Plasma homocysteine levels in patients with isolated coronary artery ectasia

OBJECTIVE: Hyperhomocysteinemia is recognized as an independent risk factor for arterial disease including coronary artery disease, cerebrovascular disease and peripheral vascular disease. Previously, an association between increased plasma homocysteine level and peripheral arterial aneurysms has been reported. However, the relationship between coronary artery ectasia (CAE) and plasma homocysteine level has not been investigated. Accordingly, this study was designed to investigate plasma homocysteine level in patients with isolated CAE. METHODS: Thirty-two patients with isolated CAE without significant stenosis and 30 control subjects with angiographically normal coronary arteries were included in this study. Fasting plasma homocysteine concentrations were measured by Fluorescence Polarization Immunoassay method using homocysteine kids. Hyperhomocysteinemia is defined as plasma homocysteine levels above the 95th percentile of the control subjects (13.6 mumol/l). RESULTS: According to the definition of hyperhomocysteinemia, 19 (59%) of patients with isolated CAE had elevated levels of plasma homocysteine compared to 2 (7%) in the control subjects with angiographically normal coronary arteries (p<0.001). In addition, patients with isolated CAE had significantly higher levels of plasma homocysteine compared to control subjects (14.9+/-4.5 micromol/l vs. 8.6+/-1.9 micromol/l respectively, p<0.001). Besides, we detected a significant positive correlation between the number of ectasic segment and plasma homocysteine level (r=0.537, p=0.002). CONCLUSION: We have shown for the first time an association between elevated plasma homocysteine level and isolated CAE. Larger prospective studies are needed to confirm the role of hyperhomocysteinemia in CAE and to evaluate the usefulness of homocysteine-lowering therapies.     

Incremental role of three-dimensional transesophageal echocardiography in the assessment of mitral-aortic intervalvular fibrosa abscess

We report a case of an elderly patient in whom live/real time three-dimensional transesophageal echocardiography (3DTEE) provided definitive diagnosis of mitral-aortic intervalvular fibrosa abscess. This could not be done by two-dimensional transthoracic echocardiography (2DTTE) and two-dimensional transesophageal echocardiography (2DTEE). 3DTEE was also helpful in ruling out associated mitral valve endocarditis, which was initially suspected by 2DTEE leading to a mitral valve sparing surgery. Thus, 3DTEE provided incremental information over 2DTTE and 2DTEE in this patient.     

Live/real time three-dimensional transthoracic echocardiographic assessment of the involvement of cardiac valves and chambers in carcinoid disease

We present an adult with metastatic carcinoid disease affecting the heart, in whom live/real time three-dimensional transthoracic echocardiography (3DTTE) provided incremental value over two-dimensional transthoracic echocardiography (2DTTE). Initial 2DTTE was able to demonstrate severe pulmonic and tricuspid regurgitation, but was unable to visualize the posterior leaflet of the tricuspid valve or the right (right anterior) leaflet of the pulmonic valve. Further analysis with 3DTTE demonstrated thickening, restricted mobility, and noncoaptation of all three leaflets of both the tricuspid and the pulmonary valves. En face viewing of tricuspid and pulmonary regurgitation vena contractas permitted more reliable quantification of regurgitation severity. In addition, localized, linear, echogenic areas consistent with carcinoid deposits were noted along the inner walls of the right atrium, atrial septum, and inferior vena cava. To the best of our knowledge, endocardial carcinoid deposits have never been reported by 2D or 3D echocardiography. En face viewing of these deposits by 3DTTE enabled measurement of their dimensions and areas. Subcostal examination also identified large circumscribed hepatic lesions consistent with metastatic disease. Neither the carcinoid deposits nor the metastatic lesions were detected by 2DTTE. This case demonstrates the usefulness of 3DTTE as a supplement to 2DTTE in more comprehensively assessing carcinoid involvement of the heart.     

