Hicham Esselmani

Dr. Hicham Esselmani


Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 July 2012 in Annales de biologie clinique
Verified
Journal Article
Closed access
ODOmar Derfoufi
Omar Derfoufi
EAEric Ngoh Akwa
Eric Ngoh Akwa
AEAissam Elmaataoui
Aissam Elmaataoui
ELElmostafa
Elmostafa
HEHicham Esselmani
Hicham Esselmani
SASarra Aoufi
Sarra Aoufi
The aim of this study was to analyze the epidemiology and evolution of hydatidosis in Morocco. This is a descriptive and retrospective study over a period ranging from 1980 to 2008. The patient data were collected from the epidemiological bulletin issued by the Department of Epidemiology and Fight against Disease that report all cases operated for hydatidosis between 1980 and 1992, and from the annual reports of parasitic diseases published annually by the same department between 2003 and 2008. We identified 23512 cases of hydatidosis with an annual increase in the number of cases and their incidence. Hydatidosis is present on any area of Morocco, with an uneven distribution from one region to the other. It is mostly observed in patients from rural areas and a predominance of female cases is observed throughout the period of study (sex ratio M/F = 0.66). All age groups are affected with a predominance of young adults. The liver is the organ most affected followed by the location of lung. These results show that hydatidosis remains a major public health problem in Morocco. Continuous monitoring of the epidemiological situation is essential to assess the measures implemented to fight against this infection and to allow rehabilitation and adjustment of these measures in order to reduce the incidence of this disease.

30 January 2025 in Neurology International
Verified
Journal Article
Open access
PDF file
HEHicham Esselmani
Hicham Esselmani
AAAbdelmohcine Aimrane
Abdelmohcine Aimrane
Hicham CHATOUIHicham CHATOUI
Hicham CHATOUI
Omar El HibaOmar El Hiba
Omar El Hiba
Mustapha NAJIMIMustapha NAJIMI
Mustapha NAJIMI
Mohamed MERZOUKIMohamed MERZOUKI
Mohamed MERZOUKI
Background/Objectives: Brown tumors are rare bone lesions associated with hyperparathyroidism, particularly secondary hyperparathyroidism (SHPT), in chronic renal failure. While brown tumors commonly affect bones rich in marrow, the involvement of the sphenoid sinus is extremely rare and can present with neurological symptoms. This study reports a case of a sphenoid sinus brown tumor in a patient on hemodialysis, highlighting its clinical presentation and diagnostic challenges. Methods: A 31-year-old woman undergoing chronic hemodialysis presented with a severe headache, diplopia, and progressive vision loss in her left eye. Laboratory tests revealed hypercalcemia, hypophosphatemia, and elevated parathyroid hormone (PTH) levels, consistent with SHPT. The diagnosis was confirmed through a clinical examination and magnetic resonance imaging (MRI). Results: The clinical examination confirmed decreased visual acuity in the left eye. The laboratory results revealed serum calcium of 15.5 mg/dL, phosphate of 1.0 mg/dL, and PTH of 2000 pg/mL, consistent with SHPT. The imaging studies identified a brown tumor in the sphenoid sinus exerting a mass effect on adjacent structures. This case underscores the rarity of brown tumors in this location, with very few similar reports in the literature. Conclusions: Although rare, brown tumors should be considered in patients with SHPT who present with neurological symptoms or cranial lesions. An early diagnosis through biochemical and imaging studies is crucial to prevent severe complications. The management involves treating the underlying hyperparathyroidism, with surgical intervention indicated in cases of neural compression.

1 January 2020 in PAMJ Clinical Medicine
Verified
Journal Article
Open access
HEHicham Esselmani
Hicham Esselmani
BABoutaina Akhatar
Boutaina Akhatar
YMYassine Al Mabrouki
Yassine Al Mabrouki
MRMustapaha El Rhrib
Mustapaha El Rhrib
Le déficit en facteur VII est très rare, sa prévalence est estimée à 1/1000000. Sa transmission est autosomique récessive. L´expression peut aller de la simple épistaxis à l´hémorragie cérébrale. Nous rapportons une découverte fortuite d´un cas d´un enfant issu de parents consanguins du premier degré, suite à la réalisation d´un bilan préopératoire pour une amygdalectomie. Le bilan biologique a montré un taux de prothrombine bas et un temps de céphaline activée (TCA) normal. Un bilan de la coagulation a montré un déficit isolé en facteur VII évalué à 28%. À travers cette observation, nous soulignons la rareté de ce trouble, la révélation fortuite et le rôle de la collaboration clinicien-biologiste pour un bilan biologique raisonné.

