Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially life-threatening idiosyncratic drug reaction. It presents with extensive rash, fever, lymphadenopathy, hematologic abnormalities (eosinophilia and/or atypical lymphocytosis) and internal organ involvement. It has been described in association with more than 50 drugs. To the best of our knowledge neither cefotaxime nor clindamycin has been previously reported to induce DRESS syndrome in children. Clindamycin was reported only in adults as a cause of DRESS syndrome in the literature. In this report, we aimed to present a child with DRESS syndrome that developed after cefotaxime and clindamycin treatment. A 6-year-old boy was diagnosed with the left lower lobe pneumonia and pleural effusion. Parenteral cefotaxime and clindamycin were then started, after which the patient improved clinically and was discharged 7 days later with oral amoxicillin clavulanate treatment. After four days he was readmitted to the hospital with fever and cough. Chest X-ray revealed left lower lobe pneumonia and pleural effusion. We considered that the pneumonia was unresponsive to oral antibiotic treatment, and therefore parenteral cefotaxime and clindamycin were re-administered. As a result, his clinical and radiological findings were improved within 10 days. On the 12th of day of hospitalization, the body temperature has risen to 39°C, which we considered to be caused by antibiotics and stopped antibiotic treatment. At the same day he developed generalized maculopapular erythematous rash, which was considered an allergic reaction secondary to antibiotics. Despite the antihistaminic drug administration, the clinical status quickly deteriorated with generalized edema, lymphadenopathies and hepatosplenomegaly. Laboratory tests revealed a white blood cell count of 4300/μl, a lymphocyte count of 1300/μl, a hemoglobin level of 11.2 gr/dl, a platelet count of 120.000/μl, an eosinophilia ratio of 10% on peripheral blood smear, a C-reactive protein level of 20 mg/dl, a procalcitonin level of 23.94 ng/ml and an erythrocyte sedimentation rate of 48 mm/h. Anti nuclear antibody, anti-double stranded DNA, the serologic tests for Epstein Bar virus, herpes simplex virus, parvovirus, mycoplasma, toxoplasmosis, rubella, cytomegalovirus were all found negative. Bone marrow aspiration was consistent with an autoimmune reaction. An echocardiographic examination was normal. Thoracic tomography revealed multiple enlarged axillary, supraclavicular and anterior mediastinal lymph nodes. As the patient met 8 out of 9 RegiSCAR criteria for the diagnosis of DRESS, we started pulse methyl prednisolone (30 mg/kg/day) for three days followed by 2 mg/kg/day. On the 2nd day fever resolved and cutaneous rash and edema improved. Ten days after developing eruptions the patient was discharged. To our knowledge, we report the first pediatric case of DRESS syndrome following treatment with cefotaxime and clindamycin. Pediatricians should be aware of this potential complication assoc...
Henoch-Schönlein purpura (HSP) is the most common form of childhood vasculitis. Various viral and bacterial infections, drugs, vaccines, food allergy and even insect bites have been considered as triggering factors in pathogenesis of HSP. Epstein-Barr virus (EBV) infection, which is associated with HSP, have been rarely reported. Herein we present HSP patient possibly caused by EBV infection. A 8-year old boy was admitted to our department with fever, rashes on legs and arms and intermittent mild abdominal pain. Multiple purpuric rashes were on his extremities, abdomen and buttock. Laboratory investigations revealed that monospot test was positive, EBV serology tests; Anti-EA-D Ig G: 3+, Anti-VCA gp125 Ig G: 3+, Anti-VCA p19 Ig M: 2+, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig M: negative, Anti EBNA-1 Ig G: negative. The patient was interpreted as the primary active acute EBV infection. A skin biopsy showed leucocytoclastic vasculitis. The other viral and bacterial investigations were negative. The patient was diagnosed as HSP vasculitis according to EULAR criteria and treated with intravenous hydration and ibuprofen. He was discharged after 15 days with normal laboratory findings and physical examination. We think that EBV infection may be stimulant factor for autoimmune reactions and may cause HSP vasculitis. Hence, it may be useful to investigate the EBV infection in etiology of HSP cases.
Valproic acid (VPA) is usually a well-tolerated anti-epileptic drug. The most commonly seen adverse effects are anorexia, nausea and vomiting, 1 but serious complications such as hematopoietic disorders may include thrombocytopenia, abnormal platelet function, hypofibrinogenemia and decreased coagulation factors, especially factor VII, von Willebrand factor and protein C. Although VPA-associated coagulopathies are commonly reported, the adverse effects in the hemostatic system (such as bruising, petechia, hematoma, and epistaxis) are mild, and serious bleeding complications are rare. 2-5 Herein, we report the case of a pediatric patient who developed hypofibrinogenemia, menometrorrhagia and hemarthrosis during treatment with oral VPA. Case reportA 13-year-old girl referred to the present clinic with swelling of the right knee. Past history including epileptic convulsions that had been under control for the last 2 years after initiation of VPA. She had recently developed a 2 week history of menometrorrhagia. Before starting VPA therapy, homocysteine, lipoprotein (a), factor VIII, factor IX, protein C, protein S, anti-thrombin III, and activated protein C resistance were normal. She had no history of abnormal bleeding prior to VPA treatment. There were also no cases of bleeding disorder in her family. Clinical examination was normal except for right knee swelling. Laboratory tests were normal except for coagulation parameters: activated partial thromboplastin time, 55.4 s; prothrombin time, 24.3 s; international normalized ratio of prothrombin time, 2.19; D-dimer, N and fibrinogen undetected (0 mg/dL). Rheumatoid factor, anti-nuclear antibody, and anti-dsDNA were negative and anti-streptolysin O titer was in the normal range. Blood VPA was screened and was within the therapeutic range. Minimal effusion of the right knee was observed on imaging. Arthrocentesis was performed and hemorrhagic fluid was obtained. The patient was diagnosed with intra-articular hemorrhage due to hypofibrinogenemia induced by VPA, and VPA was discontinued. The patient was treated with 1 unit cryoprecipitate. Congenital deficiency or abnormal function of fibrinogen was ruled out in this patient; she had no personal or family history of bleeding, and coagulation tests were normal before initiation of VPA therapy. Fibrinogen gradually increased to normal (58 mg/dL), and clinical symptoms of bleeding did not recur. The knee swelling resolved in 5 days. DiscussionAlthough VPA-associated coagulopathies are commonly reported, significant clinical bleeding complications are rare. 1 Most of the VPA side-effects are mild and transient. Thrombocytopenia is the most common hematologic adverse effect of VPA. The present platelet count was in the normal range. The exact mechanism of hypofibrinogenemia (decreased synthesis or increased consumption) is not well understood and may involve many different interrelated components. The probable mechanism is interference by VPA with the hepatic production of coagulation factors. [2][3][4][5] This may account fo...
Hemophagocytic lymphohistiocytosis (HLH) is a rare, albeit potentially fatal, condition in which fever, hepatosplenomegaly, and cytopenia predominate the clinical picture. Although it may be primary, it may also develop secondary to various etiologies. Herein, we aimed to report a patient who was diagnosed with pulmonary tuberculosis, developed fever and cytopenia during follow-up, and received immunomodulatory therapy together with antituberculosis therapy for the diagnosis of HLH. Sequencing of PRF1 showed heterozygous mutation. Although primary HLH has been detected in infants and children, genetic mutation of genes should be considered a differential diagnosis of HLH even in the adolescent.
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