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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular diseases are the leading cause of death in patients on haemodialysis. Cardiovascular mortality rate in these patients is approximately 9% per year, with the highest prevalence of left ventricular hypertrophy, ischemic heart disease and congestive heart failure being the most frequent cardiovascular complications. Risk factors for cardiac failure include hypertension, disturbed lipid metabolism, oxidative stress, microinflammation, hypoalbuminemia, anaemia, hyperhomocysteinemia, and increased concentration of asymmetric dimethylarginine, increased shunt blood flow and secondary hyperparathyroidism. Diagnostic strategy for early detection of patients with increased risk for the development of asymptomatic disturbances of systolic and diastolic left ventricular function should include echocardiografic examination, tests for determining coronary vascular disease, as well as tests of myocardial function (BNP, Nt-proBNP). Early detection of patients with a high risk of congestive heart failure enables timely implementation of adequate therapeutic strategy to provide high survival rate of HD patients.
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PMID:[Heart failure in haemodialysis patients: evaluation and treatment]. 2162 74

Cardio-renal-anemia syndrome is a combination of heart failure, kidney failure, and anemia. Many advanced chronic kidney disease patients have both anemia and chronic heart failure. They have often hyperhomocysteinemia, high dimethylarginine values and low erythropoietin levels. Nephrologists treat advanced chronic kidney disease patients with erythropoiesis stimulating agents to improve anemia, renal and heart disease. Erythropoiesis stimulating agents, though considered essential to improve anemia in chronic kidney disease patients, have shown no significant protective effect on cardiovascular disease when used in large clinical trials targeting normal hemoglobin levels. It is possible that the high amounts of these drugs, given to reach normal hemoglobin values, may have counterbalanced the positive effect on endothelium obtained with low doses. Many studies have shown that erythropoietin improves endothelial function in animals with high dimethylarginine levels, lowering asymmetric dimethylarginine and increasing nitric oxide synthesis. Advanced chronic kidney disease patients have also high homocysteine levels which further reduce endothelial function by increasing asymmetric dimethylarginine. Homocysteine-lowering vitamin B treatment has been associated to a significant reduction of cardiovascular disease in advanced chronic kidney disease patients. Low doses of epoetin and B vitamins may improve cardiovascular morbidity by reducing asymmetric dimethylarginine and by increasing nitric oxide synthase activity. This review analyses the interaction between erythropoietin, dimethylarginine and homocysteine, and their role in cardio-renal-anemia syndrome.
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PMID:Cardio-renal-anemia syndrome: a link between erythropoietin, dimethylarginine and homocysteine. 2268 Jun 36

Juvenile cobalamin deficiency is a rare disease in border collies and its diagnosis requires a high level of clinical suspicion. The goal of this study was to increase awareness of this disease by describing the clinical and laboratory findings in four young border collies with inherited cobalamin deficiency. The median age of the dogs was 11.5 mo (range, 8-42 mo), and two of the four dogs were full siblings. Clinical signs included intermittent lethargy (n = 4), poor body condition (n = 4), odynophagia (n = 2), glossitis (n = 1), and bradyarrhythmia (n = 1). Pertinent laboratory abnormalities were mild to moderate normocytic nonregenerative anemia (n = 3), increased aspartate aminotransferase (AST) activity (n = 3), and mild proteinuria (n = 3). All of the dogs had serum cobalamin levels below the detection limit of the assay, marked methylmalonic aciduria, and hyperhomocysteinemia. Full clinical recovery was achieved in all dogs with regular parenteral cobalamin supplementation, and laboratory abnormalities resolved, except the proteinuria and elevated AST activity persisted. This case series demonstrates the diverse clinical picture of primary cobalamin deficiency in border collies. Young border collies presenting with ambiguous clinical signs should be screened for cobalamin deficiency.
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PMID:Clinical and laboratory findings in border collies with presumed hereditary juvenile cobalamin deficiency. 2353 54