16例脑结核瘤抗结核治疗系列观察

目的:报告16例颅内结核瘤患者的临床、影像学表现及抗结核治疗的结果.设计:本文共纳入苏丹Khartoun市全国神经系统疾病中心连续观察的16例脑结核瘤患者.诊断则依据其临床、头颅影像学特征及对抗结核治疗有效等方面.本组中共有7例具有脑组织或脑外组织的病理组织学资料.结果与结论:本组病例最常见的临床表现是头痛(100%)、全身性抽搐(68.7%)及偏瘫(56.2%).头颅横断面电子计算机体层摄影(CT)/核磁共振成像(MRI)显示单个或多个明显增强的病变及病灶周围水肿.经抗结核治疗后,多数存活患者(13/15)病变完全吸收.病变部分吸收与就诊延迟、颅内多个大病灶及晚期粟粒性结核病有关.我们主张对颅内结核瘤,即使是拟诊病例,应早期经验性试用抗结核治疗,尤其在结核病高发地区.     

Decreased accessibility of platelet-bound fibrinogen to antibody and enzyme probes

The binding of fibrinogen to platelets is a multiphasic process leading to apparently nonreversible associations between fibrinogen and stimulated platelets. To further investigate changes in platelet- fibrinogen interactions, the present study examined the accessibility of platelet-bound fibrinogen and its GPIIb-IIIa receptor to antibody and enzyme probes as a function of time after platelet stimulation with adenosine diphosphate (ADP). Whereas only minimal changes in fibrinogen and 10E5 binding were observed within 60 minutes after platelet stimulation and equilibrium fibrinogen binding, the binding of polyclonal antifibrinogen antibodies decreased significantly (75% +/- 13%, mean +/- SD, n = 9). Similar decreases were noted with rabbit antifibrinogen Fab and F(ab')2 fragments. In addition, plasmin (32 mU/mL) added to platelets five minutes compared with 60 minutes after equilibrium fibrinogen binding dissociated 52% +/- 12% compared with 33% +/- 7% of platelet-bound fibrinogen in five minutes, and 83% +/- 15% compared with 66% +/- 14% of bound fibrinogen in 15 minutes. No difference in plasmin cleavage products was observed, however, by sodium dodecyl sulfate-polyacryl-amide gel electrophoresis (SDS-PAGE). Complete fibrinogen dissociation occurred 30 minutes after plasmin addition, confirming that fibrinogen was not internalized. In contrast, dissociation of platelet-bound fibrinogen by chymotrypsin was less affected by time after equilibrium fibrinogen binding, and minimal changes in antifibrinogen antibody recognition and plasmin-induced dissociation of fibrinogen bound to stimulated but glutaraldehyde-fixed platelets were observed. The data suggest that ADP-induced fibrinogen binding to fresh platelets is accompanied by progressive rearrangements of fibrinogen on the platelet surface.     

Histomorphometric analysis of aplastic bone disease in chronic renal failure at initiation of haemodialysis: Relation to aluminum and parathormone

SUMMARY: We studied bone histology of 134 uraemic patients without a history of vitamin D administration at the start of haemodialysis. Patients were categorized according to bone histology as follows: aplastic bone disease (ABD), ostitis fibrosa, mixed type, mild hyperparathyroidism and osteomalacia. On initiation of haemodialysis, ABD was observed in 48.5% of patients. the average age of the ABD group (50.8 ± 12.5 years) was significantly higher than that of patients with other histologies ( P <0.01). Serum parathyroid hormone (PTH) and alkaline phosphatase (ALP) concentrations were lower ( P <0.01) in the ABD group, especially in patients with diabetes mellitus. Patients with diabetes mellitus and ABD had lower serum concentrations of PTH and ALP than non-diabetic patients, suggesting that depressed PTH may be related to ABD. Eleven (55%) of the 20 patients who were receiving A1(OH)₃ also had ABD. A direct relationship was observed between serum aluminum concentration and aluminum-positive bone surface ( r =0.60; P <0.01). Aluminum staining was more frequently observed in the ABD group than in the non-ABD group ( P <0.01). Because serum intact-PTH concentrations correlate with osteoid surface area, fibrosis volume and bone formation rate, it may be a useful marker of bone histology in renal osteodystrophy. These results suggest that, in addition to conservative treatment with A1(OH)₃, other factors may be involved in the formation of ABD which is often present at the start of haemodialysis.     

