Moncef Feki

Publications (101) View all

• Article: Aminoacidopathies and organic acidurias in Tunisia: a retrospective survey over 23 years.

  Sameh Hadj-Taieb, Fehmi Nasrallah, Mohamed B Hammami, Monia Elasmi, Haifa Sanhaji, Feki Moncef, Naziha Kaabachi
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  ABSTRACT: Inborn errors of metabolism are neglected in developing countries because they are not as common as infectious and nutritional disorders. In Tunisia, no information is available on the incidence and epidemiological features of these inherited metabolic diseases. To precise the profile of aminoacidopathies other than phenylketonuria and organic acidurias and to estimate their incidences in Tunisia. Between 1987 and 2009, our laboratory received 13171 requests for analysis of patients with symptoms suggestive of inborn errors of metabolism. For these cases, ion exchange chromatography of free amino acids was performed on amino acids analyser. Urinary organic acids profiles were determined by gas chromatography-mass spectrometry. Abnormal cases were 370 (2.8%), divided into 212 cases of aminoacidopathies (57.3%) and 158 cases of organic acidurias (42.7%). The most frequent aminoacidopathies, were maple syrup disease (32.5%), tyrosinemia type I (28.8%) and nonketotic hyperglycinemia (16%). Methylmalonic aciduria (33.5%), propionic aciduria (18.4%) and 2-hyrdoxy glutaric aciduria (10.8%) were the most frequent organic acidurias. The incidences were calculated using the Hardy-Weinberg formula and were estimated at 1/13716 for maple syrup disease, 1/14804 for tyrosinemia type I, 1/16144 for methylmalonic aciduria and 1/23176 for propionic aciduria. Aminoacidopathies and organic acidurias turned out to be highly frequent in Tunisia, mainly because of a high rate of consanguinity. We believe that they are underestimated. To improve their diagnosis, it is necessary to have available sophisticated equipment which would allow early treatment of patients.
  La Tunisie médicale 03/2012; 90(3):258-61.
• Article: Congenital hyperinsulinism: review of 12 tunisian cases.

  Hadhami Ben Turkia, Karima Brahim, Hatem Azzouz, Neji Tebib, Mohamed Slim Abdelmoula, Amel Ben Chehida, Moncef Fekih, Sadok Sayed, Nejib Kaabar, Marie Francoise Ben Dridi
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  ABSTRACT: Congenital hyperinsulinism in infancy (CHI) is a heterogeneous disorder with respect to genetics and response to therapy. Data on CHI are sporadic in North African population. To characterize the clinical features and outcome of 12 Tunisian patients with CHI. data of patients diagnosed with CHI during the period 1989-2007 were retrospectively analyzed. Diagnosis was considered whenever hyperinsulinemia ≥ 10μ UI/ml was concomitant to hypoglycemia < 3mmol/l and/or high insulin to glucose ratio > 0.3 and/or positif glucagon test. Transient causes of hypoglycemia, adrenal and growth hormone deficiency were excluded. There were nine infants diagnosed at a median age of 17 months and three newborns. Permanent hyperammoniemia, found in one patient, guided to leucine-sensitive hyperinsulinism. Seven patients presented with seizures, two with psychomotor delay and one with recurrent malaises. Among 42 assays of plasmatic insulin, when in hypoglycemia, 40% only were ≥ 10μU/ml. Three patients resisted to diazoxide and underwent subtotal pancreatectomy complicated by diabetes mellitus in two cases and persistent hypoglycemia in one patient. Histological examination concluded to diffuse hyperplasia of pancreatic cells. Diazoxide was discontinued in four out the eight responders' patients. Four patients died, seven patients developed variable degrees of mental retardation and five suffered from epilepsy. Early onset forms were, as reported in the literature, mostly resistant to medical therapy. The high proportion of neurological sequelae is related to diagnosis delay or to a late surgery. We focus on the importance of a precocious diagnosis and aggressive treatment of hypoglycemia.
  La Tunisie médicale 04/2011; 89(4):369-73.
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  Available from: Moncef Feki

  Article: HLA class II alleles susceptibility markers of type 1 diabetes fail to specify phenotypes of ketosis-prone diabetes in adult Tunisian patients.

