Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) A systematic search was made for cardiac abnormalities (clinical, radiological and EKG) and for haemodynamic disorders (catheterisation of the right side of the heart and pulmonary artery). It was generally found that: -- 14 patients (37.8%) had no symptoms; -- 8 patients (21.6%) had pulmonary arterial hypertension (PAHT) with the corresponding cardiac signs; -- 15 patients (40.5%) had cardiac signs with no evidence of PAHT. 2) The 8 patients with PAHT (21.6%) had precapillary type of PAHT with an arteriocapillary gradient. The symptoms were those of PAHT and of the right ventricular failure; but this desorder could be latent. PAHT can be in relation with inflammatory lesions. In these 8 patients, S. Mansoni was to blame in 6 cases and 5 S. Hematobium in 2. 3) In 9 patients (24.3%), cardiac signs were connected indirectly with bilharziasis by anemia, iatrogenic injury or hypertensive myocardial disease of renal origin. 4) In 3 patients (8.1%), cardiac signs were found because of coexistant disease. 5) In 3 patients (8.1%), cardiac signs could have been due to bilharzia myocarditis. The authors reviewed the experimental and clinical discussions for such a possibility.
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PMID:[Systematic cardiologic study in 37 schistosomiasis patients]. 21 89

Complications are the major causes of illness and death after burning and most of them stem from the burn wound. Their origin and importance are reviewed with emphasis on problems and growing points in knowledge. Fluid leakage from the circulation into the burn is the cause of hypovolemic shock, but the underlying permeability changes in the burn are only partly understood. Other nonbacterial complications include acute cardiac failure, acute anemia, hemolytic jaundice, renal failure, encephalopathy, complex hypermetabolic effects including pseudodiabetes, gastric and duodenal ulceration, deep vein thrombosis and pulmonary embolism, pulmonary and glomerular microthrombosis, hepatic jaundice, and arterial thrombosis. Involvement of the airway in conflagrations carries special hazards like glottic edema and inhalation of irritant fumes. Nowadays, bacterial causes are dominant and these remain the main challenge. Bacterial infection and invasion of the burn are usually responsible for septicemia, bronchopneumonia, and pyelonephritis although other sources also contribute. Indirect manifestations of septicemia include paralytic ileus, acute gastric dilatation, toxic myocarditis, and some cases of renal failure. Therapeutic complications like agranulocytosis, thrombocytopenia, and colitis occur at times. High concentrations of oxygen given therapeutically can produce fatal aseptic hypoxic pneumonitis.
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PMID:A review of the complications of burns, their origin and importance for illness and death. 44 73

The review is based on three studies previously reported and involving the clinical, epidemiological and hemodynamic aspects of this problem. Schistosomasis may give frequently (21.6 p. 100) an arterial pulmonary hyperpressure related to the development of granulomas and arteriolitis. A myocarditis may be suspected but is rarely proved. Anemia and specific treatment are also responsible for myocardial deficiency. The parasitic changes of the urinary tract may give a systemic hypertension. Some very rare cases of acute pulmonary heart insufficiency have been reported and the responsibility of schistosomiasis in constrictive fibrous endomyocarditis is still questionned.
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PMID:[Heart and schistosomiasis (author's transl)]. 72 48

A 16-year-old girl with myocarditis and hepatitis in the course of mycoplasma pneumoniae infection was reported. She had fever and coughed for ten days prior to admission. At the time of admission infiltrations of the left lower lung field were revealed on the chest X-ray films. The ESR was elevated and CRP+6. There were no leukocytosis and anemia, but S-GOT, S-GPT and LDH were moderately increased. On the 11th day of admission VPC in bigeminy appeared and the third sound was heard. Subsequently biphastic and inverted T waves in leads V2 and V3 and flattening of T waves in leads II and aVF appeared. At the same time, the cardiac shadow was enlarged. Antibody titer to mycoplasma pneumoniae increased to more than 1:640 two weeks after admission and then it decreased gradually. The cold agglutinin test was 1:64 on the 8th day of the disease and then it became normal. ASO, antibodies to DNA and immunoglobulins were normal; ANA, Coombs test and LE test were negative. The abnormal ECG-findings were normalized three months later.
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PMID:A case of myocarditis caused by Mycoplasma pneumoniae. 74 5

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

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

Human parvovirus B19 is a recently recognized cause of hydrops fetalis. It is a small, single-stranded DNA virus, which preferentially infects late erythroid precursors and produces red blood cell (RBC) aplasia, fetal anemia, and cardiac failure. Infection is accompanied by characteristic intranuclear inclusions in fixed and circulating RBC precursors. These inclusions have been shown to contain virus particles by electron microscopy and in situ hybridization. Infection of the fetus, mother, and newborn infant can be diagnosed by serological and molecular methods selected to match the stage of the infection. Recent work has shown that parvovirus B19 can infect cells other than erythroid precursors, and that additional mechanisms such as myocarditis may contribute to hydrops fetalis in some cases. Infected fetuses are not always hydropic. Maternal infection results in increased abortion and stillbirth even in the absence of transplacental transmission, which occurs in approximately one third of infected mothers. The overall risk of fetal loss following maternal exposure is much less than previously thought, and may be less than 3% in the first 20 weeks of gestation or approximately 10% if the mother is actually infected. Although parvoviruses are teratogenic in animals, there is no evidence that B19 is a significant teratogen in man. The long-term outlook of survivors of intrauterine infection, including those successfully treated by intrauterine blood transfusion, appears to be good, but requires further study.
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PMID:Parvovirus infection of the human fetus and newborn. 156 88

A 38-year-old man with AIDS presented with fever of unknown origin, splenomegaly, anemia, and thrombocytopenia. Admission laboratory data revealed a positive toxoplasmosis titer in the blood. The initial chest x-ray showed small bilateral pleural effusions, a normal cardiac silhouette, no infiltrates, and no interstitial edema. Ga-67 imaging revealed markedly abnormal uptake in the myocardium. A diagnosis of toxoplasmosis myocarditis was made based on laboratory and imaging data. The patient was treated for toxoplasmosis. No myocardial uptake of tracer was demonstrated on a follow-up Ga-67 scan, performed after completion of treatment for toxoplasmosis.
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PMID:Ga-67 citrate myocardial uptake in a patient with AIDS, toxoplasmosis, and myocarditis. 205 84

Hydrops fetalis was diagnosed at 22 weeks. An ultrasound examination demonstrated cardiomegaly and a fetal blood specimen obtained by cordocentesis revealed thrombocytopenia, anaemia, and neutropenia. Fetal paracentesis yielded straw-coloured fluid with electrolytes indicative of a transudate. Non-enveloped icosahedral viral particles approximately 23 mm in diameter were visualized in the ascitic fluid by electron microscopy. Immune electron microscopy confirmed human parvovirus B19. Direct fetal digitalization led to a reduction in umbilical artery resistance, a decline in the abdominal circumference from 20.3 to 17.8 cm, and resolution of the ascites within 72 h. Despite this dramatic response to therapy, fetal death occurred on day 5 of treatment. The initial maternal serum was positive for anti-B19 IgM and IgG antibodies. Electron microscopy of fetal cardiac tissue obtained post-mortem revealed intranuclear viral particles typical of B19, confirming the antenatal diagnosis of myocarditis. This case demonstrates that direct viral identification is applicable to prenatal diagnosis. To our knowledge, this is the first reported case of the antenatal diagnosis and palliative treatment of fetal viral infection.
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PMID:Antenatal diagnosis and palliative treatment of non-immune hydrops fetalis secondary to fetal parvovirus B19 infection. 246 84

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81


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