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

This study was performed to extend the knowledge of the pathogenesis of PE in severe falciparum malaria. Sequential hemodynamic studies were conducted in 13 patients with severe falciparum malaria. Seven patients developed PE, while the other six patients had NPE. Two patients died, one in each group. Hemodynamic changes were found in both groups, including an initial reduction in SVR and PVR, along with an increased CI and variable values (normal and increased) of PCWP. All abnormalities persisted for at least two days; changes in PVR lasted especially longer (throughout five days). The initial hemodynamic changes cannot predict the development of PE; however, heavy parasitemia of more than 60 percent and severe hypoalbuminemia were found to be more common in PE than NPE. Of three patients with PE who had normal PCWP, one died, with postmortem findings of increased pulmonary capillary permeability. The increased PCWP which was found in the other four cases of PE was proven to be volume overload without evidence of CHF. It was concluded that the pathophysiologic changes in severe falciparum malaria were systemic and pulmonary vasodilation. The abnormal pulmonary vascular change was found to be the cause of PE. Volume overload and hypoalbuminemia could aggravate further pulmonary capillary leakage in these cases.
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PMID:Pulmonary edema in severe falciparum malaria. Hemodynamic study and clinicophysiologic correlation. 219 75

In this report of two patients with acute malaria, the electrocardiogram on admission showed changes of repolarisation. In both cases these electrocardiographic changes normalised after anti-parasitic treatment. The first patient recovered completely; however, the second patient developed signs of congestive heart failure compatible with cardiomyopathy. In acute malaria, an electrocardiogram should be considered to detect myocardial involvement.
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PMID:Electrocardiographic changes in acute malaria. 225 Jul 54

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

Hypoglycaemia is a relatively common cause for referral of patients to the accident and emergency departments of hospitals but most of it is iatrogenic. Occasionally, however, hypoglycaemia is due to any one of up to a hundred different disorders. In some, hypoglycaemia is the cause of intermittent neuroglycopenic symptoms that lead to their referral to medical outpatients for investigation. Only the most important are discussed here. Hyperinsulinism due to abnormal beta-cell function is an uncommon but important cause of spontaneous hypoglycaemia. The diagnosis is suspected from the history of episodes of altered consciousness confirmed by demonstrating raised plasma insulin, C-peptide and proinsulin levels in peripheral blood in the presence of hypoglycaemia. Differentiation of the various causes of endogenous hyperinsulinism before surgery is difficult if not impossible and the low predictive value of most of the localizing techniques that are available makes them an additional and unnecessary cost, producing little clinical benefit. Hypoglycaemia caused by non-islet cell tumours (NICTH) is seemingly rarer than hyperinsulinism from insulinoma and tends to occur in older patients. The clinical features are similar to those of hyperinsulinism but laboratory investigation reveals appropriately depressed plasma insulin, C-peptide and proinsulin levels in the presence of hypoglycaemia. The plasma IGF-II:IGF-I ratio is characteristically high and the concentration of the E-domain of proIGF-II is raised. Autoimmune hypoglycaemia is more common in some countries than others and is most often due to autoantibodies to insulin (AIS). It may also be caused by autoantibodies to the insulin receptor and possibly to autoantibodies that are stimulatory to pancreatic beta-cells. Contrary to popular belief, idiopathic reactive hypoglycaemia is rare and only one of the possible causes of the postprandial syndrome. It is characterized by a low blood glucose concentration in blood collected during a spontaneous symptomatic episode but not at other times. Its cause is unknown. Other causes of hypoglycaemia include endocrinopathies of various kinds; sepsis including malaria; congestive cardiac failure; hepatic and renal insufficiencies; diverse inborn errors of metabolism; and exogenous toxins, of which alcohol is probably the commonest.
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PMID:Hypoglycaemia in the adult. 837 12

