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)

The "eradication of malaria" in Taiwan was announced by WHO in 1965. From 1966 to 1989, 919 malaria cases were detected in Taiwan. Of these cases, 803 were classified as imported malaria. During 1977 to 1989, our hospital collected 11 cases of imported malaria, 6 of Plasmodium falciparum (PF), including 1 suspicious case, 2 of Plasmodium vivax (PV), 1 of mixed infection (PF plus PV), and 2 unclassified. Most of the patients presented clinically with fever and chills. Hepatosplenomegaly was the most common abnormal finding during the physical examination. Jaundice and anemia occurred in the more severe cases. No cases had lymphadenopathy which is helpful in making a differential diagnosis. Six cases had thrombocytopenia which may be considered as an indirect sign in the diagnosis. The MCV levels were within normal limits in all of the cases. This may indirectly imply a potential protective effect against malaria infection in cases of congenital hemoglobinopathy such as thalassemia or G6PD deficiency. Initially, 10 cases were given "standard treatment", which consisted of chloroquine 450 mg qd for 2 days then 300 mg qd for 2 days and primaquine 15 mg qd for 2 weeks. Four cases of chloroquine resistance were encountered, all in cases with PF infection. Two cases were grade I delayed type resistance and were successfully treated with Fansidar, tetracycline and quinine. Two cases were grade II resistance and presented clinically as cerebral malaria. Intravenous quinine was given plus Fansidar and tetracycline. The cases were resolved without sequele or recurrence. None of the cases, except for 2, received chemoprophylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Imported case of malaria in Taiwan: analysis of 11 cases]. 167 9

A preterm infant with possible congenital clinical malaria is described. The infant developed persistent pyrexia, hyperbilirubinaemia, anaemia, increasing gastric residuals and hepatosplenomegaly from the 7th day of life. Thick and thin smears of the infant's blood were heavily loaded with various asexual stages of Plasmodium falciparum. The parasite exhibited R1 resistance. There was no satisfactory response to chloroquine, but response to intravenous quinine therapy was achieved on day 15. The initial 6-month follow-up period was uneventful. The mother had apparently had chloroquine-resistant malaria which responded to sulfadoxine-pyrimethamine (Fansidar).
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PMID:Congenital malaria with chloroquine resistance. 171 26

The patient is a 39 year-old Japanese male who had traveled to Southeast Asia from March 14, 1987 and returned on April 2. On April 3 and 5, he had a high fever with chills and he was admitted to our hospital. Despite initial treatment with antibiotics, a high fever over 39 degrees C appeared with a 48 hour periodicity. On the 8th day after admission, malarial parasites were identified on the peripheral blood smear after repeated trials. Combined with a raised serum antibody titer, Plasmodium vivax malaria was diagnosed. He was successfully treated with the sulfadoxine 500 mg and pyrimethamine 25 mg (Fansidar) and body temperature was normalized after the 12th day. More interestingly, the patient showed pancytopenia without splenomegaly. The bone marrow aspiration revealed hypoplasia of erythroblasts, granulocytes and megakaryocytes. Because of this pancytopenia in the peripheral blood and hypoplasia of the bone marrow which improved after recovery from malarial infection, it was indicated that they were caused by the malarial infection. Generally, it is considered that anemia in malarial patients is caused by destruction of the blood cells by parasites and/or hypersplenism and compensatory hyperplasia of the bone marrow is seen. On the contrary, this case showed pancytopenia accompanied with hypoplasia of the bone marrow probably due to the malarial infection suggesting a new aspect of pathogenesis in the hematological abnormality of the malarial infection.
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PMID:[A case of Plasmodium vivax malaria complicated with pancytopenia due to hypoplasia of the bone marrow]. 250 94

