Hemorrhage ; pathology ; Humans ; Thrombocytopenia ; pathology

Fever ; Humans ; Plasma Cells ; pathology ; Thrombocytopenia ; diagnosis ; pathology

The authors analysed bone marrow findings of sixteen cases of culture proven typhoid fever to reveal the pathologic changes according to the disease stage. The most frequent finding was chronic granulomatous inflammation (eight cases). Infection (bacteria) associated hemophagocytic syndrome (four cases), reactive marrow (two cases), and non specific findings (two cases) were also encountered. Granulocytic hyperplasia with hemophagocytosis appeared at the early stage and was followed by infection (bacteria) associated hemophagocytosis and granuloma in proliferative stage. In lysis (late) stage, granulomatous inflammation was noted. However, resolution of granulomatous inflammation was not distinct. Some nuclear debris and phagocytosis were remarkable in well-formed granulomas. Thrombocytopenia was the most remarkable peripheral blood finding at the time of biopsy. Anemia, leukopenia, and pancytopenia were also observed in descending order.
Adult ; Bone Marrow/microbiology/*pathology ; Female ; Humans ; Male ; Middle Aged ; Salmonella typhi/isolation & purification ; Thrombocytopenia/pathology ; Typhoid Fever/microbiology/*pathology

Actinin/genetics* ; Anemia ; Blood Platelets/pathology* ; Female ; Humans ; Male ; Megakaryocytes ; Mutation, Missense ; Pedigree ; Thrombocytopenia/genetics*

Bunyaviridae Infections ; pathology ; Fever ; virology ; Humans ; Leukopenia ; virology ; Orthobunyavirus ; classification ; pathogenicity ; Thrombocytopenia ; virology

OBJECTIVE: To report on the incidence of nab-paclitaxel hypersensitivity reactions (HSRs) in patients with prior taxane HSR. METHODS: From 2005 to 2015, all patients who received nab-paclitaxel for a gynecologic malignancy were identified. Chart abstraction included pathology, prior therapy, indication for nab-paclitaxel, dosing, response, toxicities including any HSR, and reason for discontinuation of nab-paclitaxel therapy. RESULTS: We identified 37 patients with gynecologic malignancies with a history of paclitaxel HSR who received nab-paclitaxel. Six patients (16.2%) had a prior HSR to both paclitaxel and docetaxel while the other 31 patients had not received docetaxel. No patients experienced a HSR to nab-paclitaxel. Median number of cycles of nab-paclitaxel was 6 (range 2–20). Twelve patients received weekly dosing at 60 to 100 mg/m². The remainder of patients received 135 mg/m² (n=13), 175 mg/m² (n=9), or 225 mg/m² (n=3). Thirty four patients (91.9%) received nab-paclitaxel in combination with carboplatin (n=28, 75.7%), IP cisplatin (n=1, 2.7%), carboplatin and bevacizumab (n=3, 8.1%), or carboplatin and gemcitabine (n=2, 5.4%). Reasons for discontinuing nab-paclitaxel included completion of adjuvant therapy (n=16), progressive disease (n=18), toxicity (n=1), and death (n=1). There were no grade 4 complications identified during nab-paclitaxel administration. Grade 3 complications included: neutropenia (n=9), thrombocytopenia (n=4), anemia (n=1), and neurotoxicity (n=1). CONCLUSION: Nab-paclitaxel is well-tolerated with no HSRs observed in this series of patients with prior taxane HSR. Given the important role of taxane therapy in nearly all gynecologic malignancies, administration of nab-paclitaxel should be considered prior to abandoning taxane therapy.
Albumin-Bound Paclitaxel ; Anemia ; Bevacizumab ; Carboplatin ; Cisplatin ; Drug Hypersensitivity ; Drug Therapy ; Humans ; Hypersensitivity* ; Incidence ; Neutropenia ; Paclitaxel ; Pathology ; Thrombocytopenia

