Gastric mucosal vascular ectasias causing bleeding in cirrhosis. A distinct entity associated with hypergastrinemia and low serum levels of pepsinogen I

To characterize bleeding from gastric red spots in patients with cirrhosis, three groups of patients were studied: (a) 11 cirrhotic patients bleeding from gastric red spots, (b) 18 nonbleeding cirrhotic patients without gastric red spots, and (c) 13 noncirrhotic patients with endoscopic normal mucosa (controls). Histologic examination of antral biopsy specimens revealed a diffuse capillary ectasia without inflammation in 8 of the 11 cirrhotic patients with gastric lesions. Morphometric analysis disclosed a significantly greater mean mucosal capillary cross-sectional area in cirrhotic patients with gastric lesions (mean +/- SE, 1371 +/- 320 microns2) than in those without gastric lesions (541 +/- 61 microns2) (p less than 0.005) or controls (353 +/- 20 microns2) (p less than 0.001). Hypergastrinemia was detected in 8 of the 11 cirrhotic patients with lesions, in 2 of the 18 cirrhotic patients without gastric lesions, and in none of the controls (p less than 0.001). Gastrin serum levels correlated significantly (r = 0.80) with mean mucosal capillary cross-sectional area in patients with cirrhosis. Pepsinogen I serum levels below 20 ng/ml were observed in 7 of the 11 cirrhotic patients with lesions, in 1 of the 18 cirrhotic patients without lesions, and in none of the controls. These data indicate that bleeding from gastric red spots in patients with cirrhosis is a distinct entity characterized by vascular ectasia of the gastric mucosa. This condition seems to be associated with hypergastrinemia and low serum levels of pepsinogen I.     

Increased aortic stiffness in patients with coronary artery ectasia

OBJECTIVE: Alterations in aortic stiffness may reflect the elastic properties of the larger arteries. In many diseases, aortic elastic properties have been investigated to show whether the larger arteries are involved. The elastic properties of aorta in patients with coronary artery ectasia, however, have not been studied yet. We aimed to investigate aortic stiffness parameters in patients with coronary artery ectasia and to compare patients with coronary artery ectasia and coronary artery disease with the control group. METHOD: Thirty-three patients with coronary artery ectasia, 31 patients with coronary artery disease and 30 patients with angiographically normal coronary arteries were included in this study. Aortic diameters were measured on the M-mode tracing obtained at a level 3 cm beyond the aortic valve at parasternal long-axis view. Aortic diameter change, aortic strain, aortic distensibility and stiffness parameters were measured as aortic stiffness parameters. RESULTS: Aortic diameter changes were fewer in the coronary artery ectasia and coronary artery disease group than in the control group (0.4 +/- 0.1 and 0.3 +/- 0.1 vs. 0.8 +/- 0.2; P < 0.001). Aortic distensibility and aortic strain were significantly lower in patients with coronary artery ectasia and coronary artery disease than in the controls (for aortic distensibility P < 0.001 and for aortic strain P < 0.001, < 0.001, respectively). In contrast, a significantly higher aortic stiffness index was observed in patients with coronary artery ectasia and coronary artery disease than in the control group (14.2+/-2.6 and 18.1 +/- 2.9 vs. 5.9 +/- 1.8; P < 0.001, respectively). CONCLUSIONS: The impairment in aortic elastic properties in patients with coronary artery ectasia indicates that this disease is a generalized disease rather than a localized disease of the coronary arteries.     

Elevated plasma homocysteine levels in patients with isolated coronary artery ectasia

OBJECTIVE: Coronary artery ectasia is a variant of coronary atherosclerosis. Hyperhomocysteinemia has emerged as a major, independent risk factor for cardiovascular diseases. The purposes of this study were to determine plasma hyperhomocysteine levels in patients with coronary artery ectasia, and to compare patients with coronary artery ectasia, coronary artery disease, and controls with normal coronary angiogram. METHOD: The study population included 37 patients with coronary artery ectasia and 36 patients with coronary artery disease. The control group consisted of 32 patients with angiographically proven normal coronary arteries. Plasma hyperhomocysteine levels were measured in all study patients with an enzyme-linked immunosorbent assay. RESULTS: Plasma homocysteine levels were significantly higher in patients with both coronary artery ectasia and coronary artery disease than in the controls (14.8+/-1.1 and 15.9+/-0.8 vs. 2.5+/-0.6 micromol/l; P<0.001 and P<0.001, respectively). No significant differences in plasma homocysteine levels were found among CAE and CAD groups (P>0.05). CONCLUSIONS: We have demonstrated that patients with coronary artery ectasia and coronary artery disease have increased plasma hyperhomocysteine levels compared with the controls. These findings suggest that hyperhomocysteinemia may play an important role in the pathogenesis of coronary artery ectasia as in coronary artery disease.     

