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Dive into the research topics where Fernando Kemta Lekpa is active.

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Featured researches published by Fernando Kemta Lekpa.


Joint Bone Spine | 2012

Lack of efficacy of abatacept in axial spondylarthropathies refractory to tumor-necrosis-factor inhibition.

Fernando Kemta Lekpa; Valérie Farrenq; Florence Canoui-Poitrine; Muriel Paul; Xavier Chevalier; Rémy Bruckert; Sylvie Bastuji-Garin; Pascal Claudepierre

OBJECTIVE To assess the efficacy of abatacept in patients with axial spondyloarthropathies who had failed TNFα antagonist therapy. METHODS Consecutive patients fulfilling criteria for active axial spondyloarthropathy, despite at least two previous TNFα antagonists, were treated with abatacept (10mg/kg) given on days 1, 15, and 29, then every 28 days until week 24. Clinical and laboratory outcome criteria were assessed monthly for 6 months. RESULTS Seven patients were treated and followed, all women (median age, 39 years; median disease duration, 12 years), five with ankylosing spondylitis and two with undifferentiated spondyloarthropathy. After 6 months of abatacept therapy, no patient had an at least 50% decrease in the BASDAI; a single patient had an at least 2 cm decrease in the BASDAI (-3.8 cm; -49.3%). No significant changes were observed in pain or patient global assessment scores. Inflammatory back pain persisted in all seven patients. When present, enthesitis improved in most patients. Improvements in spinal mobility measures occurred in two patients. There were no clinically significant adverse events. CONCLUSION A 6-month regimen of abatacept did not meaningfully improve disease activity, function, or other disease parameters in seven patients with axial spondyloarthropathies. These preliminary results do not suggest a strong efficacy of abatacept in axial forms of spondyloarthropathies.


Arthritis Research & Therapy | 2012

Is IL-6 an appropriate target to treat spondyloarthritis patients refractory to anti-TNF therapy? A multicentre retrospective observational study.

Fernando Kemta Lekpa; Cécile Poulain; Daniel Wendling; Martin Soubrier; Michel De Bandt; Jean Marie Berthelot; Philippe Gaudin; Eric Toussirot; Philippe Goupille; Thao Pham; J. Sellam; Rémy Bruckert; Muriel Paul; Valérie Farrenq; Pascal Claudepierre

IntroductionThe aim of this study was to evaluate, under real-life conditions, the safety and efficacy of tocilizumab in patients having failed anti-TNFα therapy for spondyloarthritis.MethodsFrench rheumatologists and internal-medicine practitioners registered on the Club Rhumatismes et Inflammations website were asked to report on patients given tocilizumab (4 or 8 mg/kg) to treat active disease meeting Assessment of SpondyloArthritis International Society (ASAS) criteria for axial or peripheral spondyloarthritis, after anti-TNFα treatment failure. Safety and efficacy after 3 and 6 months were assessed retrospectively using standardised questionnaires.ResultsData were obtained for 21 patients, 13 with axial spondyloarthritis (46% men; median age, 42 years; disease duration, 11 years; HLA-B27-positive, 92.3%) and eight with peripheral spondyloarthritis (25% men; median age, 40 years; disease duration, 10 years; HLA-B27-positive, 62.5%). No patients with axial disease had at least a 20 mm decrease in the BASDAI, nor a BASDAI50 response or major ASAS-endorsed disease activity score improvements after 3 or 6 months; an ASAS-endorsed disease activity score clinically important improvement was noted at month 3 in five of 13 patients and at month 6 in one of four patients. A good DAS28 response was achieved in four patients with peripheral disease, including one in EULAR remission at month 3. Four patients were still taking tocilizumab at month 6, including one in EULAR remission and one with a good DAS28 response. Tocilizumab was well tolerated, with no serious adverse events. Initially elevated acute-phase reactants declined during tocilizumab therapy.ConclusionIn patients having failed anti-TNFα therapy, tocilizumab decreased acute-phase reactants but failed to substantially improve axial spondyloarthritis and was inconsistently effective in peripheral spondyloarthritis.


The Journal of Rheumatology | 2009

Efficacy of Etanercept in Lymphedema Associated with Psoriatic Arthritis

Fernando Kemta Lekpa; Andra Economu-Dubosc; Claire Fevre; Pascal Claudepierre; Xavier Chevalier