The Kallmann syndrome gene product expressed in COS cells is cleaved on the cell surface to yield a diffusible component

Kallmann syndrome is characterized by hypogonadotropic hypogonadism and anosmia and caused by a defect of migration and targeting of gonadotropin-releasing hormone-secreting neurons and olfactory axons during embryonic development. We previously cloned the gene responsible for the X-linked form of the disease encoding a 680 amino acid protein, KAL, which displays the unusual combination of a protease inhibitor domain with fibronectin type III repeats. Previous expression studies by northern blot and RNA in situ hybridization in human and chick indicated that the gene is expressed at very low levels in the olfactory bulb during development. Therefore, low abundance of the protein has hampered a detailed biochemical characterization. By overexpressing both the human and chick KAL cDNAs in eukaryotic cells, we now provide evidence that KAL is a glycosylated peripheral membrane protein with an apparent molecular weight of approximately 100 kDa. We show that this 100 kDa protein is proteolytically processed on the cell membrane to yield a 45 kDa diffusible component, which is detectable with an antisera against the C-terminal part of the protein and binds tightly to cell surfaces. These data provide a first step toward understanding KAL function in neuronal interactions and neurite extension in the olfactory bulb and suggest that KAL might be a diffusible chemoattractant molecule for olfactory axons.      

Predicting risk of erectile dysfunction in patients with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is one of the risk factors for erectile dysfunction (ED). We aimed to predict the risk of ED in patients with NAFLD. The study included 146 male patients complaining impotence admitted to the urology outpatient clinic aged 24–80 years without a history of alcohol use who underwent abdominal ultrasonography between February 2018 and January 2019. 106 patients with NAFLD and 40 men without NAFLD were included in the study. Clinical and laboratory parameters, ED status according to International Index of Erectile Function-5 were compared between patients with and without NAFLD. The mean age of patients was 51.47 ± 10.34 years. NAFLD was detected in 72.6% of the patients. No statistically significant difference was found regarding mean age, BMI, IIEF-5 scores, DM status, serum glucose levels (p > .05). Fasting insulin levels, hypertension (HT), insulin resistance (IR) and ED status of the patients with NAFLD were significantly higher than patients without NAFLD (p < .05). NAFLD was found to be a significantly independent associated with ED. We also found that patients with NAFLD have risk of ED 2.92 times higher than without NAFLD (OR: 2.92). For the patients presenting with erectile dysfunction, hepatic steatosis should also be considered.     

Transient myocardial bridging of the left anterior descending coronary artery in acute inferior myocardial infarction

We observed transient myocardial bridging of left anterior descending coronary artery (LAD) in 18.75% (12 of the total 64) of the patients during acute inferior myocardial infarction (MI). Myocardial bridging occurred only in the acute phase of inferior MI and not in the chronic phase. In the acute phase of inferior MI, compensatory hypercontraction of the anterior wall is assumed to occur in response to the decrease in the movement of the infarct-related walls. In the chronic phase, disappearance of the myocardial bridging observed due to the resolution of compensatory anterior wall hypercontraction, as a result of the reperfusion of infarct-related coronary artery. Most of the myocardial bridges seen in autopsy series are not seen angiographically. Variation at angiography may in part be attributable to small and thin bridges causing little compression. Adrenergic stimulation or afterload reduction by nitroglycerin facilitates diagnosis of myocardial bridging by increasing coronary compression. Both of these conditions are almost always present in acute MI. We concluded that transient myocardial bridging of LAD can be observed in some patients with acute inferior MI during acute stage.