Changes in diameter size and F-actin expression in the myocytes of patients with diabetes and streptozotocin-induced diabetes model rats

Diabetes mellitus may be an independent risk factor for disturbance of cardiac function, but the detailed mechanism remains unclear. In the present study, histological examinations were carried out on 25 hearts from diabetes model rats as well as myocardial biopsy materials from patients with diabetes (n = 25). The mean diameter of the cardiac myocytes in humans was 12.2 +/- 0.5 microns in the control group of patients without diabetes mellitus or hypertension (n = 6), 13.7 +/- 0.8 microns in the hypertension group (n = 3), 9.0 +/- 1.7 microns in the diabetes group (n = 8), and 11.9 +/- 2.0 microns in the diabetes with hypertension group (n = 8). The cardiac myocytes of diabetic patients appeared to be atrophic. Comparison of the size of myocytes in the control rats vs streptozotocin-induced diabetes model rats (n = 7, each) was 5.4 +/- 0.2 vs 5.2 +/- 0.3 microns at 2 weeks; 5.9 +/- 0.1 vs 4.9 +/- 0.9 microns at 12 weeks, and 5.7 +/- 0.1 vs 4.0 +/- 0.2 microns at 24 weeks, respectively, and gradually decreased in streptozotocin rats with aging. Immuno-histochemistry with phaloidin was used to assess F-actin in the cardiac myocytes. The relative cross-sectional area of F-actin in the cardiac myocytes of streptozotocin rats was compared to that in non-streptozotocin rat myocytes. F-actin fluorescence in streptozotocin rats was 89.9 +/- 3.9% at 2 weeks, 77.9 +/- 6.4% at 12 weeks, and 56.8 +/- 5.7% at 24 weeks, indicating a decrease in F-actin. These results suggest that the smaller myocytes observed in patients with diabetes and streptozotocin rats are related to the decrease in F-actin in myocytes.     

Expression of monocyte and lymphocyte adhesion molecules is increased in isolated coronary artery ectasia

BACKGROUND: Coronary artery ectasia is defined as localized or diffuse dilation of the coronary arteries exceeding the 1.5-fold of normal adjacent segment. Scarce data are available about the role of inflammation in coronary artery ectasia. In the present study, we aimed to evaluate the expression of CD11b and CD45 adhesion molecules in peripheral blood granulocytes, monocytes and lymphocytes from the patients with coronary artery ectasia as possible indicators of inflammation. METHOD: The study consisted of 14 patients who had angiographically normal coronary arteries with coronary artery ectasia and 13 age and sex-matched controls without coronary artery ectasia. Cell surface adhesion molecules were detected by direct immunofluorescence evaluated by flow cytometry using monoclonal antibodies tagged with fluorescent markers. Venous blood samples were taken after coronary angiography. RESULTS: Mean fluorescence intensity of CD45 (33.8+/-3.1 vs. 13.0+/-0.7, P<0.001) and CD11b (39.1+/-13.5 vs. 19.5+/-1.32, P<0.001) on the monocyte surface of patients with coronary artery ectasia were higher than those of controls. Similarly in patients with coronary artery ectasia, the expression of CD11b (7.5+/-0.61 vs. 5.6+/-0.2, P=0.009) and CD45 (47.5+/-3.6 vs. 36.2+/-2.5, P=0.02) on lymphocytes was also significantly higher than those of controls. CONCLUSION: Increased levels of cellular adhesion molecules in patients with coronary artery ectasia may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to coronary artery ectasia.     