We have prospectively collected information during resuscitation in 24 children with life-threatening malaria. All had clinical respiratory distress and 16 were severely anemic (hemoglobin < or = 5 g/dL) on admission. Central venous pressure (CVP) measurements were normal (< or = 5 cm of water) prior to treatment but all had a metabolic acidosis. The geometric mean lactate level was significantly higher in children admitted with severe anemia than in those without severe anemia (11.2 mmol/l versus 4.2 mmol/l; P = 0.009). Hypovolemia (a CVP on admission < 0 cm of water) was associated, although not significantly, with a higher admission plasma creatinine concentration (94 mumol/l versus 64 mumol/l; P = 0.06) and probably contributed to the severely reduced creatinine clearances (0-39 ml/min/1.73 ml2) found in 12 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 13 children in whom this was assessed in the first 24 hr. Treatment resulted in a rapid decrease in blood lactate in 16 of the 20 children transfused, which was most dramatic in severely anemic children, who were rapidly resuscitated. In nonanemic children, early and rapid administration of normal saline usually resulted in both metabolic and clinical improvement. However, in three children, two of whom died, acidosis persisted despite resuscitation. Metabolic acidosis often accounts for respiratory distress in life-threatening childhood malaria. Severe anemia and hypovolemia appear to play major roles in its pathogenesis, are readily treatable, and there appears to be little risk of congestive cardiac failure even with an aggressive approach to fluid replacement.
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PMID:Transfusion for respiratory distress in life-threatening childhood malaria. 894 Sep 85

Chloroquine, an agent used in treatment and prophylaxis of malaria, and also known for its antiinflammatory effects in dermatological, rheumatological, and connective tissue disorders, has been reported to cause toxicity, most commonly in the retina and the cardiovascular system. We describe a 60-year-old woman with longstanding rheumatoid arthritis receiving multidrug treatment, including prolonged administration of chloroquine. She developed complete heart block requiring a permanent pacemaker, congestive heart failure, and progressive myopathy. During hospital investigations for her myopathy, she died of acute pulmonary thromboembolism. Although hypertension and possibly amyloidosis were thought to be the cause of her cardiac disease, cardiac and skeletal muscle changes characteristic of chloroquine toxicity were observed. Chloroquine may be an important unsuspected contributing cause of cardiac dysfunction in patients with rheumatological disease. Endomyocardial biopsy should be considered early in the course of diagnosis and management.
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PMID:Chloroquine related cardiac toxicity. 963 91

Splenomegaly was studied retrospectively at the University of California, San Francisco, School of Medicine, on all patients (N = 2,056) for the years 1913 to 1962. The patients were classified into several diagnostic groups, and these groups were tested for statistical significance (chi(2)) with many clinical and laboratory variables to determine their predictive value. Hematologic disorders were associated with 57% of cases of splenomegaly and 81% of cases of massive splenomegaly. Among patients with splenomegaly, 19% had infectious diseases, 11% had hepatic diseases, and 9% had congestive or inflammatory disorders. The residual 4% were considered to have primary splenic disorders or a disorder of unknown cause. The commonest diseases associated with splenomegaly were hematologic (acute and chronic leukemias), infectious (malaria, endocarditis, and tuberculosis), hepatic (chronic liver disease), congestive (congestive heart failure), inflammatory (thyrotoxicosis), and other (cancers not metastatic to the spleen). The diseases most frequently associated with massive splenomegaly were the chronic leukemias. The disease with the highest incidence of massive splenomegaly was myelofibrosis (23 of 29 patients, 78%). Splenectomy was performed in 154 patients (7%), primarily for hematologic amelioration and hepatic hypersplenism. Hematologic diseases showed significant associations with lymphadenopathy, generalized lymphadenopathy, massive splenomegaly, and cytoses (P .001) and with progressive splenic enlargement (P < .02). Infectious diseases showed significant association with fever, and hepatic diseases showed significant association with abnormal results of liver function tests (P < .001). The findings of this retrospective study should be validated prospectively.
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PMID:Splenomegaly in 2,505 patients in a large university medical center from 1913 to 1995. 1913 to 1962: 2,056 patients. 973 88

