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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty six patients with culture-proven enteric fever and 15 patients of fever with etiology other than enteric fever as a control group were studied, with special reference to hepatic dysfunction and its relation to clinical features of the disease. Hepatomegaly was observed in 55% of enteric fever patients, and was slightly more common than splenomegaly (50%). Its incidence in typhoid fever (67%) was three times higher than in paratyphoid fever (22%). Hepatic dysfunction occurred in 55% of cases. Jaundice was noted in only 8% of the cases, whereas hyperbilirubinemia (serum bilirubin greater than 1.8 mg %) was present in 17%. Although hepatic manifestations of enteric fever were mild, a small but important group had sufficient hepatic involvement to mimick the clinical picture seen in viral hepatitis, amebic liver disease, and malaria with jaundice. It may be considered of clinical significance, since enteric hepatitis responds very well to specific therapy.
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PMID:The spectrum of hepatic injury in enteric fever. 312 48

There are many possible causes of yellow-orange discoloration of the skin. It is important to ascertain the presence or absence of scleral icterus in determining the diagnosis. Yellow sclerae are found in patients with all causes of hyperbilirubinemia due to the predilection of bilirubin for elastic tissue. The sclerae are also involved in the staining due to some drugs such as quinacrine. Hypercarotenemia, lycopenemia, and riboflavinemia do not involve the sclerae. In our case there are several possible causes for yellow-orange pigmentation of the skin. The patient had malaria, as well as a history of hepatitis, both of which could have resulted in hyperbilirubinemia. However, a bilirubin level of 1.2 mg/100 ml was not sufficient to result in jaundice. The most important finding was that his sclerae were uninvolved, leading us to consider other causes of yellow-orange coloration. The localization of the pigment to the palms and soles is consistent clinically with the diagnosis of hypercarotenemia. This was verified by a serum beta-carotene level slightly above normal. In this case, the carotenemia was due to the ingestion of red palm oil, which the patient had consumed in great quantities while living in Liberia. The surprisingly low level of serum beta-carotene is explained by the fact that he had not consumed red palm oil or another concentrated source of carotene for about three months since living in the United States. Due to the lipophilic nature of the carotenoids, sufficient amounts remained in the tissue to produce discoloration for up to five months, regardless of serum levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Xanthoderma: case report and differential diagnosis. 334 84

Severe anemia has remained a major cause of morbidity and mortality in children of Southern Ghana since the early 1960s. Cases of anemia and anemia-associated mortality in the Korle Bu Teaching Hospital (KBTH), Accra, that occurred from January to December 1991 were reviewed. Data on hemoglobin levels, hypochromia, and malaria parasitemia of children referred from January to December 1991 were collected and analyzed to determine the prevalence of moderate/severe malaria parasitemia, anemia, and severe anemia. 10,989 (71.1%) of 15,450 children attending KBTH referred to the laboratory for hematological studies had hemoglobin (Hb) levels below 11.0 g/dl; while 3049 children (27.7%) of anemic patients had Hb levels below 7.0 g/dl. Of these 3049 children with severe anemia, 2185 (71.7%) had Hb levels below 5.0 g/dl, thus requiring urgent blood transfusion. Though the Department of Child Health alone utilized 32.2% of total blood processed by the National Blood Transfusion Service at KBTH, as many as 259 (58.1%) of the 554 deaths (306 male and 248 female) in the emergency room in children beyond the neonatal period were related to severe anemia. The main causes were nutritional anemia (n = 135), anemia associated with severe malaria (n = 56), anemia associated with sickle cell disease (n = 28), anemia associated with protein-energy malnutrition (n = 22), and 18 cases of anemia complicating gastroenteritis, pneumonia, meningitis, and convulsions. 108 (19.5%) deaths occurred because of neonatal sepsis, severe neonatal hyperbilirubinemia, meningitis and bronchopneumonia, severe anemia secondary to hemorrhage of the newborn, and faulty cord ligation. A significant decline occurred in the prevalence of childhood anemia in the developed world following improved counseling in nutrition, fortification of foods with iron, and iron supplementation to infants and schoolchildren with the attendant improvement in growth velocity and intellectual performance. A planned national anemia survey and early consideration of iron supplementation to older infants and preschool children at risk are recommended.
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PMID:Childhood deaths from anaemia in Accra, Ghana. 749 16

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.
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PMID:Acute renal failure in falciparum malaria. 767 79

To demonstrate the liver profile abnormalities in jaundiced falciparum malaria patients and to determine whether jaundice was associated with other complications in falciparum malaria, 390 patients with acute falciparum malaria were studied. 124 patients were jaundiced and the others were non-jaundiced. Hyperbilirubinemia (total serum bilirubin 3 to 64 mg/dl) was found in jaundiced patients predominantly as unconjugated bilirubin. Asparatate amino-transferase and alanine minotransferase were significantly higher in jaundiced patients (p < 0.01). There was a slight decrease of serum albumin in jaundiced malaria. The complications in jaundiced patients included cerebral malaria (n = 10), acute renal failure (n = 12), pulmonary edema (n = 3), shock (n = 3), and other severe malarial complications (n = 43). Jaundice was associated with cerebral malaria (p < 0.05), acute renal failure (p < 0.01), and hyperparasitemia (p < 0.01). After successful treatment, liver profile returned to normal within a few weeks. We found that jaundiced malaria patients had transient liver profile impairment which indicated predominantly hemolysis rather than liver damage; complications were more frequent in jaundiced patients.
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PMID:Liver profile changes and complications in jaundiced patients with falciparum malaria. 771 91