Decreased nitrate-mediated dilatation in patients with coronary artery ectasia: an ultrasonographic evaluation of brachial artery

BACKGROUND: Coronary artery ectasia has been defined as localized or diffuse nonobstructive lesions of the epicardial coronary arteries with a luminal dilation exceeding the 1.5-fold of normal adjacent segment or vessel diameter. Although coronary artery disease is supposed to be responsible for more than 50% of coronary ectasia, the precise pathology of coronary artery ectasia is not clearly understood. The brachial artery ultrasound test for flow-mediated endothelial-dependent vasodilatory function includes administration of sublingual nitrates to examine the vasodilating effect of an exogenous source of nitric oxide. In the present study, we aimed to compare flow-mediated and nitrate-mediated responses of brachial artery in patients with coronary artery ectasia and patients with coronary artery disease. MATERIALS AND METHODS: Thirty-six consecutive patients with coronary artery ectasia in combination with coronary artery disease and 42 age-matched and sex-matched patients with coronary artery disease alone were included in the study. Flow-mediated and nitrate-mediated dilatations were measured in all patients using a high-resolution B-mode ultrasonographic system. RESULTS: Baseline brachial artery diameters in patients with coronary artery ectasia were not statistically different from those in patients with coronary artery disease (4.2+/-0.6 vs. 4.0+/-0.6 mm, respectively, P=0.16). Although the forearm flow-mediated dilatation of the patients with coronary artery ectasia did not differ from that of patients with coronary artery disease alone (5.5+/-3.8 vs. 4.8+/-3.6%, respectively, P=0.41), nitrate-mediated dilatation was significantly lower than that of patients with coronary artery disease alone (7.9+/-5.2 vs. 10.9+/-5.4%, respectively, P=0.02). CONCLUSION: We have shown that patients with coronary artery ectasia have decreased nitrate-mediated response of brachial artery compared with patients with coronary artery disease alone, suggesting more severe dysfunction or, possibly, destruction of the media layer in coronary artery ectasia than in coronary artery disease.     

Morphologic and morphometric light and electron microscopic studies of the spleen in patients with hereditary spherocytosis and autoimmune haemolytic anaemia

With the aim of contributing to a better understanding of the haemolytic function of the spleen, a morphologic and morphometric study of this organ fixed by arterial perfusion was performed in nine patients with hereditary spherocytosis (HS), three with autoimmune haemolytic anaemia (AHA) and six with Hodgkin's disease without splenic involvement (controls). The spleen weight in HS and AHA (621 +/- 429 g, mean +/- SD) was significantly increased with respect to controls (168 +/- 36 g) (P = 0.003). In HS the red cell retention in the cords of Billroth was significantly increased (203 +/- 68 per 10(4) microns 2) with respect to the cases with AHA (93 +/- 35 per 10(4) microns 2) and to the controls (57 +/- 28 per 10(4) microns 2) (P = 0.004). In HS and AHA the number of macrophages per 10(4) microns 2 of red pulp was significantly increased (5.41 +/- 1.10 and 7.52 +/- 2.91, respectively) with respect to the controls (3.25 +/- 0.58) (P less than 0.003). There was no statistically significant difference between the number of macrophages in HS and AHA. The transmission (TEM) and scanning electron microscopy (SEM) studies demonstrated predominantly red cell retention in the cords of HS spleens, red cell phagocytosis by cordal macrophages in AHA spleens and in a lesser intensity in HS spleens, and phagocytosis of haematic corpuscles by sinus endothelial cells (SEC) in the cases of HS. These quantitative studies allow a better understanding of splenic red cell destruction in haemolytic syndromes.     

Plasma total homocysteine in the active stage of ulcerative colitis

BACKGROUND: Homocysteine, an independent risk factor for thromboembolism, has been recently shown to be elevated in ulcerative colitis (UC). However, its relation to the activity of the disease remain unclear. METHODS: Two groups were studied: group consisted of 1-30 patients with UC (17 men, 13 women, mean age 50.3 +/- 14.7 years), including 15 patients with active disease. Group 2 (controls) consisted of 21 age-, sex-, bodyweight-matched healthy persons (12 men, nine women, mean age 53.1 +/- 12.8 years). Total plasma homocysteine (tHcy) and serum folate and vitamin B12 as well as selected coagulation parameters were assessed. RESULTS: Mean tHcy in UC patients was significantly higher than in healthy controls: 10.8 +/- 3.1 mmol/L versus 6.8 +/- 2.5 mmol/L (P < 0.001). Patients with active disease had higher tHcy than patients in remission: 11.2 +/- 3.5 mmol/L versus 9.0 +/- 2.3 mmol/L (P = 0.048). Patients with > or =4 recurrences of the disease had also higher tHcy than the others: 11.5 +/- 3.6 mmol/L versus 9.0 +/- 2.1 mmol/L (P = 0.035). The tHcy correlated with duration of disease: r = 0.6632 (P < 0.05). Folate and B12 levels were within their reference ranges in all subjects. However, in the patients with active disease the platelet count, fibrinogen and D-dimer were significantly higher than in the patients in remission and the controls. CONCLUSIONS: Ulcerative colitis is associated with elevated tHcy concentration, particularly in the active stage, and in more recurrent types of the disease; this elevation does not seem to be prevented by a normal folate status and might have an enhancing effect on the procoagulation blood profile.     

