Comparison between Mycophenolate Mofetil and Azathioprine for Preventing Renal Relapse in Lupus Nephritis: An Evidence-based Case Report

Background: Systemic Lupus Erythematosus (SLE) is an autoimmune disease which involved many organs. One of its severe manifestations is lupus nephritis (LN). Treatment of LN consists of two phases, induction and maintenance. Inappropriate treatment approach could increase morbidity and mortality in LN patients. Renal flare is among many bad outcomes of LN that should be mitigated with an appropriate therapeutic approach. Various guidelines stated usage of mycophenolate mofetil (MMF) or azathioprine (AZA) as an appropriate immunosuppresant in the maintenance phase. However, it is not clear which agent acts best in preventing renal flare. This paper presents a case of 21 years old SLE female patient with history of renal flare 1 month prior to admission. This study aimed to give evidence-based recommendation to adjust this patient’s therapy in order to prevent future renal flare episode. Method: Literature search was done on four online databases, namely PubMed, EBSCO, Cohrane Library, and ProQuest. Articles with randomized clinical trial (RCT), systematic review and meta-analysis study design were retrieved and selected based on inclusion and exclusion criterias. Critical appraisal was done using appraisal sheet provided by Oxford Centre of Evidence-based Medicine. Articles were appraised based on its validity, importance, and applicability.Results: There were 144 articles retrieved from literature searching. Further screening and full-text reading yields to 2 RCTs and 2 meta-analysis that were critically appraised. Both meta-analysis were satisfactory on their validity, while none of RCTs found were blinded studies. Both meta-analyses showed pooled risk ratio (RR) of0.70 (0.49 – 1.00) for renal flare outcome in the use of mycophenolate mofetil compared to azathioprine. Conclusion There are no significant differences between mycophenolate mofetil and azathioprinein prevention of renal flare. Based on applicability, azathioprine is more appropriate to be given in this patient, in accordance to her background.Keywords : Lupus Nephritis, Renal Flare, Mycophenolate Mofetil, Azathioprine, Systemic Lupus Erythematosu

Avascular Necrosis of the Right Femoral Head in a Systemic Lupus Erythematosus Patient

According to the 1993 Association Research Circulation Osseous, idiopathic avascular necrosis of the femoral head is defined as the presence of disease or other causes that result in ischemic osteonecrosis of the femoral head without the presence of trauma or sepsis. Based on the above defi nition, idiopathic avascular necrosis(AVN) includes those that are the result of steroid administration, systemic lupus erythematosus, alcoholic consumption, etc. The pathogenesis of AVN is still obscure; however, it is basically caused by vascular circulation disorder, cell death and decreased capability of bone repair.1,2 Systemic lupus erythematosus (SLE) is characterized by the presence of systemic immune dysregulation, autoantibody formation, immune complex in the circulation, and activation of the systemic complement. The pathology during recurrence of SLE, among others, is the presenceof vascular lesion in the form of infl ammation, thrombosis, endothelial injury in which the three of them are predispositions for atherosclerosis. The vascular lesion will cause microcirculation damage which is a risk factor for the occurrence of AVN in activation of SLE. Besides being caused by vascular lesion during activation of SLE, AVN is also triggered by fat deposition in SLE patients as a result of long term steroid therapy that causes abnormal blood fat level.1,2 Patients with SLE who have undergone pharmacologic treatment with systemic steroid either in oral or injection form will have 10 to 40 times the risk of having idiopathic AVN. High dose of systemic steroid treatment of more than 4000 mg of prednisone administered for more than three months or low dose of oral steroid administered for seven days can become a risk factor for AVN. The mechanism of AVN caused by steroid treatmentis associated with hypercoagulation, fi brinolysis disorder, and thrombosis of the bone vein.1,2,3 We report a case of AVN of the right femoral head in an SLE patient

Arthritis in leprosy without specific skin lesion

Leprosy patients could display a great variability of signs and symptoms. An overabundance of rheumatic manifestations, occuring alone or in varying combinations, are associated with leprosy, particularly with lepra reactions A study involving seventy cases of leprosy found that rheumatic manifestations were seen in 61.42% of cases: arthritis in 54.28% and soft tissue rheumatism in 17.14%. Enthesitis was seen in 2.84% of cases. Rheumatic manifestations may be the primary complaint, thus delaying accurate diagnosis. Musculoskeletal involvement in leprosy is the third most frequent manifestation after dermatological and neurological involvements. It can occur at anytime during the infection. Articular inflammation in leprosy, which closely mimics other rheumatic disorders, usually occurs in reactive states, particularly erythema nodosum leprosum (ENL).1 About 1–5% of leprosy patients are reported of developing arthritis (synovial inflammation) at some stage of the disease but this rate increases to over 50% during lepra reactions.2 Here we report a case of arthritis in leprosywithout any typical skin lesion thus causing a delay in diagnosis

Complete manifestations of Behçet’s disease

Behçet’s disease (BD) is a chronic, relapsing, inflammatory disease characterized by recurrent oral aphthae and any of several systemic manifestations that include genital aphthae, ocular disease, skin lesions, neurologic disease, vascular disease, or arthritis. Hippocrates may had described BD in the fifth century B.C.; however, the first official description of the syndrome was attributed to the Turkish dermatologist Hulusi Behçet in 1924. In 1930, the Greek physician Adamantiades reported a patient with inflammatory arthritis, oral and genital ulcers, phlebitis, and iritis.1 Since then, the syndrome has been referred to as BD.1,2 The manifestations of BD are thought to be caused by an underlying vasculitis. Although this disease is recognized worldwide, the prevalence is highest in the eastern Mediterranean, the Middle Eastern, and East Asian countries, thus the nickname Silk Road disease. The disease tends to be more severe in areas where it is more common. Prevalence rates all over the world are increasing, probably because of improved recognition and reporting. Behçet’s disease occurs primarily in young adults. The mean age at onset is between 25 and 30 years. The incidence of disease in males and females is approximately equal along the Silk Road, but in Japan, Korea, and Western countries the disease occurs more frequently in women. Caseconfirmation can be challenging because many patients labeled as having BD have oral ulcers as the primary or sole manifestation.

Management of Salmonella Septic Bursitis in Immunocompromised Host Post Renal Transplant

Salmonella as a causative agent in septic bursitis is considered rare. We report a case of 56 year old male with history of renal transplantation and using mycophenolate mofetil, cyclosporine and methylprednisolone as maintenance, admitted due to 3-week-fever associated with tenderness and swelling on left shoulder. Upon investigation, a diagnosis of septic bursitis was established. Salmonella enteritidis as the definitive causative agent was revealed. He was treated with meropenem 1g IV three times daily and levofloxacin 500 mg IV once a day for 3 weeks, followed by oral ciprofloxacin 500 mg twice a day for 2 weeks and oral metronidazole 500 mg three times a day for 1 week with a total duration of 5 weeks of antibiotics. On the subsequent follow up there was no recurrence episode of fever and the swelling of the left shoulder subsided, no tenderness noted and the patient has no limitation of range of movement. Since immunocompromised state complicates the management, the duration of therapy may twice longer than the typical management of septic bursitis. Salmonella as etiologic agent should be considered as differential in immunocompromised patient with septic bursitis