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

Anemia with splenomegaly and signs of glomerulonephritis were found associated with the acute and post-acute phase of Trypanosoma lewisi infections of laboratory rats. The onset of the anemia was associated with the peak of parasitemia and the development of cold-active hemagglutinin (HA) for trypsinized rat erythrocytes. It persisted with gradual recovery for as long as the trypanosomes and HA were detected in the blood. Signs of glomerulonephritis consisted of hypercellularity of the glomerular tuft, swelling of vascular endothelium and tubular epithelium, thickening of Bowman's membrane and tubular basement membrane, and abnormal numbers of hyaline casts in the distal convoluted tubules. Residual damage to the kidneys was not evaluated.
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PMID:Anemia, splenomegaly, and glomerulonephritis associated with autoantibody in Trypanosoma lewisi infections. 35 13

In this paper demographic characteristics, etiology, pathology and clinical features of infective endocarditis are reviewed simultaneous presentation of the data from our series of 50 cases with infective endocarditis. The peak incidence of infective endocarditis is between 11 and 15 years. Both sexes are equally affected. Patients with congenital or acquired heart disease tend to have hemodynamic trauma to the endocardium and vascular endothelium. These sites form the nidus for circulating bacteria of either spontaneous origin or the result of any oro-dental, genitourinary or other surgery or procedures and produce vegetations characteristic of infective endocarditis. The location of the vegetation is dependent upon the predisposing cardiac lesion. Embolic phenomenon is another cardinal feature of endocarditis and may occur in any organ system. Although a large variety of microbes have been known to cause endocarditis, streptococci and staphylococci remain the most frequent offenders. Clinical diagnosis of infective endocarditis is difficult because of the insidious onset and varied clinical features. A high degree of suspicion is essential for early diagnosis. Any patient with known heart disease and unexplained fever should be suspect for endocarditis. Splenomegaly, petechiae and embolic phenomena support this diagnosis. New or changing murmurs, splinter hemorrhages, Osler's nodes. Janeway's lesions and Roth's spots may be present. Elevated sedimentation rate, microscopic hematuria, leukocytosis with a shift-to-the-left and anemia may further support the diagnosis. Congenital or acquired heart disease and fever are all that will be present in many cases. Only isolation of the causative agent from the blood can confirm the diagnosis.
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PMID:Infective endocarditis: a review. I. Incidence, etiology, pathology and clinical features. 72 71

The nomenclature, life cycles, and pathogenicity of Sarcocystis of domestic animals are reviewed. Sarcocystis had a 2-host life cycle, with carnivores as definitive hosts and herbivores as intermediate hosts. The following species are found in domestic animals (with the definitive hosts given in parentheses): 3 species in the ox: S cruzi (dog, wolf, coyote, raccoon, fox), S hirsuta (cat), S hominis (man, monkey); 2 species in the sheep: S ovicanis (dog), S tenella (cat); 3 species in the pig: S miescheriana (dog), S porcifelis n sp (cat), S porcihominis n sp (man); and 1 species in the horse: S bertrami (dog). Sarcocystis cruzi, S ovicanis, and S porcifelis are highly pathogenic to the ox, the sheep, and the pig, respectively. Clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42 C, or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation, and loss of hair at the tip of the tail. Anemia, anorexia, ataxia, and abortions are the chief clinical signs of acute ovine sarcocystosis. These signs are evident at the time of vascular endothelium is parasitized by schizonts. The schizonts disappear in about 1 month, and cysts are formed in the muscles. The cystic phase of sarcocystosis is virtually nonpathogenic. Carnivores shed sporocysts in their feces after ingesting the intramuscular cysts from the herbivores. Sarcocystis is nonpathogenic to the definitive host. Feline and canine coccidia are also reviewed. The following 11 species are found in cats: Toxoplasma gondii, Hammondia hammondi, Isospora felis, Isosporarivolta, Besnoitia besnoiti, Besnoitia sp, and 5 types of Sarcocystis (S hirsuta from the ox, S tenella from the sheep, S muris from the mouse, S porcifelis from the pig, and Sarcocystis sp from Grant's gazelle). The following 10 species are found in canine feces (Isospora canis, Isospora ohioensis, Isospora wallacei n sp; and 7 types of Sarcocystis (S cruzi from the ox, S ovicanis from the sheep, S bertrami and Sarcocystis sp from the horse, S miescheriana from the pig, S hemionilatrantis from mule deer, and Sarcocystis sp from Grant's gazelle). The history of Isospora begemina in dogs is reviewed; life cycles of feline and canine coccidia are given; oocysts of common feline and canine coccidia are compared and illustrated; and public health significance of Toxoplasma gondii oocysts is discussed, especially in relation to cats in the household of pregnant women.
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PMID:A review of Sarcocystis of domestic animals and of other coccidia of cats and dogs. 82 60