Fluorescence microlymphography: diagnostic potential in lymphedema and basis for the measurement of lymphatic pressure and flow velocity

Fluorescence microlymphography (FML) is an almost atraumatic technique used to visualize the superficial skin network of initial lymphatics through the intact skin of man. Visualization was performed with an incident light fluorescence microscope following subepidermal injection of minute amounts of FITC-dextran 150,000 using microneedles. Emanating from the bright dye depot, the surrounding network of microvessels is filled, documentation performed by photography or video film. In congenital Milroy lymphedema, a lack of microlymphatics (aplasia) is typical while in other primary lymphedemas and in secondary lymphedema after mastectomy or irradiation of proximal lymph nodes, the network remains intact but the depicted area is enlarged. Lymphatic microangiopathy characterized by obliterations of capillary meshes or mesh segments develops in phleboedema with trophic skin changes, progressive systemic sclerosis and Fabry's disease. In lipedema, lymphatic microaneurysms are stained. Microlymphatic pressure may also be measured using FML. For this purpose, glass micropipettes are inserted into the capillaries by means of a micromanipulator and pressure is determined by the servo-nulling technique. Normal subjects produced significantly lower pressure (7.9 +/- 3.4 mmHg) compared to patients with primary lymphedema (15.0 +/- 5.1 mmHg, p<0.001). This characteristic lymphatic hypertension may be improved by complex physiotherapy or local application of prostaglandins. Additionally, a modification of the FML procedure can be used to measure lymphatic capillary flow velocity in controls and patients. FML is suited to confirm the clinical diagnosis of lymphedema, contributes to distinguish among various forms of edema, and is useful in clinical research. In addition, FML has also become a tool for experimental animal studies including the depiction of gastric microlymphatics, the measurement of flow velocity in the naked mouse tail, and in evaluation of lymphangiogenesis in a model of Milroy disease.     

Oestrogen agonistic effects of tamoxifen in the uterus of newborn guinea pigs after short and long treatment. Biological and histological studies

Tamoxifen (TAM) alone or combined with oestradiol (E2) or progesterone (P) was administered to newborn guinea pigs (2 days old) for short (2 days) or a long (12 days) treatment period. TAM alone provoked a great stimulatory effect on uterine growth and DNA content and the effect was particularly intense after the long treatment. These actions were markedly enhanced when TAM was administered together with E2. Following short treatment, the values of the uterine wet weights (mg +/- SD) were as follows: control animals, 142 +/- 15; animals treated with TAM, 298 +/- 53; E2, 335 +/- 15; (TAM + E2), 362 +/- 16. The values after the long treatment were 177 +/- 30, 555 +/- 93, 709 +/- 117 and 1263 +/- 222, respectively. Histological studies showed that TAM provoked morphological changes in both the endometrium and the myometrium. The effects were particularly great on the height of the luminal epithelial cells and on the uterine glands. After 2 days of treatment with E2, TAM and P, the thickness of the luminal epithelium, which was 13.5 micron +/- 1.5 in the control animals, increased as follows: TAM, 19 microns +/- 1.7; E2, 20.3 microns +/- 3.3; (TAM + E2), 30.5 microns +/- 5; P, 12 microns +/- 0.9 and (P + TAM), 19.7 microns +/- 1.2. The values after the 12 day treatment were: controls, 20.8 microns +/- 1.8; TAM, 27.4 microns +/- 2.1; E2, 32 +/- 3; (TAM + E2), 43 microns +/- 5; P, 17.8 microns +/- 1.2 and (P + TAM), 23.6 microns +/- 1.5.(ABSTRACT TRUNCATED AT 250 WORDS)     

Constipation caused by colonic inertia and distal obstruction: electromyographic study