Death from malaria occurs from the complications of the infection: cerebral manifestations leading to coma and a severe and refractory anemia leading to hypoxia and cardiac decompensation. Several mechanisms have been identified to play a role in the pathogenesis of malarial anemia, such as erythrocyte lysis and phagocytosis, and sequestration of parasitized red blood cells, but recent data indicate that these mechanisms (singly or in combination) do not adequately explain the severity of this anemia. By contrast, hematologic studies have shown that bone marrow suppression and ineffective erythropoiesis contribute importantly to the severe anemia of malaria infection. The host mechanisms responsible for suppression of erythropoiesis may involve an excessive or sustained innate immune response or a pathologic skewing of the T-cell differentiation response with the attendant production of certain proinflammatory cytokines. Experimental data also indicate that severe malarial anemia is associated with the immunologic expression of a circulating inhibitor of erythropoiesis that functionally antagonizes the action of erythropoietin. We review the clinical and experimental basis for these concepts and discuss ongoing experimental and genetic studies aimed at unraveling the molecular basis of this malaria-induced bone marrow suppression.
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PMID:The anemia of malaria infection: role of inflammatory cytokines. 1496 85

Congestive cardiac failure (CCF) is a common paediatric emergency with diverse aetiologies. The objective of this study is to define the current prevalence rate and common causes of CCF among children hospitalized in a Nigerian Tertiary Hospital. The study was prospectively done over a 1-year period in the Paediatric Wards of the hospital. Consecutive children aged 0-14 years, who fulfilled the standard diagnostic criteria for CCF were recruited. Data obtained from them included the age, sex, duration of illness and the socioeconomic status of the parents. Each subject was given a specific diagnosis based on the clinical, laboratory and radiological features. Out of a total of 1552 admissions, 109 had CCF giving the prevalence of 7.02%. The mean age of children with CCF was mean of 2 +/- 3.1 years (range: 1 day to 14 years). Ninety-five (91%) of them were concentrated in the lower socioeconomic classes III-V. The aetiologies of CCF identified in this study were as follows: severe anaemia occurring alone (48; 46%), lower respiratory tract infections (LRTI) (30; 29%), anaemia with LRTI (12; 11.5%), congenital heart diseases (CHD) (11; 10.5%), rheumatic heart disease (1; 1%), myocarditis (1; 1%) and chronic renal disease (1; 1%). Malaria was the commonest cause of anaemia while bronchopneumonia was the commonest form of LRTI in the subjects. Measles infection was associated with LRTI in 10 (23.8%) children. Three children had HIV-related anaemia. Infants formed the bulk of the subjects with CCF due to anaemia, LRTI and CHD. Ventricular septal defect was the commonest CHD identified. The prevalence obtained from this study was higher than rates obtained from some previous studies in the country. Severe anaemia is the commonest cause of CCF probably from the effects of severe malaria and increasing poverty. Stringent attention to poverty alleviation and malaria control may reduce the burden of CCF among Nigerian children.
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PMID:Current trends in the prevalence and aetiology of childhood congestive cardiac failure in Sagamu. 1716 31

Viral hepatitis is common in Nigeria and may present with jaundice in pregnancy. The objective of this study was to determine the contribution of viral hepatitis among other aetiological factors, to the development of jaundice during pregnancy. Data on viral hepatitis among gravidae with jaundice in pregnancy over a 10-year period from 1st January 1992 through 31st December 2001 were retrieved and analyzed. Fifty-two cases of jaundice in pregnancy were seen among 16,566 pregnancies registered in the hospital over the 10-year period. Of the 52 cases of jaundice in pregnancy, only 48 case records were retrievable, on which this analysis is based. Viral hepatitis (VH) occurred in 1 in 591.6 pregnancies and was diagnosed in 28 (58.3%) cases of jaundice in pregnancy. Other causes of jaundice were malaria 8 (16.7%), sickle-cell anaemia in pregnancy 6 (12.5%) and sepsis 2 (4.2%). Of the 28 patients with viral hepatitis, 8 (28.5%) were positive for HBsAg. The liver function tests (LFTs) were done in 26 of the 28 patients and it showed hyperbilirubinaemia in 24, 11 had serum albumin >3.5 g/dl. All had spontaneous vaginal delivery with no maternal death. Complications associated with viral hepatitis were, anaemia 14 (50%), intrauterine growth retardation (14.3%), intrauterine foetal death 2 (7.1%), congestive cardiac failure 1 (3.57%) early neonatal death 1 (3.57%) and 2 (7.1%) cases of systemic hypertension. Viral hepatitis contributes significantly to jaundice in pregnancy and there is associated fetal and maternal morbidity.
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PMID:Viral hepatitis in the aetiogenesis of jaundice in pregnancy at the University College Hospital, Ibadan. 1920 72


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