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1.
Kisangani méd. (En ligne) ; 12(2): 525-532, 2022. tables
Article in English | AIM | ID: biblio-1426221

ABSTRACT

changes occur commonly among patients affected with malaria. This study aimed to assess lipid changes in blood among patients with malaria in Butembo, a hypoendemic region. Methods: This cross-sectional study, conducted in the Departments of Internal and Parasitology of Matanda Hospital, located in Butembo, from July 1st, 2020, to November 2, 2020; involved 100 patients diagnosed with malaria. Biochemical analyses carried out by three lab technicians were performed among patients who had positive malaria using positive thick film. Plasmodial species, the parasite density, the triglycerides, the total cholesterol, the HDL-cholesterol, the LDL-cholesterol were assessed. Results: Cholesteroleamia and HDLemia demonstrated a low level in 93% and in 61% of participants respectively; whereas 73% of cases showed an increased level of triglycerides in the blood. Lipidemia profile was independently associated with parasite density among patients with malaria. Conclusion: Although the lipid changes in the blood are not specific in the diagnosis of malaria, this study highlighted their status among patients with malaria. Further researches should be conducted to determine their impact on malaria outcomes. Therefore, dyslipidemia could be used in malaria screening.


Subject(s)
Humans , Male , Female , Blood , Cholesterol , Dyslipidemias , Hyperlipidemias , Malaria , Triglycerides , Lipids
2.
S. Afr. med. j. (Online) ; 107(2): 145-148, 2017. ilus
Article in English | AIM | ID: biblio-1271153

ABSTRACT

Background. Familial hypercholesterolaemia (FH) is usually caused by mutations in three genes (LDLR, APOB and PCSK9). Objective. To identify the spectrum of FH-causing mutations in black South African (SA) patients.Methods. DNA samples of 16 unrelated South African FH patients with elevated low-density lipoprotein cholesterol levels, tendon xanthomas and corneal arcus (3 clinically homozygous FH and 13 heterozygous FH) of ethnic African origin were screened for mutations in the LDLR (coding region, promoter and intron/exon boundaries), APOB (part of exon 26) and PCSK9 genes (exon 7), using high-resolution melting.Results. Eight LDLR mutations were identified, for an overall detection rate of 8/19 predicted FH-causing alleles (42.1%). The previously reported six base pair deletion p.(D47_G48del) was found in two patients, and two novel variants (c.1187-25T>C and c.1664T>G p.(L555R)) were found, both predicted to be pathogenic using in silico web-based predictive algorithms. No pathogenic variants in APOB or PCSK9 were found.Conclusions. These findings contribute to the knowledge of allelic heterogeneity in the spectrum of FH-causing mutations in black SA patients, signifying their ancestral diversity. The relatively low overall detection rate may reflect locus heterogeneity of the FH phenotype in black SA FH patients


Subject(s)
High-Density Lipoproteins, Pre-beta , Lipid Metabolism , South Africa , Triglycerides
3.
Article in English | AIM | ID: biblio-1271592

ABSTRACT

Background: Dyslipidaemia is reported to occur in patients with sickle cell disease as well as patients with chronic kidney disease irrespective of the haemoglobin genotype. This study aimed at evaluating lipid profile in subjects with sickle cell anaemia (HbSS); sickle cell trait (HbAS) and normal haemoglobin genotype (HbAA); and comparing the lipid parameters between sickle cell disease patients with and those without chronic kidney disease. Methods: A total of 66 patients with chronic kidney disease: 26 HbAA; 24 HbAS and 16 HbSS and 60 apparently healthy controls were recruited for the study. Lipoproteins; urea; creatinine; estimated glomerular filtration rate and electrolytes were determined using standard procedures in both patients and controls. Results: The mean total cholesterol; low density lipoproten cholesterol and high density lipoproten cholesterol in stable HbSS subjects were significantly lower (p


Subject(s)
Anemia , Kidney Diseases , Lipoproteins , Triglycerides
4.
JEMDSA (Online) ; 15(1): 11-17, 2010.
Article in English | AIM | ID: biblio-1263738

ABSTRACT

The bulk of plasma triglycerides are carried by chylomicrons in the fed and very low-density lipoproteins in the fasted state. These triglyceride-rich lipoproteins are metabolised to remnant lipoproteins by lipoprotein lipase (LPL). Hypertriglyceridaemia results if triglyceride-rich lipoproteins accumulate either due to defective clearance; overproduction or a combination of both mechanisms. Genetic and environmental factors interact in the genesis of hypertriglyceridaemia but occasionally a single factor may be dominant. At a molecular level the most common cause of severe primary hypertriglyceridaemia is loss of function mutations in both alleles of LPL. The most common environmental contributors include diabetes; diet; alcohol and medications (including oestrogen; steroids; retinoids and protease inhibitors). Severe hypertriglyceridaemia can trigger acute pancreatitis while mild to moderate hypertriglyceridaemia is an independent cardiovascular risk factor. Treatment strategies are determined by the severity and aetiology of hypertriglyceridaemia as well as the patient's cardiovascular risk profile. General strategies include lifestyle modifications with restriction of dietary fat intake; cessation of alcohol intake and increased exercise. Contributing metabolic disorders should be controlled and aggravating medications withdrawn or reduced where possible. Moderate hypertriglyceridaemia may be treated with high doses of omega-3 fatty acids (4 g/day); fibrates; niacin or statins. Fibrates are the agents of choice in severe hypertriglyceridaemia


Subject(s)
Disease Management , Hypertriglyceridemia , Lipoprotein Lipase , Triglycerides
6.
Med. Afr. noire (En ligne) ; 42(4): 213-216, 1995.
Article in French | AIM | ID: biblio-1266023

ABSTRACT

Deux cent cinquante donneurs de sang adultes-jeunes ont ete etudies aux fins de determiner les valeurs usuelles de certains parametres lipidiques (cholesterol total; triglycerides; HDL-cholesterol); apolipoproteiques (Apo AI; Apo B) et de la Lp (a). Les resultats sont compares a ceux obtenus sur une population caucasienne. Il en ressort que la distribution des valeurs entre les hommes et les femmes est conforme aux donnees de la litterature; mais tous les chiffres obtenus sur la population; excepte la Lp (a); sont inferieurs a ceux de la population de comparaison. Ces resultats etant mis en parallele avec la tendance evolutive des maladies cardiovasculaires; les auteurs preconisent des etudes complementaires pour mieux preciser le role des facteurs lipidiques dans l'etiopathogenie de ces maladies


Subject(s)
Apolipoproteins , Blood Donors , Cardiovascular Diseases , Cholesterol , Triglycerides
7.
Publications Medicales Africaines ; 26(123): 23-27, 1993.
Article in French | AIM | ID: biblio-1268857

ABSTRACT

Les auteurs rapportent un cas d'ascite chyleuse chez un nouveau-ne de 3 semaines. L'evolution sous nutrition parenterale puis alimentation enterale elementaire excluant les triglycerides a chaine longue a ete malheureusement defavorable au 37eme jour de vie dans un tableau de choc septique. Une revue de la litterature a permis de souligner le caractere en regle idiopathique de l'ascite chyleuse du nouveau-ne; et la necessite d'une nutrition parenterale ou enterale comportant des triglycerides a chaine moyenne : seul gage d'une evolution habituellement favorable


Subject(s)
Ascites , Ascites/therapy , Enteral Nutrition , Infant , Infant Nutrition , Parenteral Nutrition , Triglycerides
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