Colonic motility was evaluated in 15 patients with chronic constipation and 12 healthy subjects by both measuring the transit time of 20 radiopaque markers and recording the colonic myoelectric signals by means of a silastic tube equipped with 4 ring contact electrodes. The tube was introduced by flexible sigmoidoscopy so as the electrodes be located at 50, 40, 30 and 20 cm from the anal verge. Constipation resulted from colonic inertia in 7 patients, the markers being delayed over the whole length of the colon. In the 8 other patients, constipation was due to distal obstruction, the markers accumulating electively in the rectum. The myoelectric tracings showed in the control subjects, on one hand rhythmical stationary spike potentials that occurred at only one electrode site at a mean rate of 10 per minute; on the other hand sporadic (non-rhythmic) spike potentials that were either propagating over the colonic segment (sporadic propagating potentials) or not (sporadic non-propagating potentials). In the constipated patients, the following changes were observed: 1) the number of sporadic propagating potentials was significantly decreased in colonic inertia (2.5 +/- 1.3 bursts of spikes per hour) compared to the controls (8.5 +/- 1.1 bursts/h) or distal obstruction (7.9 +/- 1.3 bursts/h); 2) sporadic propagating potentials usually moved aborally; however, 19.8 +/- 0.9 p. 100 moved orally in colonic obstruction, while 4.6 +/- 0.2 p. 100 in the controls and 4.7 +/- 0.1 p. 100 in colonic inertia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Isoprostane 8-epi-prostaglandin F2 alpha decreases lymph capillary pressure in patients with primary lymphedema

In patients with lymphedema, reduced lymph drainage capacity results in an overloaded superficial microlymphatic network and microlymphatic hypertension. In in vitro experiments, it has been shown that 8-epi-prostaglandin F2 alpha (PGF) induced contractions in human lymphatics. Since lymphatic contractility plays a crucial role in the regulation and generation of lymph transport, we studied the effect of PGF on microlymphatic dynamics by measuring lymph capillary pressure (LCP). Twenty healthy volunteers and 13 patients with primary lymphedema were studied after either PGF or placebo was applied to the skin and occlusively covered for 30 min. Glass micropipettes (7-9 microm) were inserted under microscopic control into initial lymphatics visualized by fluorescence microlymphography and pressure measurements were performed using the servo-nulling technique. The mean LCP in patients with lymphedema was significantly higher (19.8 +/- 12.1 mm Hg) than that in healthy controls (8.4 +/- 4.1 mm Hg) at the placebo-treated site and decreased to normal values after PGF (10.0 +/- 7.7 mm Hg). In healthy volunteers, there was no significant decrease of LCP with PGF compared to placebo. PGF normalizes microlymphatic hypertension in patients with lymphedema by improving lymph transport into deeper channels.     

Dysplastic intramyocardial arteries with subaortic septum in patients with hypertrophic obstructive cardiomyopathy]

Abnormal, dysplastic intramyocardial arteries were reported in autopsied hearts of hypertrophic cardiomyopathy. To elucidate their significance, the operatively-excised myectomy specimens of 24 patients with hypertrophic-obstructive cardiomyopathy (HOCM), of 18 patients with valvular aortic stenosis and of 10 postmortem normal hearts were investigated. Eight patients with HOCM had dysplastic intramyocardial arteries (greater than 100 microns external diameter) as well as dysplastic arterioles (less than 100 microns external diameter). The value of the scores for the thickness and fibroelastosis of the media was nearly doubled, the tunica intima was frequently thickened, and the lumen was relatively reduced in dysplastic vessels. Neither in controls nor in aortic stenosis dysplastic arteries were found. Volume density of patchy fibrosis (scars) was increased in patients with dysplastic arterial vessels (HOCM II) (7.2 +/- 4.4 Vv%) (p less than or equal to 0.05) as compared with HOCM without dysplastic vessels (HOCM I) (0.8 +/- 2.3 Vv%), with aortic stenosis (0.9 +/- 1.6 Vv%) or with controls (0 Vv%), Patients with HOCM II were significantly (p less than or equal to 0.05) younger (30 +/- 13 years) than those with HOCM I (53 +/- 12 years), aortic stenosis (56 +/- 12 years), or controls (63 +/- 21 years). The anterior septum was significantly thicker in HOCM II (29 +/- 7 mm) than in HOCM I (22 +/- 4 mm), in aortic stenosis (19 +/- 3 mm), or in controls (12 +/- 2 mm). Syncopes were complained by about 75% (6/8) of patients in HOCM II, by 54% (9/16) in HOCM I, and by 44% (8/18) in aortic stenosis (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)     

