Myringosclerosis incidence among children with acute otitis media in relation to the isolated pathogens

Patients with acute otitis media [AOM] or otitis media with effusion [OME] and treated with tympanostomy tube insertion can develop myringosclerosis. The aim of this study was to investigate and compare the incidence of myringosclerosis among children with acute otitis media in relation to the isolated aerobic and anaerobic pathogens in their ear discharge. This study as conducted on two groups of patients. Group [1] included 23 subjects of OME had been treated with tympanostomy tubes and some of them had the complication of otorrhea, and group [2] included 48 subjects with AOM with or without otorrhea. Otorrhea of discharging ears of both groups was cultured and the status of their tympanic membranes was followed regularly by otoscopic examination during follow-up duration in scheduled visits to detect the incidence rate, time of appearance and severity of myringosclerosis in relation to the type of isolated pathogens. [GI] had 6 cases [10 ears] of myringosclerosis detected at 2-3 months average duration, and [G II] had 11 cases [20 ears] of myringosclerosis detected at 1-2 months average duration. The highest number of isolated pathogens was Streptococcus pneumoniae [S.P] and Haemophilus influenzae [H.I], and they were the only pathogens accompanied the incidence of myringosclerosis with more incidence and severity in [S.P] infected ears. These findings support the inflammatory theory of development of myringosclerosis. Our study considered myringosclerosis an inflammatory condition rather than to be traumatic reaction from tympanostomy tubes insertion, where Streptococcus pneumoniae is the most liable organism can induce myringosclerosis in improper treated cases of AOM .Anaerobic organisms cannot afford the hyperoxic environment which is suggested by some researchers to be a necessary factor in the development of myringosclerosis and proper treatment of cases of AOM diminishes the chance of incidence of myringosclerosis

Natural inhibitors of coagulation and markers of coagulation activation: the hypercoagulable state in sickle cell disease

This study was designed to clarify abnormalities of the natural coagulation inhibitors and of the markers of thrombin generation in patients with homozygous sickle cell disease [HbSS] in the steady-state, and to evaluate their role in the contribution of the increased thrombotic risk in these patients that could result in new therapeutic interventions. This study was carried out on 50 subjects. They were divided into two groups. Group [A] included 30 patients with homozygous sickle cell disease [HbSS]. Group [B] included 20 apparently healthy age- and sex-matched control subjects; with normal baseline hematologic parameters and haemoglobin electrophoresis as well as no apparent increased thrombotic risk. All patients were tested during steady-state phase with no symptoms or signs of crises or infection for at least 8 weeks and had not had any blood transfusion during the preceding two weeks. They were not on medications other than folic acid 5mg tablets. HbSS was diagnosed by family studies and haemoglobin electrophoresis on cellulose-acetate at pH 8.6. Both patients and control groups were subjected to initial laboratory investigations including complete blood count [CBC], bleeding time [BT], prothrombin time [PT] and INR, activated partial thromboplastin time [aPTT] and haemoglobin electrophoresis. Then, both groups were tested for: [1] Natural coagulation inhibitors including Protein C [antigen and activity], Protein S [total and free levels], Antithrombin-III activity, Heparin cofactor II level, and Tissue factor pathway inhibitor [TFPI] and [2] Markers of coagulation activation; Prothrombin fragments 12 [Fl.2] and Thrombin-antithrombin complex [TAT]. HbSS patients had significantly higher leukocytic count [x 10 [3]/cmm] than control subjects [10.4 +/- 2.8 compared to 6.2 +/- 2.4, p < 0.01]. There was no significant difference between both groups regarding platelet count, bleeding time, prothrombin time [and INR] and activated partial prothrombin time. HbSS patients had significantly lower values than the control group regarding the level of protein C antigen, protein C activity, protein S total and protein S free as well as heparin cofactor TI [p < 0.001, each]. Although FIbSS had lower antithrombin-III activity and tissue factor pathway inhibitor than the control group, the difference was not significant. On the other hand, markers of coagulation activation [namely prothrombin fragments 1.2 and thrombin-antithrombin complex] were significantly higher in HbSS patients compared to the control group [p < 0.001, each]. Comparative studies showed no significant correlation between the level of haemoglobin SS and any of the studied coagulation inhibitors or markers of activation. These data shows that steady state SCD is associated with significant reduced level and/or function of the majority of naturally occurring anticoagulants as well as increased markers of thrombin generation denoting a state of chronic hypercoagulability with increased thrombotic and vasoocclusive tendency. Such changes might justify the prophylactic use of low dose coumadin and/or antiplatelet drugs in HbSS

Erythro-thrombocytopoiesis in hemodialysis patients: possible interaction between thrombopoietin and erythropoietin? is there a role for arterio-venous fistula?