Forty cases of imported malaria (1978 to 1988) are reviewed and management principles are discussed. All 15 cases of Plasmodium falciparum malaria were acquired in Africa, 5 of which were probably chloroquine-resistant. Most cases of Plasmodium vivax (80%) were acquired on the Indian subcontinent, including 2 cases of congenital malaria. Six children developed P. falciparum malaria despite chemoprophylaxis. All children had a history of fever, usually with other influenza-like symptoms. Two-thirds had splenomegaly, and one-third were afebrile on admission. Thrombocytopenia (70%) and anemia (70%) were often present. Forty-five percent received previous wrong diagnoses and treatments. Quinine or quinidine with either Fansidar or clindamycin were used to treat P. falciparum malaria. Clindamycin may be more effective if given for 7 instead of 3 days. There were no deaths or residual complications. As the prevalence and severity of drug-resistant P. falciparum spreads, prophylaxis and treatment choices become more difficult. Diagnosis requires a travel history and a high index of suspicion.
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PMID:Review of 40 children with imported malaria. 259 48

In the treatment of severe Plasmodium falciparum infection antimalarial drugs should, ideally, be given by controlled rate intravenous infusion until the patient is able to swallow tablets. In cases where infection has been acquired in a chloroquine resistant area, and where it has broken through chloroquine prophylaxis or where the geographical origin or species are uncertain, quinine is the treatment of choice. When access to parenteral quinine is likely to be delayed, parenteral quinidine is an effective alternative. A loading dose of quinine is recommended in order to achieve therapeutic plasma concentrations as quickly as possible. In the case of chloroquine sensitive P. falciparum infection, chloroquine, which can be given safely by slow intravenous infusion, may be more rapidly effective and has fewer toxic effects than quinine. There is limited experience with parenteral administration of pyrimethamine sulphonamide combinations such as Fansidar, and resistance to these drugs has developed in South East Asia and elsewhere. Mefloquine and halofantrine cannot be given parenterally. Qinghaosu derivatives are not readily available and have not been adequately tested outside China. Supportive treatment includes the prevention or early detection and treatment of complications, strict attention to fluid balance, provision of adequate nursing for unconscious patients and avoidance of harmful ancillary treatments. Anaemia is inevitable and out of proportion to detectable parasitaemia. Hypotension and shock ('algid malaria') are often attributable to secondary gram-negative septicaemia requiring appropriate antimicrobial therapy and haemodynamic resuscitation. Many patients with severe falciparum malaria are hypovolaemic on admission to hospital and require cautious fluid replacement. Failure to rehydrate these patients may lead to circulatory collapse, lactic acidosis, renal failure and severe hyponatraemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of severe malaria. 269 26

Some 200 cases of malaria are officially reported yearly in Switzerland. It is estimated that 2000-8000 Swiss travellers are infected by the anopheles mosquito annually, with 90% protected by chemoprophylaxis. An attack of malaria appears to have a better prognosis when the symptoms start in Africa, since treatment is initiated immediately, than in industrialized countries where the mortality is 1-4%. Failure to inquire into travel history is often responsible for the delay in initiating treatment. Severe falciparum malaria is treated by repeated slow quinine infusions followed by 1500 mg sulfadoxine, 75 mg pyrimethamine and 750 mg mefloquine (single dose). This adult dose corresponds to 3 tablets of Lariam and 3 of Fansidar (or 3 of Fansimef). The increase in chloroquine resistance among falciparum strains has led to the use of Fansidar for chemoprophylaxis, followed by the use of mefloquine when Fansidar resistance occurs. The dosage of mefloquine is 250 mg weekly (1 tablet Lariam) for 4 weeks, followed by 1 tablet every fortnight. Treatment is continued for 1 month after return. If the risk of transmission is low, chemoprophylaxis may be replaced by prescription of a reserve drug to be taken in case of fever and headache. A sulfadoxine-pyrimethamine-mefloquine combination (i.e. 3 tablets Fansimef) has been tested in this indication. Ineffective chemoprophylaxis may lead to atypical clinical syndromes, e.g. anemia, hepatosplenomegaly and jaundice, without episodes of fever. HIV positive subjects may risk travelling in tropical countries if they have undergone correct chemoprophylaxis.
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PMID:[Malaria in Switzerland]. 306 91