  Lilia Laadhar, Fatma Harzallah, Mondher Zitouni, Maryam Kallel-Sellami, Moncef Fekih, Naziha Kaabachi, Hádia Slimane, Sondès Makni
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  ABSTRACT: We aimed to characterize the different subgroups of ketosis-prone diabetes (KPD) in a sample of Tunisian patients using the Aβ scheme based on the presence or absence of β-cell autoantibodies (A+ or A-) and β-cell functional reserve (β+ or β-) and we investigated whether HLA class II alleles could contribute to distinct KPD phenotypes. We enrolled 43 adult patients with a first episode of ketosis. For all patients we evaluated clinical parameters, β-cell autoimmunity, β-cell function and HLA class II alleles. Frequency distribution of the 4 subgroups was 23.3% A+β-, 23.3% A-β-, 11.6% A+β+ and 41.9% A-β+. Patients from the group A+β- were significantly younger than those from the group A-β- (P = .002). HLA susceptibility markers were significantly more frequent in patients with autoantibodies (P = .003). These patients also had resistance alleles but they were more frequent in A+β+ than A+β- patients (P = .04). Insulin requirement was not associated to the presence or the absence of HLA susceptibility markers. HLA class II alleles associated with susceptibility to autoimmune diabetes have not allowed us to further define Tunisian KPD groups. However, high prevalence of HLA resistance alleles in our patients may reflect a particular genetic background of Tunisian KPD population.
  Experimental Diabetes Research 01/2011; 2011:964160. · 1.20 Impact Factor
• Article: Moderate phenotypic expression of familial hypercholesterolemia in Tunisia.

  Awatef Jelassi, Afef Slimani, Imen Jguirim, Mohamed Najah, AbdelMajid Abid, Lamia Boughamoura, Jawhar Mzid, Moncef Fkih, Fawzi Maatouk, Mustapha Rouis, Mathilde Varret, Mohamed Naceur Slimane
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  ABSTRACT: Autosomal Dominant Hypercholesterolemia (ADH) is an autosomal dominant disease caused by mutations in the low density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. Xanthomas and coronary heart diseases (CHD) at an early age are the major clinical manifestations of the disease. 16 families with familial hypercholesterolemia from different regions in Tunisia participated in the study. Mutations within the LDLR gene were screened through DNA sequencing. Lipids values were measured by standard enzymatic methods. We present here thirty five homozygotes and fifty six heterozygotes. Homozygotes presented extensive xanthomatosis, variable clinical manifestations of CHD, and total cholesterol levels in males and females of 17.26+/-4.18 and 17.64+/-2.59 mmol/L respectively. HDL-cholesterol levels were 0.62+/-0.24 and 1.00+/-0.61 mmol/L for males and females, respectively. None of the heterozygotes had tendon xanthomas (except for one female aged 62), eight had corneal arcus, and nine developed CHD mean between 46 and 88 years old. Total cholesterol levels in males and females ranged from 4.60 to 8.90 and from 4.30 to 10.50 mmol/L, respectively. Tunisian FH heterozygotes are characterized by a moderate clinical and biological expression of the disease.
  Clinica chimica acta; international journal of clinical chemistry 02/2010; 411(9-10):735-8. · 2.54 Impact Factor
• Article: Adiponectin and metabolic syndrome in a Tunisian population.

  Samir Ben Ali, Riadh Jemaa, Bouchra Ftouhi, Amani Kallel, Moncef Feki, Hedia Slimene, Naziha Kaabachi
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  ABSTRACT: The aim of this study was to investigate the relationship between the adiponectin levels and various characteristics of the metabolic syndrome (MS) in a sample of the Tunisian population. Three hundred and fifty-four individuals were included in this study. Body mass index, blood pressure, HDL-cholesterol, triglycerides, glucose, insulin, and adiponectin concentrations were measured. Insulin resistance was assessed by homeostasis model assessment of insulin resistance (HOMA-IR). MS was identified with the NCEP-ATP III criteria. Subjects with MS showed significantly lower adiponectin levels compared to those without MS. For both genders, the prevalence and the number of MS components increased significantly as the adiponectin concentrations decreased. Subjects with the lowest adiponectin quartile had an increased risk of MS adjusted for age, gender, and HOMA-IR. Our findings suggest that hypoadiponectinemia is strongly associated with the risk of MS independent of insulin resistance.
  Inflammation 09/2011; 35(3):828-33. · 1.75 Impact Factor