Stroke is a leading cause of mortality and morbidity worldwide. Traditional cardiovascular risk factors - hypertension, diabetes and dyslipidemia - are related to the incidence of stroke. Chronic kidney disease has also been recognized to be a major public health problem as a cardiovascular risk factor. Growing evidence has suggested that chronic kidney disease is associated with an increased risk of cardiovascular disease including stroke in general populations. Those with chronic kidney disease have a greater prevalence of traditional cardiovascular risk factors. Several meta-analyses assessing the association between chronic kidney disease and stroke have found that the magnitude of the risk estimates adjusted for known traditional cardiovascular risk factors were reduced as compared with the age-adjusted risk estimates. While these findings on the surface seem to downplay the effect of chronic kidney disease on stroke, they may actually suggest that an accumulation of traditional cardiovascular risk factors in those with chronic kidney disease increases the risk of stroke, and that applying appropriate treatments to those with chronic kidney disease is important for reducing the risk of stroke. Additionally, other large-scale meta-analyses demonstrated that chronic kidney disease was a significant risk factor for stroke independent of known cardiovascular risk factors. Chronic kidney disease may also be associated with an increase in nontraditional risk factors such as hyperhomocysteinemia, inflammation, asymmetric dimethylarginine, oxidative stress, and anemia, and thrombogenic factors such as left ventricular hypertrophy, endothelial dysfunction, and arterial stiffness. Herein, we review the results of meta-analyses of published cohort studies for a better understanding of the precise nature of the relationship between chronic kidney disease and stroke, important to both the clinical and public health fields. Further studies are warranted to determine whether interventions to prevent the progression of kidney impairment are effective at reducing the risk of stroke.
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PMID:Risk of stroke in kidney disease. 2365 49

It has been estimated that up to 10% of hypercoagulable state manifestations in patients with inflammatory bowel disease (IBD) are ischemic strokes. The literature search through MEDLINE and EMBASE highlighted 33 case reports of IBD patients complicated with cerebral arterial infarction during the course of their disease. Most of these patients presented with either left or right sided hemiparesis on admission, while the most common site of arterial infarction was either the right or the left middle cerebral artery. Thrombocytosis and anemia were the most commonly observed potential risk factors for stroke in the laboratory analysis. Other coagulation abnormalities, hereditary thrombotic mutations, hyperhomocysteinemia, hyperlipidemia, structural cardiac abnormalities, endocarditis and cerebral artery vasculitis have also been reported in some of the cases that were reviewed. Even though many of these findings are commonly observed in IBD patients, literature data is still controversial about their causal relationship to ischemic stroke. Similarly, there is also lack of steady evidence and official guidelines for stroke management in both children and adults with IBD comorbidity. Finally, an algorithm based on both the American Heart Association and European Stroke Organization guidelines for stroke management and prevention in the general population, is presented as a reference point for the treatment of IBD patients who are complicated by an ischemic cerebral event.
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PMID:Cerebral arterial infarction in inflammatory bowel diseases. 2402 31

Impairment of cognitive functions occurs frequently in chronic kidney disease (CKD). The conditions most associated with this decline are depression, delirium, mild cognitive impairment and dementia. The mechanisms involved have not been established yet, but some factors, as neuronal damage by uremic toxins, cerebrovascular ischemic lesions, oxidative stress, chronic inflammation, anemia, hyperhomocysteinemia, the endothelial dysfunction may play a critical role. The neuropsychological performance improves with the initiation of dialysis, although some cognitive dysfunctions remain even after treatment, especially in the areas of attention, cognitive flexibility, memory and learning. Kidney transplantation may improve and even reverse some cognitive deficits detected in the dialysis period, despite some compromise in verbal memory and executive functions remain after transplantation. The diagnosis of cognitive decline in patients with CKD may have an important impact on the management and prognosis. This paper presents an update on the decline of cognitive function in patients with CKD.
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PMID:Cognitive alterations in chronic kidney disease: an update. 2505 65