1 January 2014 in Pan African Medical Journal
Verified
Journal Article
Open access
HEHicham Esselmani
Hicham Esselmani
MBMounya Bouabdellah
Mounya Bouabdellah
LBLaila Benchekroun
Laila Benchekroun
SESanae Elalami
Sanae Elalami
NHNajat Handor
Najat Handor
LCLayachi Chabraoui
Layachi Chabraoui
L'hyperparathyro?die primaire (HPP) est une affection fr?quente, aujourd'hui d?couverte fortuitement dans 75 ? 80% des cas par un dosage syst?matique de la calc?mie biologique. Le diagnostic de cette affection se base sur la mise en ?vidence concomitante d'une calc?mie ?lev?e, d'un taux de parathormone (PTH) ?lev? (80% des cas) ou normal (20% des cas), et d'une calciurie sup?rieure ? 150 mg/24 heures. Les manifestations squelettiques graves (ost?ite fibrokystique, tumeurs brunes, fractures pathologiques) sont rares de nos jours. Les tumeurs brunes constituent un mode de r?v?lation rare de l'hyperparathyro?die primaire et leur localisation au niveau des maxillaires est exceptionnelle. Nous rapportons ici la longue histoire de la maladie d'un homme de 42 ans atteint d'une hyperparathyro?die primitive d?couverte devant une tum?faction jugale, une hypercalc?mie majeure ? 3.92 mmol/l et une tumeur brune maxillaire et nous soulignant le r?le du bilan biologique raisonn? et de son interpr?tation en tant que r?v?lateur diagnostique pour orienter le clinicien vers l'hyperparathyro?die primaire.

12 June 2026 in Livers
Verified
Journal Article
Open access
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RERAHMA ENNADI
RAHMA ENNADI
HEHicham Esselmani
Hicham Esselmani
YNYoussef Nadir
Youssef Nadir
Mustapha NAJIMIMustapha NAJIMI
Mustapha NAJIMI
Mohamed MERZOUKIMohamed MERZOUKI
Mohamed MERZOUKI
Background: Liver diseases are an increasing public health concern in Morocco; reliable national population-based estimates of liver fibrosis and cirrhosis in Morocco are currently unavailable. Existing evidence is largely limited to selected high-risk groups and hospital-based cohorts. Generating reliable prevalence data is crucial for designing evidence-based screening pathways, targeting high-risk groups and informing prevention and treatment policies. Objectives: Our aim was to comprehensively review studies on the prevalence of liver fibrosis and cirrhosis in Morocco, focusing on characterizing study populations, specifically high-risk populations and hospital-based cohorts, diagnostic methods and thresholds used. The review also summarizes hospital-based cirrhosis cohorts without merging them with prevalence estimates, and identifies gaps in the literature, particularly the absence of population-based prevalence studies and national epidemiological data in Morocco. Methods: The study systematically reviewed literature up to 26 October 2025, including studies conducted in Morocco among high-risk populations or hospital-based cirrhosis cohorts, using multiple databases. Two reviewers independently screened and extracted data, assessing bias with the Joanna Briggs Institute (JBI) checklist. Due to heterogeneity in study populations and diagnostic approaches, a narrative synthesis was performed. Hospital-based cohorts were analyzed separately to provide contextual information and were not included in prevalence estimates. Results: From 1198 records, four Moroccan studies providing prevalence data on liver fibrosis and cirrhosis were included, primarily involving patients with hepatitis C, HIV, or rheumatoid arthritis. Additionally, three hospital-based cirrhosis cohorts were incorporated for a contextual analysis of disease severity and complications. In total, seven studies were included, with prevalence and hospital-based data analyzed separately to ensure clarity. Conclusions: Current evidence on liver disease in Morocco is limited but suggests a significant burden among high-risk groups. The findings highlight major gaps in national epidemiological data and underscore the urgent need for comprehensive nationwide data and improved diagnostic tools to guide effective screening, prevention, and resource allocation.

22 April 2026 in BioMedInformatics
Verified
Journal Article
Open access
PDF file
YNYoussef Nadir
Youssef Nadir
HEHicham Esselmani
Hicham Esselmani
AOAnass Oukhdouch
Anass Oukhdouch
HNHabiba Nechchadi
Habiba Nechchadi
RERAHMA ENNADI
RAHMA ENNADI
Mohamed MERZOUKIMohamed MERZOUKI
Mohamed MERZOUKI
Background: Liver fibrosis arises from chronic liver injury and remains a major clinical challenge due to its progression toward cirrhosis and hepatocellular carcinoma, as well as the absence of approved antifibrotic therapies. This study aimed to characterize the transcriptomic behavior of the EGR1-FOS axis in liver fibrosis and its evolution into hepatocellular carcinoma, and to identify genes shared between liver fibrosis and cirrhosis. Methods: An integrated bioinformatics approach was applied to GEO transcriptomic datasets. Differentially expressed genes in hepatic fibrosis were identified using GSE139602, GSE84044, and GSE49541, with GSE62232 as control when needed, while GSE14323 and GSE89377 were used to detect genes common with cirrhosis. GEPIA, TIMER, and TISCH2 were used to assess the involvement of the EGR1-FOS axis in hepatocellular carcinoma. External validation of EGR1 expression dynamics and its coregulation with FOS was performed using the GSE135251 dataset. Results: Eleven hub genes were identified, with emphasis on the EGR1-FOS axis. EGR1 expression fluctuated across liver fibrosis etiologies, whereas FOS was predominantly downregulated. A strong correlation between EGR1 and FOS (r = 0.77) was observed, remaining stable across fibrosis stages (all p < 0.001) and in hepatocellular carcinoma (r = 0.698, p = 1.81 × 10−55). Despite overall downregulation, both genes increased progressively with advancing fibrosis (EGR1: p = 0.0008–0.0035; FOS: p = 0.0001–0.0188). Four genes were shared between fibrosis and cirrhosis (SOX9, CD24, CXCR4, and CYP2C19). Conclusions: The EGR1-FOS axis acts as a dynamic regulator of liver fibrosis and its progression, and both this axis and the four shared genes identified may serve as valuable biomarkers and potential therapeutic targets.