The causes of cytopenia in patients with severe fever with thrombocytopenia syndrome (SFTS) are not fully understood until now. We reviewed the bone marrow (BM) findings of patients with SFTS to unravel the cause of the cytopenia. Three Korean SFTS were enrolled in this study. Thrombocytopenia, neutropenia, and anemia were detected in all three patients. Severe hypocellular marrow (overall cellularity <5%) and a decreased number of megakaryocytes were noted in one patient, and hypo-/normocellular marrow and an increased number of hemophagocytic histiocytes were observed in two patients. Megakaryocytes were relatively preserved in two patients. Although a limited number of cases are available, our observations suggest that both BM suppression and peripheral destruction or sequestration are causes of cytopenia of patients with SFTS. To the best of our knowledge, this is the first well documented pathologic evaluation of Korean SFTS.
Aged ; Aged, 80 and over ; Bone Marrow/*pathology ; Female ; Fever/*complications ; Histiocytes/*pathology ; Humans ; Male ; Middle Aged ; Neutropenia/complications ; Pancytopenia/complications ; Syndrome ; Thrombocytopenia/*complications/*immunology

BACKGROUND/AIMS: The endoscopic findings and clinical relevance of portal hypertensive colopathy are not well described in Korea. We aimed to do a retrospective study of mucosal changes in the colon of patients with liver cirrhosis and to find their association with clinical characteristics. METHODS: We reviewed the clinical data and endoscopic findings of 48 patients with liver cirrhosis and 48 patients, matched for age and sex, with irritable bowel disease (IBS) who underwent colonoscopy over a 5 year span. RESULTS: Patients with liver cirrhosis were more likely to have colitis-like lesions and vascular abnormalities than IBS patients. Low platelet count (p=0.005) and severe esophageal varices (p=0.011) were associated with portal hypertensive colopathy, whereas the etiologies and severity of cirrhosis were not associated with these findings. CONCLUSIONS: Portal hypertensive colopathy can be defined with colitis-like lesions or vascular lesions. These lesions are more frequently present in patients with more severe esophageal varices and thrombocytopenia.
Adult ; Aged ; Colonoscopy ; Esophageal and Gastric Varices/etiology ; Female ; Humans ; Hypertension, Portal/complications/*pathology ; Intestinal Mucosa/pathology ; Irritable Bowel Syndrome/complications/*pathology ; Liver Cirrhosis/complications/*pathology ; Male ; Middle Aged ; Platelet Count ; Retrospective Studies ; Severity of Illness Index ; Thrombocytopenia/etiology

The study was purposed to investigate the expression and function of non-muscle myosin heavy chain-IIA (NMMHC-IIA) in Fechtner syndrome in order to explore the pathologic changes of kindy disease and the mechanism of granulocyte inclusion body formation. NMMHC-IIA levels in granulocytes were analyzed by Western-blot, the expressions of NMMHC-IIA, IIB in HEK-293 cells were detected by RT-PCR and were analyzed by co-immunoprecipitation. The results indicated that the IIA/beta-actin ratio for Fechtner syndrome granulocytes was (0.35 +/- 0.12), and obviously decreased as compared with that of normal control (0.87 +/- 0.18) (p < 0.01). The IIA and IIB expressed higher in HEK-293 cells. The interaction of IIA and IIB was confirmed by co-immunoprecipitation in HEK-293 cells. It is concluded that dominant-negative effect of NMMHC-IIA is involved in the formation of inclusion bodies. IIA and IIB show obvious interaction, IIB partly compensates the IIA defect derived from MYH9 mutations, and may delay or prevent the development of clinically relevant abnormalities.
Blood Platelet Disorders ; genetics ; metabolism ; pathology ; Cell Line ; Granulocytes ; pathology ; Humans ; Inclusion Bodies ; pathology ; Kidney ; cytology ; embryology ; metabolism ; Mutation ; Nonmuscle Myosin Type IIA ; genetics ; metabolism ; physiology ; Nonmuscle Myosin Type IIB ; genetics ; metabolism ; physiology ; Syndrome ; Thrombocytopenia ; genetics ; metabolism ; pathology

No abstract available.
Bone Marrow/pathology ; *Chromosome Deletion ; Diagnosis, Differential ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Middle Aged ; Purpura, Thrombocytopenic, Idiopathic/diagnosis ; Thrombocytopenia/*diagnosis