Alterations of the nailfold capillary morphology associated with Raynaud phenomenon in patients with systemic lupus erythematosus

Quantitative analysis of nailfold capillary morphology was performed in age and sex matched groups of 29 patients with systemic lupus erythematosus (SLE) presenting Raynaud phenomenon (RP), 29 RP negative patients with SLE with the same duration of the disease, and 29 healthy controls. Percentages of tortuous, meandering and bushy capillaries were significantly increased in both groups of patients without influence of RP. Capillary density was lower, mean diameters of the capillary loops were higher in patients, especially when RP was present (at the venular branch in microns, mean +/- SD: controls: 15.0 +/- 2.0, RP negative patients with SLE: 17.6 +/- 3.6, RP positive patients with SLE: 20.5 +/- 6.3). In a subgroup of 13 patients with frequent Raynaud's attacks (more than 1/week), diameters were still higher (22.1 +/- 7.1, p to controls less than 0.0005; p to RP negative patients less than 0.05). In patients with SLE, the prevalence of RP seems not to be associated with the increased number of abnormal capillaries but with capillary enlargement, correlating with the frequency of attacks.     

神经生长因子在哮喘患者诱导痰炎性细胞的表达

目的　通过观察神经生长因子 (NGF)在哮喘气道炎性细胞的表达 ,探讨NGF与哮喘气道炎症形成的关系。方法　取 11例哮喘急性发作期、19例哮喘非急性发作期患者及 11例健康对照者的诱导痰 ,其中 12例哮喘非急性发作期患者予丙酸氟替卡松 (ICS)治疗 2周后再取诱导痰。做诱导痰炎性细胞分类计数 ;SP法测诱导痰炎性细胞NGF表达 ;ELISA测其上清中白细胞介素 (IL) 5浓度。结果　 (1)诱导痰巨噬细胞、淋巴细胞、粒细胞NGF表达阳性率哮喘组较健康对照组高 (P值均<0 0 1) ,且急性发作期较非急性发作期高 (P <0 0 1)。急性发作期IL 5水平较非急性发作期和健康对照组高 (P值均 <0 0 1)。 (2 ) 12例非急性发作期患者经ICS治疗后 ,诱导痰巨噬细胞、淋巴细胞、粒细胞NGF表达阳性率及IL 5水平均较治疗前下降 (P值均 <0 0 1)。 (3)巨噬细胞、粒细胞NGF表达阳性率与淋巴细胞相对计数构成比、IL 5水平均呈正相关。结论　哮喘患者气道内巨噬细胞、淋巴细胞和粒细胞NGF表达增加 ,提示NGF可能与哮喘气道炎症的形成有关。     

Assessing local tissue edema in postmastectomy lymphedema

Overall limb lymphedema can be assessed by several methods but none are suitable to determine local edema. Quantifying local edema could provide important information not previously available. Our goal was to determine the suitability of using the tissue dielectric constant (TDC) as and index of local tissue water to detect and quantify edema in postmastectomy patients with unilateral arm lymphedema. Segmental arm volume and TDC were measured in both arms of 18 women with unilateral lymphedema, and in 15 premenopausal and 15 postmenopausal controls. TDC was measured at a frequency of 300 MHz using open-ended coaxial probes with effective measuring depths of 0.5, 1.5, 2.5 and 5.0 mm. For patients and controls, absolute TDC depended on measurement depth but for any depth the TDC of lymphedematous segments was significantly greater than for non-affected contralateral arms (p<0.001). At a depth of 2.5 mm, the TDC ratio between arms for patients was 1.64+/-0.30 vs.1.04+/-0.04 for both control groups (p<0.001). No patient's TDC ratio was as low as 1.2 and no control subject's TDC ratio was as great as 1.2. Results suggest that this method is a good quantitative discriminator of the presence of lymphedema in patients with unilateral limb lymphedema.     

Evaluation of maximal Na K ATPase activity in the erythrocytes of patients with various types of arterial hypertension using the Na-23-NMR method

The paper provides measurements of maximal Na+, K(+)-ATPase activity in 20 patients with hypertensive disease, 20 patients with secondary hypertension and 20 healthy donors. The investigation was made by high-resolution nuclear magnetic resonance using sodium nuclei. A significant decrease was found in Na+, K(+)-ATPase activity in the patients with hypertensive disease (9.0 +/- 0.3 mg-equiv. per lites cells an hour) as compared with those with secondary hypertension (10.3 +/- 0.3 mg-equiv. per liter cells an hour) and the controls (10.5 +/- 0.3 mg-equiv. per liter cells an hour), which supports the findings of impaired membrane morphology in hypertensive disease.     