Nine patients of acute falciparum malaria with severe hyperbilirubinemia developed acute renal failure (ARF). All of them had evidence of intrahepatic cholestasis and needed hemodialysis for several weeks; 7 survived and 2 died, one due to cerebral malaria, the other multiple organ failure. Interestingly, referal diagnosis did not include malaria as a cause of ARF in 8 out of 9 patients.
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PMID:Falciparum malaria complicating cholestatic jaundice and acute renal failure. 786 Apr 65

Six cases of severe jaundice and encephalopathy due to falciparum hepatitis initially diagnosed as fulminant hepatic failure are reported. This rare presentation of falciparum malaria should be suspected in patients with persistent fever, jaundice, encephalopathy and hepatomegaly. The diagnosis should be further suspected when the liver function tests show a predominantly conjugated hyperbilirubinemia with only modest elevation of liver enzymes and alkaline phosphatase. Liver biopsy is valuable in establishing the diagnosis at all stages of the disease.
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PMID:Falciparum malaria or fulminant hepatic failure? 811 50

Thirty five patients with imported malaria were hospitalised in a period of 1980-93 in Department of Infectious Diseases of Pomeranian Medical School, Szczecin, Poland. The diagnosis of malaria was established on a base of clinical feature, the presence of Plasmodium in peripharal blood smears and, in some cases, on positive serological tests. Thirty two patients were Polish citizens, and three persons were foreigners. Malaria was caused mostly by invasion of Plasmodium falciparum (62.8), then P. vivax (31, 4), in 1 case--P. ovale and 1 case--mixed invasion occurred (P. falciparum and P. vivax). The majority of cases caused by P. falciparum were imported from Central Africa. Invasions of P. vivax were brought from North Africa, India and Middle East. Malaria in Polish patients was connected with occupational exposure and lack of proper antimalarial prophylaxis was obvious. A clinical course of disease was serious, with one mortal case. Fever, headache, abdominal pain, weakness, jaundice, insomnia were main complaints. Anemia, leucopenia, thrombocytopenia, hyperbilirubinemia, hypertransaminasemia and high serum concentration of urea were observed. A level of parasitemia in peripheral blood varied from minimal to very high (22.5%) in cases of P. falciparum invasions. In treatment chloroquine, fansidar, quinine, primaquine, halfan were used.
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PMID:[Observation of patients with malaria hospitalized during the years 1980-1993 in the Clinic of Infectious Diseases in Szczecin]. 886 94

We studied 38 patients with acute renal failure (ARF) due to malaria over a 5-year period between 1990 and 1994 at the Institute of Urology and Transplantation. There were 30 males and 8 females who ranged in age from 13 to 75 years. Most were critically ill on presentation with blood urea levels between 116 and 587 mg% and serum creatinine concentrations between 3 and 30 mg%. Anemia accompanied by hyperbilirubinemia was a result of severe hemolysis. Antimalarial therapy consisted of quinine sulfate, chloroquine, or both. Of the 38 patients, 32 required hemodialysis and eventually recovered normal (n = 29) or near normal (n = 3) function. Six patients died.
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PMID:Predictors of outcome in malarial renal failure. 887 97

The goal of our study was to determine the epidemiological and clinical features of imported malaria seen at our military hospital in Hawaii. We reviewed the records of malaria cases seen from January 1, 1979, to December 31, 1995, and compared our results with published reviews from civilian hospitals in North America. Seventy-nine patients were diagnosed with malaria by blood smears. All acquired malaria abroad, mostly in southeast Asia. Sixty-seven percent of cases were vivax malaria, 22% were falciparum malaria, and 11% were caused by undetermined species. Common symptoms were fever (100%), alternate day fever (41%), rigors (91%), headache (59%), nausea (41%), fatigue (39%), dark urine (32%), and vomiting (31%). Ninety-one percent had fever during hospitalization, but 39% were afebrile on admission. Splenomegaly was detected in 49% of cases. The white blood cell count was normal in 65%, low in 31%, and elevated in 4% of cases. Other laboratory findings were anemia (58%), thrombocytopenia (74%), and mild hyperbilirubinemia (64%). Military physicians initially considered the diagnosis of malaria in only 54% of patients. The epidemiological features of our patients differ from those described in the civilian hospitals. Most of our patients were nonimmune, U.S.-born, military personnel infected in southeast Asia, whereas patients described in reviews from U.S. civilian hospitals were usually foreign-born civilians who were infected in Africa or India. The clinical features of malaria, and the problems of initial misdiagnosis in our patients, were similar to those reported from civilian hospitals. Military physicians, like their civilian colleagues, need more training and experience in malaria.
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PMID:A review of 79 patients with malaria seen at a military hospital in Hawaii from 1979 to 1995. 950 98


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