Interleukin-2 (IL-2) is increasingly used to treat patients with cancers refractory to conventional treatment. Flu-like syndromes are extremely frequent but usually mild. A variety of skin complications (mostly erythema and mucositis) have been reported. Life-threatening skin reactions have also been described. Acute reactivation of psoriasis can also occur. Immediate hypersensitivity reactions have so far not been described, but IL-2 treatment has been shown to predispose to acute hypersensitivity reactions to iodine-containing contrast media. Hypothyroidism is the major endocrine complication and antithyroid antibodies have been detected in approximately 50% of patients. Neurological and psychiatric disturbances with moderate or severe mental status changes are common and sometimes treatment-limiting. The occurrence of peritumoural oedema in patients with brain metastases can also be a major practical problem. Musculoskeletal disorders are transient and resolve spontaneously. The vascular leak syndrome is the most frequent and severe complication of IL-2 of which weight gain, generalised oedema, hypotension and impaired renal function are the main features. Even though a damaging effect on vascular endothelium cells by various cytokines released by activated lymphoid cells or mediated by non-lymphocyte-dependent factors has been proposed to be involved, the mechanism remains unclear. Other cardiovascular injuries, possibly life-threatening, including myocarditis, angina pectoris and myocardial infarction, can occur during the first days of treatment. Supraventricular arrhythmias are the most common rhythmic disorder. Decreases in myocardial contractility and haemodynamic pattern similar to those of septic shock have been encountered in most cases. Acute renal dysfunction is common but resolves with symptomatic management. Intrahepatic cholestasis with hyperbilirubinaemia is observed in most patients but permanent liver damage has not been described. Several cases of pancreatitis have been reported. Anaemia, thrombocytopenia, lymphocytopenia and eosinophilia are frequent and occur in most if not all patients. Some data suggest a high incidence of infectious complications, particularly in patients with surgically tunnelled catheters, but marked flu-like syndromes may be confounding. Finally, death directly related to IL-2 treatment has been noted in less than 1% of all patients. Investigations are under way to minimise IL-2 toxicity with varying dose regimens and combined treatments.
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PMID:Clinical toxicity of interleukin-2. 141 98

Four groups of 6 pigs each were given 5 x 10(5) to 3 x 10(6) sporocysts of a Georgia isolate of Sarcocystis suicanis. Only the 6 pigs given 3 x 10(6) sporocysts became acutely ill at postinoculation days (PID) 12 to 15, and 3 of the 6 diet at PIG 14 or 15. Clinical signs included purpura of the skin of the ear, snout, and buttocks and dyspnea, muscle tremors, and severe locomotor difficulties. Clinical abnormalities were accompanied by laboratory findings of pyrexia, severe anemia, leukopenia, thrombocytopenia, megathrombocytosis, prolonged prothrombin time and activated partial thromboplastin time, and hypofibrinogenemia. Seemingly, excessive intravascular coagulation may be involved in the pathogenesis of this disease in swine. Pigs given 5 x 10(5) to 1 x 10(6) sporocysts did not exhibit clinical signs; however, leukopenia and thrombocytopenia were demonstrated in the pigs at all dosage levels. Growth rates were impaired in surviving pigs. Second-generation schizonts containing merozoites were found in vascular endothelium of pigs dying on PID 14 or 15. Nonsuppurative myocarditis and hepatitis were present. Numerous developing cysts were in the musculature of pigs enthanatized on PIG 35 to 52. Cyst dissolution and resorption occurred concomitantly, indicating that swine may be able to clear the infection.
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PMID:Experimental Sarcocystis suicanis infections: disease in growing pigs. 680 76

Excessive binding of Plasmodium falciparum-infected red blood cells (pRBCs) to the vascular endothelium (cytoadherence) and to uninfected erythrocytes (rosetting) may lead to occlusion of the microvasculature and thereby contribute directly to the acute pathology of severe human malaria. A number of endothelial receptors have been identified as targets for the pRBCs, including CD36, intercellular adhesion molecule-1 (ICAM-1) and chondroitin-4-sulfate (CSA). In vitro, CD36 is the most frequent target of strains from patients with mild as well as severe P. falciparum malaria, but is expressed at low levels on the cerebral microvasculature and therefore seems unlikely to be involved in the evolution of cerebral disease. Strains of P. falciparum that form rosettes are associated both with the occurrence of cerebral malaria and severe anemia. Here we report that malaria-infected RBCs adhere to platelet/endothelial cell adhesion molecule-1 (PECAM-1/CD31) on the vascular endothelium. pRBCs bind to endothelial cells, to PECAM-1/CD31 transfected cells, and directly to recombinant PECAM-1/CD31 absorbed onto plastic. Soluble PECAM-1/CD31 and monoclonal antibodies specific for the amino-terminal segment of PECAM-1/CD31 (domains 1-4) blocked the binding. Interferon-gamma (IFN-gamma)-essential for the development of cerebral malaria in the mouse-was found to augment adhesion of human pRBCs to PECAM-1/CD31 on endothelial cell monolayers. Our results suggest that PECAM-1/CD31 is a virulence-associated endothelial receptor of P. falciparum-infected RBCs.
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PMID:PECAM-1/CD31, an endothelial receptor for binding Plasmodium falciparum-infected erythrocytes. 939 93

