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 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty patients of inflammatory brain disease were diagnosed and classified according to clinico-investigational criteria by Ahuja et al into tuberculous meningitis group (36 patients) and non-tuberculous meningitis group (24 patients). Tuberculous meningitis (TBM) patients were classified as probable (9 patients) and possible (27 patients) TBM. Non-TBM group comprised of pyogenic meningitis (8.3%), viral encephalitis (23.3%), cerebral malaria (5%) and enteric encephalopathy (3.3%). Cerebrospinal fluid-adenosine deaminase (CSF-ADA) activities were measured in both TBM and non-TBM groups. Mean CSF-ADA levels in TBM patients was 9.61 +/- 4.10 IU/L and was significantly elevated as compared to viral encephalitis and enteric encephalopathy cases; but difference was insignificant in comparison to pyogenic meningitis (7.92 +/- 0.95 IU/L) and cerebral malaria. Using 8 IU/L as cut off value for diagnosis of TBM a sensitivity of 44% and specificity of 75% was observed.
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PMID:Evaluation of CSF-adenosine deaminase activity in tubercular meningitis. 1099 88

Malaria is a problem of global importance, responsible for 1-2 million deaths per year, mainly in African children, as well as considerable morbidity manifested as severe anaemia and encephalopathy in young children. Fundamental to the development of new tools for malaria control in humans is an increased understanding of key features of malaria infection, such as the diversity of outcome in different individuals, the understanding of different manifestations of the disease and of the mechanisms of immunity that allow clinical protection in the face of ongoing low-grade infection (concomitant immunity or premunition). Here, Graham Brown and colleagues review some of the ways in which molecular approaches might be used to increase our understanding of the epidemiology and clinical manifestations of malaria, as discussed at the Molecular Approaches to Malaria conference (MAM2000), Lorne, Australia, 2-5 February 2000.
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PMID:Molecular approaches to epidemiology and clinical aspects of malaria. 1100 78

Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94

Human cerebral malaria is a frequent encephalopathy that occurs in the endemic tropical-subtropical zones. There are a smaller number of imported cases in continental zones where the diagnosis sometimes remains difficult to establish. Fifteen days after the death of a 36-year-old male French citizen in Africa, an investigation to determine the cause of death was conducted. Histologic examination of the brain permitted the diagnosis of cerebral malaria. Because of the popularity of overseas tourism and because this disorder may appear as "sudden death," these victims may be referred to a forensic pathologist. This case demonstrates the role a forensic pathologist may play in determining the cause of death in cerebral malaria.
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PMID:Postmortem diagnosis of cerebral malaria. 1111 99

Severe falciparum malaria, with its associated hyperpyrexia, distorts plasma levels of large neutral amino acids (NAA) and consequently, brain uptake of individual NAA. Since brain levels of NAA determine cerebral synthesis of monoamines (serotonin, histamine, catecholamines), we measured plasma concentrations of NAA, and also plasma histamine (Hm) in children with falciparum malaria and in uninfected controls. Malaria elicited a marked (P < 0.025) increase in plasma histidine (His) with a 5-fold significant (P < 0.001) elevation in histamine, as well as a 2.5-fold increase (P < 0.005) in plasma phenylalanine (Phe), with no changes in the other NAA. Using kinetic parameters of NAA transport at human blood-brain barrier (BBB), we showed that malaria significantly altered calculated brain uptake of His (+30%), Phe (+96%), Trp (-30%) and Ile (-27%), with no change in the other NAA, compared with controls. Our data suggested enhanced cerebral synthesis of Hm with impaired production of serotonin and the catecholamines in the patients, and therefore, the need to evaluate the encephalopathy in severe malaria within the context of abnormalities in metabolism of Hm and other monoamines resulting from imbalance in plasma levels of the large neutral amino acids. Of clinical relevance also is the impaired inactivation of increased brain Hm by antimalarials such as the widely used aminoisoquinolines leading to elevated brain levels of imidazole-4-acetic acid (IAA), a potent inducer of a sleep-like state often accompanied by seizures, analgesia, decreased blood pressure and other effects.
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PMID:Increased plasma levels of histidine and histamine in falciparum malaria: relevance to severity of infection. 1114 3

