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Wernicke encephalopathy is considered a complication of dialytic therapy, but there are few reports of this complication. We report a 57 years old man and a 45 years old woman, with grade IV renal failure, who after acute peritoneodialysis and chronic hemodialysis respectively, had a confusional syndrome that responded to the administration of thiamine. CT scans in both patients discarded abnormal blood collections or new cerebrovascular episodes. The man bad two previous cerebrovascular episodes, a severe anemia that was corrected, angina and an episode of arrhythmia during the dialytic procedure previous to the confusional episode. The woman had an acute uremic syndrome and a concomitant urinary tract infection during the confusional episode. Wernicke encephalopathy must be suspected in patients in dialysis with confusional episodes.
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PMID:[Wernicke's encephalopathy and dialysis: report of two cases]. 949 80

Even with the reservations that exist regarding the accuracy of tools to measure quality of life, there is little doubt that epoetin has dramatically improved the quality of life in patients with the anemia of chronic renal failure. Patients feel better and have increased energy levels, greater capacity for physical exercise, fewer symptoms of lethargy and tiredness, improved memory and concentration, and less angina and breathlessness. Cardiac, sexual, and cognitive functions all improve, and quality of life assessments suggest enhancements in both physical and social aspects of well-being. Furthermore, circumstantial evidence suggests that treatment with epoetin is quite likely to reduce cardiovascular morbidity and mortality in patients with renal anemia. While chronic anemia has common characteristics irrespective of the etiology, the implications on quality of life in patients with chronic renal failure vary in a number of ways from those in patients with cancer.
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PMID:Quality of life and anemia: the nephrology experience. 967 29

A 72-year-old patient presented himself with typical symptoms of coronary heart disease and was scheduled for invasive diagnostic procedures. Cardiac risk factors were smoking and arterial hypertension. The physical examination was inconspicious. In the laborchemistry a hemoglobin of 79 g/l with a mean corpuscular volume of 63 fl and a mean corpuscular hemoglobin of 20 pg was conspicuous. The serum iron was with 42 micrograms/dl in the lower norm. Transferrin, bili-rubin and lactate dehydrogenase were normal. Then in the gastrointestinal investigations he was diagnosed with a leiomyoma of the intestine that led to chronic anaemia and additionally to chest pain characteristic for angina pectoris. After the removal of the tumor and normalization of hemoglobin this patient was free from symptoms of the disease. The coronary angiography revealed a complex stenosis of the right coronary artery with collaterales and not significant stenosis both of the left coronary arteries. In patients with angina pectoris anaemia as the possible and only cause of angina ought to be verified. It is therefore necessary after normalization of hemoglobin and clarification of the cause for the anaemia to apply a test for coronary ischemia.
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PMID:[Angina pectoris in leiomyoma]. 975 77

Anemia is a common complication of chronic renal failure (CRF). With the availability of recombinant human erythropoietin (rhEPO) over the last decade, much progress has been made in the management of anemia in patients with end-stage renal disease (ESRD) [Eschbach 1995, Gimenez and Scheel 1994, Muirhead et al. 1995, Winearls 1995]. The clearest benefit of rhEPO in ESRD is a substantial reduction in transfusion dependency, which reduces the need for hospital admission and the risk of viral transmission. Improvements in hemostasis and a decrease in human leucocyte antigen (HLA) antibodies have also been reported. Beneficial effects of rhEPO on the cardiovascular system in ESRD include regression of left ventricular hypertrophy (LVH), improvement of angina, and a modest increase in aerobic work capacity. Treatment of anemia with rhEPO has also been shown to improve cognitive function, socialization and quality of life in dialysis patients, although this has not led to better vocational rehabilitation or employment status. It has also been reported that a lower hemoglobin (Hb) content is an independent risk factor for increased mortality in hemodialysis patients [Harnett et al. 1995]. Clearly, therefore, treatment of anemia associated with ESRD is required and beneficial. The optimum treatment of anemia prior to dialysis, however, is still a matter for debate.
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PMID:Does early anemia correction prevent complications of chronic renal failure? 998 40

