiatric hospital by his colleagues where he was admitted and treated for acute mania with electroconvulsive
therapy (EST) and antipsychotic medication. After a few days, the patient was discharged on anti-psychiatric medications. Six months later while on antipsychotic medication he developed fever and lymphadenopathy. He was admitted to another hospital where a lymph node biopsy revealed follicular hyperplasia, without any abnormal cell. The patient’s HBV, HCV and HIV tests were all negative. The patient developed progressive weakness, anorexia, malaise, and virtually become bed bound. He was admitted to the King Abdul Aziz hospital in Taif, Saudi Arabia where the examination revealed pallor, generalised lymph-adenopathy, palmer rash, alopecia and mouth ulcers.
On evaluation, he had significant proteinuria, and ANA dsDNA was positive. The patient had mild pericardial effusion and mitral regurgitation (MR ++ noted on echocardiography).
Lupus anticoagulant was negative. With all these signs and symptoms, the patient was diagnosed with SLE and was managed with steroids which he tolerated well and improved progressively on the follow-up investigations. On follow up, proteinuria persisted and a kidney biopsy showed class IV lupus nephritis. The lupus nephritis was treated with pulse cyclophosphamide and later the patient was started on tablet Mycophenolate.
The patients showed improvement in that his haemoglobin levels increased (Shown in Table 1) and he was clinically well and mobilising. Two years on, on follow up the patient rejoined work and no longer required his anti-psychotic medications.
Click here to read further: British Journal of Medical Practitioners
A 27-year-old male suddenly developed aggressiveness and violent behaviour within 24 hours while at his workplace. The patient had no insight into his illness and was brought to the local psychiatric hospital by his colleagues where he was admitted and treated for acute mania with electroconvulsive
therapy (EST) and antipsychotic medication. After a few days, the patient was discharged on anti-psychiatric medications. Six months later while on antipsychotic medication he developed fever and lymphadenopathy. He was admitted to another hospital where a lymph node biopsy revealed follicular hyperplasia, without any abnormal cell. The patient’s HBV, HCV and HIV tests were all negative. The patient developed progressive weakness, anorexia, malaise, and virtually become bed bound. He was admitted to the King Abdul Aziz hospital in Taif, Saudi Arabia where the examination revealed pallor, generalised lymph-adenopathy, palmer rash, alopecia and mouth ulcers.
On evaluation, he had significant proteinuria, and ANA dsDNA was positive. The patient had mild pericardial effusion and mitral regurgitation (MR ++ noted on echocardiography).
Lupus anticoagulant was negative. With all these signs and symptoms, the patient was diagnosed with SLE and was managed with steroids which he tolerated well and improved progressively on the follow-up investigations. On follow up, proteinuria persisted and a kidney biopsy showed class IV lupus nephritis. The lupus nephritis was treated with pulse cyclophosphamide and later the patient was started on tablet Mycophenolate.
The patients showed improvement in that his haemoglobin levels increased (Shown in Table 1) and he was clinically well and mobilising. Two years on, on follow up the patient rejoined work and no longer required his anti-psychotic medications.
Click here to read further: British Journal of Medical Practitioners
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