The aim of the study was to identify maternal risk factors for perinatal asphyxia in Malawi. Records of 100 mothers who delivered neonates with Apgar scores less than 6 at 5 minutes of birth during March to September 1998 were analyzed. The majority of the mothers were primigravidas (79%) and were within the normal childbearing ages of 20 to 34 years (61.2%). Sixty-one percent of the mothers started antenatal care at 20 to 28 weeks' gestation. Sixty-five percent of the mothers developed obstetric and medical problems that contributed to perinatal asphyxia, and of these, 12 mothers (18.5%) had more than one problem. The problems were premature labor and delivery (21%), preeclampsia (10%), cephalopelvic disproportion (8%), breech presentation (12%), prolonged second stage (11%), fetal distress (7%), cord prolapse (4%), antepartum hemorrhage (2%), prolonged rupture of membranes (1%), and malaria (1%). Forty-six percent had assisted deliveries, and these were cesarean section (18%), vacuum extraction (14%), breech delivery (12%), and forceps delivery (2%). Eighty-one percent of the neonates were admitted to the neonatal nursery, and of these, 56 neonates (67.1%) developed complications; the most common was hypoxic ischemic encephalopathy (38 neonates; 67.9%). Thirty-three percent of the neonates died within 6 days postdelivery. Morbidity and mortality related to perinatal asphyxia can be reduced if staff are knowledgeable and skilled in basic neonatal resuscitation and necessary equipment is available. Mothers should be encouraged to report early for antepartum and intrapartum care for adequate surveillance. The quality of neonatal care, with a focus on thermoregulation and infection prevention, needs to be improved.
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PMID:Risk factors for perinatal asphyxia at Queen Elizabeth Central Hospital, Malawi. 1127 Nov 18

Encephalopathies are the most feared complications of sleeping sickness treatment with melarsoprol. To investigate the existence of risk factors, the incidence of encephalopathic syndromes and the relationship between the development of different types of encephalopathies and the clinical outcome was studied in a clinical trial with 588 patients under treatment with melarsoprol. The 38 encephalopathy cases were classified into three types according to the leading clinical picture: coma type, convulsion type and psychotic reactions. Nine patients were attributed to the convulsion type, defined as a transient event of short duration with convulsions followed by a post-ictal phase, without signs of a generalized disease. None of these patients died from the reaction. Febrile reactions in the 48 h preceding the reaction were generally not observed in this group. Twenty-five patients were attributed to the coma type, which is a progredient coma lasting several days. Those patients often had signs of a generalized disease such as fever (84%), headache (72%) or bullous skin (8%) reactions. The risk of mortality was high in this group (52%). About 14/16 patients with encephalopathic syndrome of the coma type were infected with malaria. Patients with psychotic reactions or abnormal psychiatric behaviour (3/38) and one patient who died after alcohol intake were excluded from the analysis. The overall rate of encephalopathic syndromes in the cases analysed (n=34) was 5.8%, of which 38.2% died. We did not find any parameters of predictive value for the risk of developing an encephalopathic syndrome based on the symptoms and signs before treatment initiation. The appearance during treatment of febrile reactions (RR 11.5), headache (RR 2.5), bullous eruptions (RR 4.5) and systolic hypotension (RR 2.6) were associated with an increased risk for the occurrence of encephalopathic syndromes especially of the coma type.
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PMID:Clinical description of encephalopathic syndromes and risk factors for their occurrence and outcome during melarsoprol treatment of human African trypanosomiasis. 1134 33