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

In childhood, coeliac disease (gluten enteropathy) tends to show itself with failure to thrive and growth retardation; in adult life with malabsorption syndromes. We report six cases in adults who presented atypically, with features including clotting disorder, hypoglycaemia, weight loss, anaemia and angina pectoris, all of which responded to gluten withdrawal.
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PMID:Coeliac disease in adults: variations on a theme. 1069 14

A prospective phase II study was conducted to determine the response, toxicity and survival rate of lung cancer patients treated with combination paclitaxel and carboplatin in stage IIIB and IV NSCLC. Eligible patients required measurable and/or evaluable diseases; performance status (ECOG) 0-2; no previous chemotherapy; adequate hepatic, renal and bone marrow function. Paclitaxel was administered at a dose of 200 mg/m2, 3 h infusion, followed by carboplatin at an AUC of 6. Treatment was repeated every 3 weeks for six courses. G-CSF 5 microgram/kg was subcutaneously injected during subsequent courses if there was grade 3-4 leucopenia or granulocytopenia in the previous course. From April 1996 through July 1997, 53 patients were enrolled; all are assessable for toxicity and response. The median age was 56 years (range, 20-77 years). Sixty four percent were male, 64% had adenocarcinoma and 62% had stage IV disease. Two hundred and seventy two courses were administered; 36 patients (68%) completed all six cycles. Two patients achieved a complete response (4%) and 27 patients achieved a partial response (51%), for an overall response rate of 55%. Sixteen patients had stable disease (30%) and 8 patients had progressive disease (15%). The median progression free survival time for all patients, stage IIIB and stage IV patients was 28 weeks (range, 18-37 weeks), 31 weeks (range 21-41 weeks) and 22 weeks (range 16-29 weeks), respectively. The median survival time and 1 year survival rate for all patients was 55 weeks (range, 51-59 weeks) and 55%, respectively. Stage IIIB patients had better median survival time and 1-year survival rate than stage IV patients (75 vs. 46 weeks, P = 0.007; 80% vs. 42%, P = 0.003). Grade 3 and 4 granulocytopenia, anemia and thrombocytopenia were observed in 25, 3, and 1%, respectively, of the 272 courses administered. G-CSF was required in 28% of the 272 courses. There were four episodes of febrile neutropenia (1.5%), three episodes of angina pectoris (1%) and one episode of anaphylaxis (0.4%). Other common toxicities, generally mild, included myalgia, arthralgia, peripheral neuropathy and asthenia. Most toxicities showed cumulative effect. Paclitaxel plus carboplatin is a moderately active regimen in advanced NSCLC. Toxicities of this regimen are well tolerated.
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PMID:Phase II study of paclitaxel and carboplatin for advanced non-small-cell lung cancer. 1059 28

A 41-year-old woman who had been given a diagnosis of aplastic anemia 14 years before was admitted because of recurrence of the disease. Despite therapy, the anemia progressed gradually. The patient refused blood product transfusions for religious reasons. Angina pectoris-like chest pain without ischemic changes on electrocardiograms appeared at a hemoglobin concentration (Hb) of 1.6 g/dl. The patient died of heart failure at Hb 1.5 g/dl. Autopsy showed enlargement of the heart, fatty changes in the myocardium and liver due to chronic hypoxia, and no changes in coronary arteries.
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PMID:[An aplastic anemia patient died of severe anemia who refused transfusion]. 1069 2