A 42-year-old man was admitted to hospital with, previously wrongly diagnosed, fulminant falciparum malaria, 14 days after a two-week trip to Kenya. He had a high fever and was jaundiced, with severe anaemia and thrombocytopenia. He was given quinine intravenously and pyrimethamine/sulfadoxine (Fansidar) by mouth. He developed acute renal failure and increasingly severe cerebral symptoms, at times coma. An exchange transfusion and several plasmaphereses were, therefore, performed. The cerebral symptoms quickly abated during the exchange transfusion, but renal function failed to improve. Because of continuing fever, mefloquin (Lariam) and doxy-cycline (Vibramycin) were also administered. After several dialysis periods the patient improved gradually and was discharged after three weeks in generally good condition with normal renal function.
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PMID:[Exchange transfusion and (or) plasmapheresis: effective measures in severe tropical malaria?]. 328 61

We present two cases of Plasmodium falciparum malaria contracted in Douala despite adequate prophylaxis by Fansidar for one and by chloroquine for the other. Failure of curative treatment by Fansidar for the first case (in vitro chloroquine-resistant strain) and by amodiaquine plus erythromycin for the second. After these therapeutic failures, both patients presented without fever, but with splenomegaly and anaemia. The successful therapeutic was mefloquine.
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PMID:[2 cases of multiresistant Plasmodium falciparum malaria contracted in Douala with atypical clinical presentation]. 331 53

The demographic and clinical features of severe malaria in children on the south coast of Papua New Guinea have never been clearly documented. This prospective study sought to define the associations between ethnic origin, domain, age, nutritional status and severe malaria in this group and to assess significant clinical features, evaluate the use of a coma score as a prognostic indicator in cerebral malaria and to determine the ultimate outcome. Twenty patients with severe malaria (17 cerebral malaria and 3 severe anaemia) were studied. Their mean age of 4.96 years was significantly greater than that of matched controls with uncomplicated. Plasmodium falciparum infection with mean age 3.79 years (0.02 < p < 0.05). Nutritional status was not a significant independent risk factor when controlled against inpatients with other diagnoses. Low coma scores (Adelaide scale 4/14 or less) sensitively predicted the risk of dying vs survival. The mortality of 18% was comparable with other series. Current standard treatment with quinine and Fansidar was effective and no early recrudescence was encountered in the survivors. The degree of intermarriage and migration between regions precluded firm conclusions from being drawn as to the relevance of ethnic and geographical factors in the epidemiology of severe malaria in this region.
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PMID:Severe malaria in children at Port Moresby General Hospital, Papua New Guinea. 748 99

Whether children with malarial anaemia should receive supplementation with iron or folic acid is uncertain. Therefore, the effects of supplementary treatment with iron or folic acid, given together with chloroquine or pyrimethamine-sulfadoxine (Fansidar), has been assessed in 600 Gambian children with uncomplicated falciparum malaria. After one month, haematological recovery was significantly better in the group treated with Fansidar than in the chloroquine-treated group (difference in mean haemoglobin level = 0.54 g/dL, P = 0.01). Children who received iron had a significantly better response than those given placebo (differences in mean haemoglobin level after one month and at dry season follow-up = 0.70 g/dL, P = 0.006, and 0.81 g/dL, P = 0.001, respectively). Iron supplementation was not associated with increased prevalence of malaria. Supplementation with folic acid did not improve the haematological response but, among children who received Fansidar, the treatment failure rate was significantly higher among those given folic acid than among those given placebo. Thus, supplementation with iron, but not folic acid, improves haematological recovery without increasing susceptibility to malaria.
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PMID:Iron, but not folic acid, combined with effective antimalarial therapy promotes haematological recovery in African children after acute falciparum malaria. 859 93


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