The author has divided his work into parts. The first part entitled "Premature Death of Physicians" is dedicated to those who started their research, scientific works and fruitful medical practice but the premature death has stopped their lives and activities. Death causes are presented in ten chapters (groups of causes), i.e. Tuberculosis - Other Lung Diseases - Heart and Vessel Diseases - Septicaemiae - Infectious Diseases in Subgroups: Typhus, Plague, Cholera, Yellow Fever, Diphtheria, Influenza, Malaria, Smallpox, etc. - Encephalopathies and Mental Diseases - Malignant Neoplasms - Noninfectious Unit Diseases - Accidents - Manslaughters - Death Sentences - Suicides - Not Settled Causes of Death. There are in total 283 biographies in the first part. The second part "Longevity of Physicians" is much longer than the first one and contains 509 biographies of doctor, scientists, research workers and practitioners, meritorious in the history of medicine who attained at least 80 years of age. The biographies are arranged in 22 chapters, one for every year from 80 years of age assumed as the beginning of longevity up to 104 years in one of the cases. In each chapter the biographies are arranged in the alphabetical order. In the Epilogue the author presents shortly his conclusions and observations related to the first part and wider commentaries for the second part.
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PMID:[Premature death and longevity of physicians]. 1185 80

The pathogenesis of fatal cerebral malaria (CM) is not well understood, in part because data from patients in whom a clinical diagnosis was established prior to death are rare. In a murine CM model, platelets accumulate in brain microvasculature, and antiplatelet therapy can improve outcome. We determined whether platelets are also found in cerebral vessels in human CM, and we performed immunohistopathology for platelet-specific glycoprotein, GPIIb-IIIa, on tissue from multiple brain sites in Malawian children whose fatal illness was severe malarial anemia, CM, or nonmalarial encephalopathy. Platelets were observed in 3 locations within microvessels: between malaria pigment and leukocytes, associated with malaria pigment, or alone. The mean surface area of platelet staining and the proportion of vessels showing platelet accumulation were significantly higher in patients with CM than in those without it. Platelet accumulation occurs in the microvasculature of patients with CM and may play a role in the pathogenesis of the disease.
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PMID:Platelet accumulation in brain microvessels in fatal pediatric cerebral malaria. 1255 30

Physiologically in the brain, cytokines such as tumor necrosis factor-alpha (TNalpha) are released by the immune system and can modulate neurological responses. Conversely, the central nervous system (CNS) is also able to modulate cytokine production. In the case of CNS disorders, cytokine release may be modified. Cerebral malaria (CM) is a complication of Plasmodium falciparum infection in humans and is characterized by a reversible encephalopathy with seizures and loss of consciousness. Central clinical signs are partly due to sequestration of parasitized red blood cells in the brain microvasculature due to interactions between parasite proteins and adhesion molecules. TNFalpha is produced and released by host cells following exposure to various malarial antigens. The increase of TNFalpha release is responsible for the overexpression of adhesion molecules. This article reviews the involvement of TNFalpha in cerebral malaria and the relation with all the processes involved in this pathology. It shows that (i). TNFalpha levels are increased in plasma and brain but with no clear correlation between TNFalpha levels and occurrence and severity of CM; (ii). TNFalpha is responsible for intercellular adhesion molecule-1 upregulation in CM, the relation being less clear for other adhesion molecules; (iii). TNFalpha receptors are upregulated in CM, with TNF receptor 2 (TNFR2) showing a higher upregulation than TNFR1 in vivo; (iv). in murine CM, low doses of TNFalpha seem to protect from CM, whereas excess TNFalpha induces CM and anti-TNFalpha therapies (antibodies, pentoxifylline) did not show any efficiency in protection from CM. Moreover, the involvement of lymphotoxin a, which shares with TNFalpha the same receptors with similar affinity, appears to be an interesting target for further investigation.
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PMID:Tumor necrosis factor alpha in the pathogenesis of cerebral malaria. 1450 53


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