Proven invasive pulmonary mucormycosis successfully treated with amphotericin B and surgery in patient with acute myeloblastic leukemia: a case report

INTRODUCTION: Invasive mucormycosis (zygomycosis) is the third most frequent fungal infection in patients with hematologic malignancies. It often results in a fatal outcome mainly due to the difficulty of early diagnosis and its resistance to antimycotics. CASE PRESENTATION: A 52-year-old Caucasian man was diagnosed with acute myeloblastic leukemia. Following the induction chemotherapy he developed febrile neutropenia. Meropenem (3×1000mg/day) was introduced empirically. A chest computed tomography showed soft-tissue consolidation change in his right upper lobe. A bronchoscopy was performed and the histology indicated invasive pulmonary aspergillosis based on fungal hypha detection. Also, high risk patients are routinely screened for invasive fungal infections using commercially available serological enzyme-linked immunosorbent assay tests: galactomannan and mannan (Bio-Rad, France), as well as anti-Aspergillus immunoglobulin G and/or immunoglobulin M and anti-Candida immunoglobulin G and/or immunoglobulin M antibodies (Virion-Serion, Germany). Galactomannan showed low positivity and voriconazole therapy (2×400mg/first day; 2×300mg/following days) was implemented. The patient became afebrile and a partial remission of disease was established. After 2 months, the patient developed a fever and a chest multi-slice computed tomography showed soft-tissue mass compressing his upper right bronchus. Voriconazole (2×400mg/first day; 2×300mg/following days) was reintroduced and bronchoscopy was repeated. Histologic examination of the new specimen was done, as well as a revision of the earlier samples in the reference laboratory and the diagnosis was switched to invasive pulmonary mucormycosis. The treatment was changed to amphotericin B colloidal dispersion (1×400mg/day). The complete remission of acute myeloblastic leukemia was verified after 2 months. During his immunerestitution, a high positivity of the anti-Aspergillus immunoglobulin M antibodies was found in a single serum sample and pulmonary radiography was unchanged. A lobectomy of his right upper pulmonary lobe was done and the mycology culture of the lung tissue sample revealed Rhizopus oryzae. He remained in complete remission for more than 1 year. CONCLUSIONS: Invasive mucormycosis was successfully treated with amphotericin B, surgery and secondary itraconazole prophylaxis. As a rare disease invasive mucormycosis is not well understood by the medical community and therefore an improvement of education about prevention, diagnosis and treatment of invasive mucormycosis is necessary

Somatic mutations of isocitrate dehydrogenases 1 and 2 are prognostic and follow-up markers in patients with acute myeloid leukaemia with normal karyotype

Mutations in the isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) genes are frequent molecular lesions in acute myeloid leukaemia with normal karyotype (AML-NK). The effects of IDH mutations on clinical features and treatment outcome in AML-NK have been widely investigated, but only a few studies monitored these mutations during follow-up

Pregnancy complicated with deficiency of antithrombin: Review of current literature

Antithrombin deficiency, although the rarest thrombophilia, carries the highest risk of thromboembolism. This risk is increased especially for pregnant women due to physiological coagulation changes in pregnancy. Therefore, in cases of positive personal and/or family history of thromboembolic events as well as recurrent pregnancy loss women should be tested for antithrombin deficiency. Antithrombin deficiency is caused by numerous mutations of serpin peptidase inhibitor clade C 1 gene (SERPINC) and is classified according to antithrombin plasma activity and antigen levels into Type I (quantitative defect) and Type II (qualitative defect). Complications during pregnancy can be divided into those regarding the mother and those concerning the fetus. The main clinical manifestation of antithrombin deficiency regarding the mother is thromboembolism occurring spontaneously or recurrently during pregnancy. Numerous major gestational complications such as miscarriage, intrauterine growth restriction or fetal death, placental abruption, preeclampsia and hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome can be linked to antithrombin deficiency. Close monitoring with early and adequate prophylaxis and treatment nowadays can mostly assure the positive pregnancy outcome for both mother and child. Prophylaxis/therapy with both low molecular weight heparin and antithrombin concentrate should start as soon as pregnancy is planned or at least as early as possible in pregnancy and continue until the end of the puerperium