Ginseng has been used in the Orient for several thousand years as an 'adaptogenic' as well as a 'restorative' agent. It has been used to treat nervous disorders, anaemia, wakefulness, dyspnoea, forgetfulness and confusion, prolonged thirst, decreased libido, chronic fatigue, angina and nausea. Although the mechanisms underlying the alleged effects of ginseng remain to be elucidated, there is an extensive animal literature dealing with the effects of ginseng on the cardiovascular system, central nervous system, endocrine system, metabolism, and immune system. In our previous review dealing with the efficacy of ginseng, we concluded that while studies with animals show that ginseng, or its active components, may prolong survival to physical or chemical stress, there is generally a lack of controlled research demonstrating the ability of ginseng to improve or prolong performance in fatigued humans. In this review, we extend our earlier analysis on the potential efficacy of ginseng use in the enhancement of physical performance and modification of fatigue states. Our analysis reveals that published literature appearing since our earlier review has not resolved the equivocal nature of research evidence involving animals or humans. Also, the lack of unanimity in this research can be explained on the basis of various methodological problems such as inadequate sample size and lack of double-blind, control and placebo paradigms. In addition, the absence of acceptable approaches to the problem of 'sourcing', in concert with an absence of compliance data in human research, further complicates the interpretation of this research literature. Nevertheless, the use of ginseng continues to grow, and current sales are estimated to be over $US300 million annually. There is clearly a need for systematic research dealing with the efficacy of ginseng, and this research needs to take into account basic, fundamental design considerations if there is to be any hope of establishing whether or not ginseng possesses efficacy.
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PMID:Evaluation of the ergogenic properties of ginseng: an update. 1070 14

The amount of oxygen delivered to an organ depends on three factors: blood flow and its distribution; the oxygen-carrying capacity of the blood, i.e. haemoglobin concentration; and oxygen extraction. Non-haemodynamic and haemodynamic mechanisms operate to compensate for anaemia. Non-haemodynamic mechanisms include increased erythropoietin production to stimulate erythropoiesis, and increased oxygen extraction (displacement of the haemoglobin oxygen dissociation curve). This decreased affinity of oxygen for haemoglobin is mediated by increased 2,3-diphosphoglycerate concentrations. Increased cardiac output is the main haemodynamic factor, mediated by lower afterload, increased preload, and positive inotropic and chronotropic effects. Decreased afterload is due to vasodilatation and reduced vascular resistance as a consequence of lower blood viscosity, hypoxia-induced vasodilatation, and enhanced nitric oxide activity. Vasodilatation also involves recruitment of microvessels and, in the case of chronic anaemia, stimulation of angiogenesis. With decreased afterload, the venous return (preload) and left ventricular (LV) filling increase, leading to increased LV end-diastolic volume and maintenance of a high stroke volume and high stroke work. High stroke work is also due to enhanced LV contractility attributed to increased concentrations of catecholamines and non-catecholamine inotropic factors. In addition, heart rate is increased in anaemia, due to hypoxia-stimulated chemoreceptors and increased sympathetic activity. In the long term, these haemodynamic alterations lead to gradual development of cardiac enlargement and LV hypertrophy (LVH). The LVH is eccentric, characterized by increased LV internal dimensions and a normal ratio of wall thickness to cavity diameter, as occurs in other forms of volume overload. When anaemia-related LVH develops in an otherwise 'healthy' humoral environment, the lesions are reversible and the type of LVH is primarily physiological and is not associated with impaired diastolic function. In the absence of underlying cardiovascular disorders, severe anaemia (Haemoglobin concentration < 4-5 g/dl) leads to congestive heart failure. In the presence of heart disease, especially coronary artery disease, anaemia intensifies angina and contributes to a high incidence of cardiovascular complications. In end-stage renal disease (ESRD), LVH is influenced by many other factors, leading to intense interstitial fibrosis, to alterations in diastolic function, and usually to poor reversibility. The chronic increase in cardiac output contributes to arterial remodelling of central elastic arteries such as the aorta and common carotid artery. This remodelling consists principally of arterial enlargement and compensatory arterial intima--media thickening. In ESRD, these geometric changes are accompanied by arterial stiffening. The principal consequences of arterial alterations are increased systolic pressure and high inertia due to higher blood mass in the dilated arterial system. These alterations contribute to the development of LVH and abnormal coronary perfusion.
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PMID:Pathophysiology of anaemia: focus on the heart and blood vessels. 1103 52


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