Increased circulating calcitonin gene-related peptide in congestive heart failure caused by congenital heart disease

Calcitonin gene-related peptide has potent vasodilatory and inotropic actions. The aim of this study was to characterize the changes in this peptide in children with varying degrees of heart failure secondary to congenital heart disease with left to right shunt and to assess its relationship to systolic pulmonary arterial pressure. Plasma calcitonin gene-related peptide levels were measured in 131 children including 13 healthy ones, 43 with various degrees of heart failure secondary to congenital heart disease, and 75 with congenital heart disease without heart failure. In patients with heart failure, calcitonin gene-related peptide concentrations were markedly elevated (15.8 +/- 2.1 pg/mL) as compared with healthy control subjects (7.0 +/- 0.8 pg/mL, P < 0.05) or patients with congenital heart disease but without heart failure (18.6 +/- 1.2 pg/mL, P < 0.01). Compared with the controls, there were highly significant stepwise increases in the calcitonin gene-related peptide levels in the mild (n = 15), moderate (n = 12), and severe (n = 16) heart failure subgroups by 1.5, 1.7 and 3.4 fold, respectively. The plasma calcitonin gene-related peptide levels also correlated directly with the pulmonary arterial systolic pressure (r = 0.515, P < 0.0001). The results of this study indicate that congestive heart failure secondary to congenital heart disease with increased pulmonary flow is associated with elevated levels of calcitonin gene-related peptide that are related to disease severity. Pulmonary overcirculation may play a role in upregulation of calcitonin gene-related peptide in congestive heart failure.     

The influence of iron deficiency on erythrocyte deformability.

The influence of iron deficiency on erythrocyte deformability is controversial. The present study was designed to analyse cell deformability in 14 patients with iron deficiency and controls in a comprehensive way by three different methods, namely erythrocyte filtration, erythrocyte elongation, and measurement of membrane elasticity. Suspensions of washed erythrocytes (haematocrit 0.10) free of leucocytes were used. Erythrocyte deformability measured by filtration was increased by iron deficiency: The relative filtration resistance of a cell in a 3 microns pore was 26.5 +/- 6.9 and 75.8 +/- 23.8 in iron deficiency and controls, respectively (P less than 0.0001). In 5 microns pores the values were 2.80 +/- 1.23 and 3.46 +/- 0.51 (not significant); when the red cell number/volume was adjusted to that in control samples, the value for iron deficiency became significantly lower than in controls (2.32 +/- 0.60, P less than 0.0001). Erythrocyte elongation by centrifugation was unaffected (ratio length/width 1.66 +/- 0.11 and 1.60 +/- 0.10 in iron deficiency and controls, respectively). Membrane elasticity, as assessed by a filter aspiration technique, was also unchanged (membrane elastic modulus 3.94 +/- 0.31 and 3.94 +/- 0.37 x 10(-3) dyn/cm, respectively). It is concluded that iron deficiency does not affect erythrocyte membrane elasticity and that the deformability of whole cells is not impaired, but improved under certain conditions such as the passage of 3 microns pores because of microcytosis with preserved surface/volume ratio. These results are in contrast to earlier studies and they have pathophysiological and clinical implications.     

Protease inhibitors and ectasia in coronary atherosclerosis

The possibility of elastase contributing to degradation of the arterial wall in atherosclerosis and to the formation of ectasia has prompted us to assay the main protease inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, in patients with angiographic coronary disease with and without coronary ectasia. Serum concentrations of these two proteins were measured by immunonephelometry in 203 patients admitted for coronary arteriography. The results obtained were analyzed according to the presence of atheromatous lesions and their severity and to the presence or absence of ectasia. There was no correlation between the values observed and the presence or severity of coronary atherosclerosis, but the concentration of alpha 1-antitrypsin was significantly higher in patients with coronary ectasia (247.2 +/- 40.5 mg/ml) than in patients without ectasia (213.5 +/- 36.6 mg/100 ml; p less than 0.001). This study shows that coronary ectasia is associated with disturbances in the protease-antiprotease system, which may be consecutive to initial changes in elastase activity. Our results support the theory that elastase and protease inhibitors play a specific role in some atheromatous processes.