We present the case of a woman of 62 years old with changes history in the intestinal habit, weak, thing, anemia, violet injuries in the gums and hemoptysis of small quantity. After the various tests accomplishment of image and biopsy of the injuries gingival and of lymphadenopathy supraclavicular was demonstrated the existence of a angiosarcoma of high degree of malignity. This neoplasm is originated in the cells of vascular endothelium and constitutes 1% of all the sarcomas and solely 4% appear the the oral cavity. These tumors has a high mortality (superior to the 20%) to five years. Once diagnosed its manage must be aggressive in spite of its wrong therapeutic response.
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PMID:[Angiosarcoma of gingival presentation]. 952 1

Southeast Asian ovalocytosis (SAO) occurs at high frequency in malarious regions of the western Pacific and may afford a survival advantage against malaria. It is caused by a deletion of the erythrocyte membrane band 3 gene and the band 3 protein mediates the cytoadherence of parasitized erythrocytes in vitro. The SAO band 3 variant may prevent cerebral malaria but it exacerbates malaria anemia and may also increase acidosis, a major determinant of mortality in malaria. We undertook a case-control study of children admitted to hospital in a malarious region of Papua New Guinea. The SAO band 3, detected by the polymerase chain reaction, was present in 0 of 68 children with cerebral malaria compared with six (8.8%) of 68 matched community controls (odds ratio = 0, 95% confidence interval = 0-0.85). Median hemoglobin levels were 1.2 g/dl lower in malaria cases with SAO than in controls (P = 0.035) but acidosis was not affected. The remarkable protection that SAO band 3 affords against cerebral malaria may offer a valuable approach to a better understanding of the mechanisms of adherence of parasitized erythrocytes to vascular endothelium, and thus of the pathogenesis of cerebral malaria.
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PMID:Prevention of cerebral malaria in children in Papua New Guinea by southeast Asian ovalocytosis band 3. 1040 43

In Plasmodium falciparum-parasitized pregnant women, erythrocytes infected by mature stages of the parasite sequester into placental intervillous spaces. The presence of parasites in the placenta causes maternal anaemia and low birth weight of the infant. In-vitro studies suggest placental sequestration may involve the cytoadherence of infected erythrocytes to chondroitin sulphate A (CSA) and/or intercellular adhesion molecule 1 (ICAM-1) expressed by human placental syncytiotrophoblast. We identified P. falciparum receptors expressed on the surface of human syncytiotrophoblast using immunofluorescence of placental biopsies from Cameroon, a malaria-endemic area. In all placentas, a strongly positive staining was observed on the syncytiotrophoblast for CSA, but not for ICAM-1, vascular endothelium cell adhesion molecule-1, E-selectin, nor CD36. The cytoadherence ability of parasites from pregnant women and nonpregnant subjects was assessed on in-vitro cultured syncytiotrophoblast. Parasites from pregnant women bound to the trophoblast via CSA but not ICAM-1. Parasites from nonpregnant hosts either did not bind to the trophoblast culture or bound using ICAM-1. Our data support the idea that placental sequestration may result from cytoadherence to placental trophoblast and that pregnant women are parasitized by parasites that differ from parasites derived from nonpregnant host by their cytoadherence ability.
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PMID:Cytoadherence of Plasmodium falciparum-infected erythrocytes in the human placenta. 1076 Jan 85

Because of the breakdown of malaria control programs, the constant emergence of drug resistant parasites, and, possibly, climatic changes malaria poses a major problem for the developing countries. In addition, because of the speed of international travel it is being seen with increasing frequency as an imported disease in non-tropical countries. This update explores recent information about the pathophysiology of the disease, its protean hematological manifestations, and how carrier frequencies for the common hemoglobin disorders have been maintained by relative resistance to the malarial parasite. In Section I, Dr. Louis Miller and colleagues consider recent information about the pathophysiology of malarial infection, including new information about interactions between the malarial parasite and vascular endothelium. In Section II, Dr. David Roberts discusses what is known about the complex interactions between red cell production and destruction that characterize the anemia of malaria, one of the commonest causes of anemia in tropical countries. In Section III, Dr. David Weatherall reviews recent studies on how the high gene frequencies of the thalassemias and hemoglobin variants have been maintained by heterozygote advantage against malaria and how malaria has shaped the genetic structure of human populations.
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PMID:Malaria and the red cell. 1244 18


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