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Objective: To study the effects of chronic severe anemia on the aging heart. Methods: We studied 41 elderly patients (mean age 69.8 yr, standard deviation [SD] 3.9 yr) suffering from [...]

Splenomegaly is a common finding in ß-thalassemia; however, its hemodynamic features and its potential correlations with high output state and hepatic disorders, both also frequent in thalassemia, have not yet been assessed in these patients. Eight ß-thalassemia patients with the indication for splenectomy and no symptoms or signs of heart disease, aged 25.6±5.5 years, were studied. Preoperative assessment included hematological profile, liver biology, hepatitis virus serology, and echocardiography. During splenectomy, splenic artery blood flow and splenic vein pressure were directly measured and liver biopsies were taken. Preoperative echocardiographic data were compared with those of 34 healthy controls. The preoperative cardiac index was significantly elevated in patients (4.8±1.3 vs 3.4±1.1 l/min per m2 in controls,p<0.001). Splenic blood flow, although increased, was not particularly high, being 285±56 ml/min or 0.13±0.04 ml/min per g of splenic mass, representing 4.1±0.9% of total cardiac output (CO). Splenic vein pressure was considerably elevated (29.7±5.5 cmH2O). Hepatic fibrosis, iron deposition, and extramedullary foci were found in all eight biopsies. Serology was positive in five of eight cases. ß-thalassemia patients with extensive splenomegaly requiring splenectomy are characterized by high output state, increased splenic blood flow, which probably makes a limited contribution to CO elevation, and portal hypertension, manifest by increased splenic vein pressure and hepatic histopathological abnormalities. [ABSTRACT FROM AUTHOR]

A case of pyomyositis is presented. This case is unique in the literature as at least 29 abscesses were detected, affecting the vast majority of big muscle groups. We outline the origin of this diseaseentity which selectively affects striated muscles. We also discuss its natural history and management strategy. [ABSTRACT FROM AUTHOR]

Background: Despite the severe derangement of gas exchange in the advanced stages of idiopathic pulmonary fibrosis (IPF), secondary erythrocytosis is either absent or much lower than is seen in chronic obstructive pulmonary disease (COPD) with comparable hypoxemia. This study investigates the differences in erythropoiesis between IPF and COPD, searching for the possible underlying mechanisms., Material/methods: The study included 32 patients with COPD, 18 patients with IPF, all with overt hypoxemia (PO(2) <65 mmHg), and 34 healthy controls. Erythrocytic parameters and serum erythropoietin (EPO) levels were assessed for all subjects. In a number of patients from both groups, the development of erythroid colonies grown from peripheral blood mononuclear cells was assayed in semisolid methylcellulose cultures and compared to cultures of control cells, in the presence of patient or control serum., Results: Hb and serum EPO levels were significantly higher in the COPD group than in IPF patients and controls. However, the number of BFU-E colonies obtained from mononuclear cells of IPF patients was clearly higher than in COPD patients when the same culture medium was used. Unlike COPD sera, IPF sera induced a significant growth inhibition of erythroid bursts arising from mononuclear cells of both patients and controls., Conclusions: Our findings suggest a kind of ineffective erythropoiesis in IPF. Defective EPO production and inhibitory effect on erythropoiesis exerted by pro-inflammatory cytokines released from alveolar macrophages may be implicated in the suboptimal erythropoietic response. However, the possible involvement of other factors affecting erythropoiesis in IPF requires further investigation.

Six hundred and thirty-eight patients who presented with clinical symptoms and/or electrocardiographic findings suggestive of stable angina pectoris were studied; they were also investigated by coronary arteriography. Hemoglobin electrophoresis was performed on all patients to detect the presence of the beta-thalassemia trait. Results were analyzed by logistic regression analysis to determine whether the latter confers any protective effect against advanced coronary artery disease (aCAD; defined as the presence of atheromas in coronary arteries, resulting in stenosis at least 70%). The role of the currently accepted risk factors (smoking, hypertension, hypercholesterolemia, and diabetes) in developing aCAD were reconfirmed, while at the same time it was found that beta-thalassemia heterozygosity is associated with a reduced risk against aCAD (odds ratio 0.39, 95% confidence interval 0.16-0.98). The lipoprotein and blood rheology profile of these individuals may be the underlying causes of this protective effect.