[Clinical, aetiological and therapeutic features of severe sickle cell related vaso-occlusive crisis at the Sylvanus Olympio University Hospital, Lomé].

Introduction: vaso-occlusive crisis (VOC) is the most common manifestation of sickle cell disease and the leading cause of hospitalization among affected children. The purpose of this study is to describe the clinical features of severe VOCs, to determine the etiologies of infectious syndromes that accompany them and to describe their management.

Methods: we conducted a descriptive cross-sectional study of 137 adult patients with sickle cell disease hospitalised for severe VOC in the Paediatric Department of the Sylvanus Olympio University Hospital from 1 January 2009 to 31 December 2011.

Severe Acute Bacterial Infections in Children With Sickle Cell Disease in Togo.

Background: Bacterial infections are considered a major cause of morbidity and mortality in patients, especially children, with sickle cell disease.

Objectives: This study aims at determining, a year after the introduction of the 13-valent pneumococcal conjugate vaccine the distribution of severe acute bacterial infections and germs in children with sickle cell disease.

Patients And Methods: Records of children 0 to 15 years of age and admitted from January 1, 2015 to December 31, 2019 (5 y), were examined retrospectively in the four sickle cell monitoring units in Lomé.

Management of acute sickle cell priapism in an African (Togo) pediatric department includes conservative measures and intracavernous epinephrine which is safe and efficacious.

Priapism is a well-known urologic complication of sickle cell anemia. This study describes the results of a protocol for the treatment of acute priapism by intracavernous injection of epinephrine due to unavailability of etilefrine. A descriptive cross-sectional study of 18 cases of acute priapism in sickle cell patients treated in the pediatric department of the Sylvanus Olympio CHU from January 1 to December 31, 2020.

MG132 Induces Progerin Clearance and Improves Disease Phenotypes in HGPS-like Patients' Cells.

Progeroid syndromes (PS), including Hutchinson-Gilford Progeria Syndrome (HGPS), are premature and accelerated aging diseases, characterized by clinical features mimicking physiological aging. Most classical HGPS patients carry a de novo point mutation within exon 11 of the gene encoding A-type lamins. This mutation activates a cryptic splice site, leading to the production of a truncated prelamin A, called prelamin A ∆50 or progerin, that accumulates in HGPS cell nuclei and is a hallmark of the disease.

Child mortality infected with HIV1 followed in 40 pediatric care sites in Togo.

Introduction: The infection in pediatric HIV is the reason a lot of problems in Africa The objective of our study were to identify factors associated with mortality during follow-up of children receiving antiretroviral therapy in Togo.

Methods: It was a cross-sectional study of 870 children aged files from 7 weeks to 15 years infected with HIV on antiretroviral treatment, covering the period 1 January 2001 to 31 December 2010 taking in 40 sites medical management in Togo. Data processing was done with the software Epi-Info 6.

Knowledge, attitude and practice of the mothers with anemia of children under five years old in the peadiatric department at Sylvanus Olympio teaching hospital in Lomé.

Background: Anemia remains a major cause of morbidity and mortality of children in Togo despite of prevention effort, due to the parents lack of implication.

Aim: To determine the knowledges, attitudes and practices of mothers, with anemia ofchildren under five years old Methods : Knowledge Attitudes and Practice survey from the first of february to 31 ofmarch 2012, about an interview of a hundred mothers with children under 5, randomly selected in the consultation, vaccination waiting rooms and in the hospitalisation.

Results: Forty mothers had never heard about anemia.

Antisense-Based Progerin Downregulation in HGPS-Like Patients' Cells.

Progeroid laminopathies, including Hutchinson-Gilford Progeria Syndrome (HGPS, OMIM #176670), are premature and accelerated aging diseases caused by defects in nuclear A-type Lamins. Most HGPS patients carry a de novo point mutation within exon 11 of the LMNA gene encoding A-type Lamins. This mutation activates a cryptic splice site leading to the deletion of 50 amino acids at its carboxy-terminal domain, resulting in a truncated and permanently farnesylated Prelamin A called Prelamin A Δ50 or Progerin.