Thrombotic thrombocytopenic purpura (TTP) has high mortality and necessitates prompt recognition of microangiopathic hemolytic anemia (MAHA) and initiation of plasmapheresis. We present a challenging diagnostic workup and management of a 42-year-old man who presented with anemia, thrombocytopenia, and schistocytes on peripheral smear, all pointing to MAHA. Plasmapheresis and steroid therapy were promptly initiated, but hemolysis continued. Further workup showed megaloblastic anemia, severe Vitamin B12 deficiency, high iron saturation, and absent reticulocytosis, none of which could be explained by TTP. Severe Vitamin B12 deficiency can lead to hemolytic anemia from the destruction of red cells in the marrow that have failed the process of maturation. However, this should not cause thrombotic microangiopathy. Previous reports of B12 deficiency presenting with MAHA and a TTP-like manifestation have identified acute hyperhomocysteinemia as a missing link between B12 deficiency and MAHA, so this possibility was further explored. Our patient similarly had significantly elevated serum homocysteine levels, confirming this suspicion of Vitamin B12 deficiency. Vitamin B12 replacement led to normalization of the elevated levels of homocysteine, the disappearance of schistocytes on the peripheral smear, and resolution of the microangiopathic hemolysis, thereby confirming the diagnosis. It is pertinent that intensivists not only know the importance of early recognition and treatment of TTP but are also familiar with rare conditions that can present in a similar fashion.
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PMID:When the picture is fragmented: Vitamin B12 deficiency masquerading as thrombotic thrombocytopenic purpura. 2730 58

Dietary folic acid deficiency induced early hearing loss in C57BL/6J mice after 2-months, corroborates the epidemiological association previously described between vitamin deficiency and this sensory impairment. However, this strain is prone to early hearing loss, and hence we decided to analyze whether the effects exerted by folate deprivation follow the same pattern in a mouse strain such as CBA/Ca, which is resistant to hearing impairment. Here, we show results of a long-term study on hearing carried out on CBA/Ca mice subjected to dietary folate deprivation. Systemic changes included decreased serum folate levels, hyperhomocysteinemia and signs of anemia in the group fed with folate-deficient (FD) diet. Initial signs of hearing loss were detected in this strain after 8-months of vitamin deficiency, and correlated with histological damage in the cochleae. In conclusion, the data presented reinforce the importance of adequate folic acid levels for the auditory system and suggest that the impact of dietary deficiencies may depend on the genetic background.
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PMID:Long-Term Dietary Folate Deficiency Accelerates Progressive Hearing Loss on CBA/Ca Mice. 2763 May 60

Transcobalamin deficiency (OMIM 275350) is a rare autosomal recessive disease presenting with nonspecific clinical features in early infancy. We report the clinical and laboratory manifestations of 7 children diagnosed with transcobalamin deficiency. All patients were admitted between 2 and 4 months of age with anemia, thrombocytopenia, and hyperhomocysteinemia. The most common complaints at admission were pallor, weakness, and poor feeding. Genetic analysis was performed in 5 patients and it revealed the same homozygous mutation. We initially treated all patients with intramuscular injections of a maximum of 1 mg cyanocobalamin (CN-Cbl) daily and with a final dose of 1 mg per week. Hemoglobin and platelet counts significantly decreased upon decrease or cessation of CN-Cbl therapy. The patients were reevaluated between 2 and 4 years of age and all had delay in speech and walking. In conclusion, 1 mg of intramuscular CN-Cbl every week suffices for hematological improvement but not for normal neurological development in patients who all had relapse due to decrease or cessation of treatment.
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PMID:Seven Patients With Transcobalamin Deficiency Diagnosed Between 2010 and 2014: A Single-Center Experience. 2782 40

Pernicious anemia (PA) is an autoimmune disease of multifactorial etiologies characterized by autoimmune chronic atrophic gastritis, cobalamin deficiency (CD) due to defective absorption of dietary cobalamin from the terminal ileum, and by the presence of intrinsic factor and parietal cell antibodies. PA is a very common cause of CD-related anemia worldwide. Despite advances in the understanding molecular biology and pathophysiology of PA, the diagnosis of PA remains challenging in many circumstances for many clinicians because of its diverse clinical manifestations and the limitations of currently available diagnostic tools. Diagnostic dilemmas could occur when patients with PA present with spuriously normal or high cobalamin levels, normocytic or microcytic anemia, non-anemic macrocytosis, autoimmune hemolytic anemia, pseudo-thrombotic microangiopathy, hyperhomocysteinemia-associated thromboembolism, pseudoleu-kemia, bone marrow failure, bone marrow ring sideroblasts, and neurologic manifestations without anemia or macrocytosis. Herein, we provide an overview of the challenging clinical presentations of PA, diagnostic approach, and management.
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PMID:Challenging clinical presentations of pernicious anemia. 2897 79


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