This study was carried out to evaluate the thrombopoietic status of patients with ESRD, to postulate possible causes of altered thrombopoiesis [if any], to verify the clinical significance of endogenous thrombopoietin on both erythropoiesis and thrombopoiesis as well as to assess the contribution of arteriovenous fistula on TPO activity. It included 60 subjects divided into two groups. Group [A] included 40 patients with ESRD on regular hemodialysis three times a week. All included patients had no history of thrombosis [local or systemic, arterial or venous] or a hemorrhagic event within the previous 6 months and they were negative for hepatitis B antigen [HBsAg] and for hepatitis C virus RNA [HCV-RNA] and have normal aminotransferases for the previous 6 months. Patients with a history of malignancy, autoimmune disease, or a documented infection were not included in this study. None of the patients received medication known to interfere with haemostasis [i.e. oral contraceptives, anticoagulants] except for heparin administered during hemodialysis as well as antihypertensives [but not angiotensin-converting enzyme inhibitor or angiotensin II-receptor antagonist] when indicated. Group [A] patients were further subdivided into two subgroups according to their need to rHu-Epo therapy; group [AI] included 19 hemodialysis patients treated with recombinant erythropoietin at a dose of 170 +/- 30 U/kg/sc per week, and group [AII] included 21 patients treated only with oral iron supplementation. Group [B] included 20 age-and sex-matched healthy as the control group. Both patients and control groups were subjected to the following tests: Complete blood count [including blood smear], BUN, serum creatinine, ALT, AST, serum iron, total iron binding capacity [TIBC], serum ferritin, serum erythropoietin [EPO], serum thrombopoietin [TPO] and absolute reticulated platelets count. Furthermore, serum TPO was measured from both the venous return of the AVF and the contra-lateral peripheral vein in each patient with ESRD. Serum erythropoietin was significantly lower [p < 0.01] in HD patients [7.6 +/- 0.8] than in the control group [10.1 +/- 1.3]. Also, serum thrombopoietin was significantly lower [p < 0.001] in the HD patients [60.6 +/- 6.9] than in the control group [120.7 +/- 50.9]. Furthermore, the absolute count of reticulated platelets [x10 [3]/cmm] was significantly lower [p < 0.01] in the HD patients [9.4 +/- 3.7] than in the control group [2 1.7 +/- 4.3]. Hemoglobin and hematocrit were slightly higher in Group AII [10.2 +/- 0.8, 32.7 +/- 5.2, respectively] than in group AI [10.1 +/- 0.9, 32.5 +/- 4.3, respectively]. Such difference was not significant. Platelet count [x10 [3]/cmm] was significantly higher [p < 0.01] in group AI [190 +/- 24.6] than in group AII [150 +/- 30.8]. On the other hand, the absolute count of reticulated platelets [x10 [3]/cmm] was lower in group AI [8.8 +/- 1.5] than group AII [9.3 +/- 1.1], and such difference was not significant. Furthermore, serum TPO was significantly higher [p < 0.05] in group AII [64.7 +/- 5.9] than group AI [55.6 +/- 6.8]. The serum EPO level was significantly higher [p < 0.01] in group AI [8.3 +/- 1.1] than in group AII [6.3 +/- 0.7]. In hemodialysis patients, comparative studies showed significant positive correlation between s. TPO and hematocrit and reticulated platelet count particularly group AII [p < 0.02 and p < 0.01 respectively]. But there was insignificant inverse correlation between s. TPO and platelet count in HD patients. On the other hand, there was significant inverse correlation between s. TPO and endogenous s. EPO in dialysis patients [p < 0.01]. In ND patients, s. TPO concentrations in AVF samples were significantly lower than in the peripheral veins [60.6 +/- 6.9 vs 40.4 +/- 3.9, p < 0.01]. These data confirm the presence of impaired erythro-thrombocytopoiesis in HD patients. This could be partly due to impaired thrombopoietin production and/or increased thrombopoietin destruction and partly due to impaired bone marrow response to the endogenous thrombopoietin. Thrombopoietin appears to induce marrow erythropoiesis either directly or indirectly by augmenting the action of endogenous erythropoietin. Also, it suggests possible involvement of the arteriovenous fistula in the production and/or catabolism of this growth factor. These findings serve as a starting point for further studies to determine the regulatory mechanisms of TPO levels and its precise erythrothrombocytopoietic role in end-stage renal disease