scholarly journals Mononeuritis multiplex due to thrombotic ischemia of primary antiphospholipid antibody syndrome without vasculitis: an autopsy case report

2015 ◽  
Vol 55 (12) ◽  
pp. 897-903
Author(s):  
Masatoshi Takahashi ◽  
Fumiaki Katada ◽  
Susumu Sato ◽  
Hidehiro Shibayama ◽  
Toshio Fukutake ◽  
...  
2000 ◽  
Vol 39 (10) ◽  
pp. 856-859 ◽  
Author(s):  
Reiko MIZUNO ◽  
Shinichi FUJIMOTO ◽  
Takashi FUJIMOTO ◽  
Toshihiko NISHINO ◽  
Hideo SHIIKI ◽  
...  

2001 ◽  
Vol 77 (6) ◽  
pp. 517-21
Author(s):  
Célia S. Macedo ◽  
Roberta S. Martinez ◽  
Márcia C. Riyuzo ◽  
Herculano D. Bastos

Lupus ◽  
2016 ◽  
Vol 26 (7) ◽  
pp. 777-782 ◽  
Author(s):  
X-J Zhou ◽  
M Chen ◽  
S-X Wang ◽  
F-D Zhou ◽  
M-H Zhao

Background Microvascular manifestations of antiphospholipid antibody syndrome in the kidneys include acute renal failure, thrombotic microangiopathy and hypertension. Therapy has been largely empiric. Case report A 49-year-old Chinese man presented with anuric acute renal failure without abundant proteinuria and heavy haematuria, but markedly low levels of urinary sodium, potassium and chlorine upon admission. On day 1 of hospitalization, his thrombocytopenia, anaemia and renal failure showed rapid progression. The presence of lupus anticoagulant and vascular ischaemia of the small vessels in renal arteriography were also observed. Anticoagulants, continuous renal replacement therapy, glucocorticoids and six sessions of plasma exchange were started. After the fourth plasma exchange (on day 20), his urine output increased and began to normalize. On day 25, haemodialysis was stopped and his general condition gradually improved. A renal biopsy was subsequently performed, and the histopathological diagnosis was thrombotic microangiopathy due to antiphospholipid antibody syndrome. A further 3-year follow-up showed that his haemoglobin level, platelet count and serum creatinine were within the normal range, with stable blood pressure. Conclusion Treatment modalities such as anticoagulation, immunosuppression and plasma exchange are likely to be necessary when severe acute renal failure combined with thrombotic microangiopathy present in nephropathy of antiphospholipid antibody syndrome.


2020 ◽  
pp. 107815522093549
Author(s):  
Gizem Yassa ◽  
Abdur R Shakir ◽  
Kuppuswamy Jagarlamudi ◽  
Ahmet E Yassa

Introduction Immune thrombocytopenia is an autoimmune disorder associated with increased thrombocyte destruction and impaired production in the bone marrow. Proposed mechanisms include an antibody or autoreactive T-cell-associated autoimmunity and thrombopoietin deficiency among others. Clinical manifestations are predominantly mucocutaneous hemorrhages including petechiae, purpura, mucosal bleeding in the urinary or the gastrointestinal tracts, menorrhagia, and epistaxis. The purpose of the treatment is to prevent bleeding rather than normalizing the platelet counts. First-line treatments include corticosteroids ± intravenous immunoglobulin and Anti-D which mainly decrease antibody-mediated platelet destruction and increase the number of peripheral Tregs. Second-line and subsequent therapies include splenectomy, chimeric anti-CD20 antibody (rituximab), which eliminates B cells and act as an immunomodulatory agent, and Thrombopoietin receptor agonists (romiplostim), which promote platelet production. Case report We describe a 40-year-old male patient diagnosed with immune thrombocytopenia that was refractory to first-line corticosteroid and intravenous immunoglobulin and second-line romiplostim monotherapy treatments. Management and outcome: The patient was given the romiplostim and rituximab combination which not only successfully treated thrombocytopenia but also resulted in grade 3 bone pains and the patient’s subsequent refusal to continue therapy. Discussion Common adverse effects of rituximab are infusion reactions and prolonged immunosuppression; those of romiplostim include thrombosis, headaches, arthralgia–myalgia, and gastrointestinal symptoms. This case shows that romiplostim has not caused any discernible side effects when given alone, while combination with rituximab resulted in severe bone and joint pains. We hypothesize that this combination regimen shows a synergistic effect both in terms of efficacy and adverse-effect probability and/or severity.


2018 ◽  
Vol 9 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Augusto Ferreira Correia ◽  
Dinaldo Cavalcanti Oliveira ◽  
Marcio Sanctos

2014 ◽  
Vol 2 (1) ◽  
pp. 35-37
Author(s):  
G Dewan

Association of hypercalcemia with SLE is very rare. Since initial report in 1991 only hand full cases have been described mainly in adult patients sporadically. Three pattern observed in this rare presentation. Commonly it is associated with serositis and lymphadenopathy or lymphedema known as hypercalcemia-lymphadenopathy SLE {HL-SLE) or hypercalcemia- lymphedema syndrome. Second group do not show this particular association. Concomitant primary hyperparathyroidism is responsible for third variety. This report describes a case of hypercalcemia associated with SLE from Bangladesh. DOI: http://dx.doi.org/10.3126/jucms.v2i1.10490   Journal of Universal College of Medical Sciences (2014) Vol.2(1): 35-37


Lupus ◽  
2020 ◽  
Vol 29 (6) ◽  
pp. 640-643
Author(s):  
Gökçe Kenar ◽  
Kadri Atay ◽  
Gül Emek Yüksek ◽  
Burak Öz ◽  
Süleyman Serdar Koca

Background Patients with systemic lupus erythematosus may present with variable gastrointestinal manifestations including peritonitis, pancreatitis, enteritis, and vasculitis. Gastrointestinal vasculitis is one of the most devastating complications of systemic lupus erythematosus, with a mortality rate of 50% when it progresses to bowel ischemia and is complicated by hemorrhage or perforation. Case report A young female patient known to have systemic lupus erythematosus, lupus nephritis, and antiphospholipid antibody syndrome, on immunosuppressive treatment presented to the emergency department with acute abdominal pain and nausea. The clinical findings were first associated with an acute flare of lupus nephritis according to the assessments with active laboratory parameters. However, over a short time the abdominal pain worsened and was accompanied by peritonitis and gastrointestinal hemorrhage. The computed tomography scans demonstrated a dilated bowel and thickening of the bowel compatible with gastrointestinal vasculitis. The upper and lower gastrointestinal endoscopy supported the diagnosis of vasculitis by showing multiple ulcerative lesions along the gastrointestinal tract. The patient was successfully treated with pulse corticosteroids urgently, with a fast response to subsequent rituximab therapy without any relapses. Treatment with cyclophosphamide was not preferred because the patient had a high cumulative dose. Conclusion Gastrointestinal vasculitis should be a primary differential diagnosis in patients with systemic lupus erythematosus presenting with abdominal pain because of its rapid progression and high mortality. The treatment choice has been suggested as cyclophosphamide for severe cases in the literature. In this case report, a patient successfully treated with rituximab without any relapses was documented.


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