Lymphedema is a rare complication of psoriatic arthritis (PsA) whose management is not standardized. We report the prompt resolution of left upper limb lymphedema in a patient with PsA treated with etanercept. A 43-year-old man presented to our department in June 2003 with oligoarthritis affecting the hands, wrists, and elbows. He had been diagnosed 9 years earlier with PsA based on a combination of asymmetric oligoarthritis, dactylitis affecting all digits of the right hand, swan-neck deformity of the fifth fingers of both hands, psoriasis at the navel and nails, and negative tests for rheumatoid factor and anti-cyclic citrullinated peptide (anti-CCP) antibodies. His left forearm was swollen following diagnosis of its rheumatic disease (Figure 1A). The axillary nodes were not enlarged. An erythematous plaque developed a few months later over the swollen forearm. Laboratory evaluation revealed elevated acute-phase reactants [C-reactive protein, 27 mg/l (normal < 5); erythrocyte sedimentation rate, 62 mm/h (normal < 20)]. He was negative for the HLA-B27 antigen. Serological tests for filarial infections were negative. A skin biopsy showed psoriasiform epidermal hyperplasia with marked dermal edema and no evidence of infection. Bilateral sacroiliitis grade 3 was seen on radiographs of the pelvis. Radiographs of the left forearm, elbow, and wrist were normal. Magnetic resonance imaging of the left forearm showed swelling of the subcutaneous fat with normal signal from soft tissues, muscle, and bone. The final diagnosis was left upper limb lymphedema stage II (International Society of Lymphology). Sulfasalazine (SSZ; 2 g/day) prescribed for 7 months and then methotrexate (MTX, up to 20 mg/wk) prescribed during 33 months, both combined with nonsteroidal antiinflammatory drugs (rofecoxib 25 mg/day or flurbiprofen 200 mg/day), failed to adequately control the disease. The oligoarthritis recurred and the lymphedema remained unchanged. Etanercept was administrated subcutaneously 50 mg once a week, initially in combination with MTX 7.5 mg/week. After 8 weeks of treatment, arthritis and laboratory test abnormalities resolved completely. Further, the forearm swelling decreased markedly (Figure 1B). In 2008, after 34 months of treatment, the difference in forearm circumference between the 2 sides at the olecranon was only 0.5 cm. Lymphedema is a rare manifestation of PsA1,2. The upper limbs are the most common sites of involvement, with the right side being preferentially affected1. It could be difficult to link lymphedema to the rheumatic condition. Other causes of upper limb edema such as thrombophlebitis, allergic reaction, septic cellulitis, panniculitis, or edema due to filarial infections should be excluded. The pathogenesis of lymphedema associated with PsA is unclear. Arthritis or tenosynovitis alone does not impair lymphatic drainage2. Lymphedema may be chiefly related to lymphatic function abnormalities, which can be documented by lymphoscintigraphy2-5. The management of lymphedema in patients with chronic inflammatory joint diseases such as PsA is a challenge. Treatments with various degrees of success include corticosteroids injected intravenously4 or intraarticularly3, D-penicillamine5, chloroquine5, SSZ1,6, MTX7, cyclosporine1, and physical therapy1,5. In our patient, the recombinant human soluble receptor for tumor necrosis factor-α (TNF-α), etanercept, was effective, whereas SSZ and MTX were not. Successful treatment with etanercept of lymphedema has been reported in another patient with PsA4. TNF-α antagonists have also been found effective in the treatment of lymphedema associated with other chronic inflammatory diseases including rheumatoid arthritis (etanercept)7, ankylosing spondylitis (infliximab)6, and Crohn’s disease (infliximab)8. The small number of published cases precludes an evaluation of specific effects of each TNF-α antagonist. TNF-α is among the cytokines involved in the pathogenesis of PsA as part of a cascade of proinflammatory molecules that also includes interleukin 8 (IL-8), IL-17, IL-23, and interferon type 19. In a study of TNF-α transgenic mice, TNF-α stimulated osteoclast precursors to produce the vascular endothelial growth factor-C (VEGF-C, a lymphatic growth factor) via the nuclear factor-κB (NF-κB) pathway10. The increase in VEGF-C production led to a significant increase in lymphangiogenesis, an abnormality also seen in the joints of mice with serum-induced arthritis10. TNFα antagonist therapy significantly decreased the joint inflammation in our case, but unfortunately failed to diminish the lymphatic vasculature10.


Presse Medicale | 2013

Isolated camptocormia revealing sporadic late onset nemaline myopathy.

Fernando Kemta Lekpa; Xavier Chevalier; Odile Dubourg; Dalia Dimitri

La Presse Medicale - In Press.Proof corrected by the author Available online since lundi 18 mars 2013


Joint Bone Spine | 2015

Spondyloarthritis: Criteria, limitations, and perspectives throughout history.

Fernando Kemta Lekpa; Daniel Wendling; Pascal Claudepierre

Joint Bone Spine - In Press.Proof corrected by the author Available online since mercredi 30 septembre 2015


Open Access Rheumatology : Research and Reviews | 2018

Refractory relapsing polychondritis: challenges and solutions

Fernando Kemta Lekpa; Xavier Chevalier

Relapsing polychondritis is a severe systemic immune-mediated disease characterized by an episodic and progressive inflammatory condition with progressive destruction of cartilaginous structures. This disease has for nearly a century kept secrets not yet explained. The real incidence and prevalence of this rare disease are unknown. The multiple clinical presentations and episodic nature of relapsing polychondritis cause a significant diagnosis delay. No guidelines for the management of patients with relapsing polychondritis have been validated to date. The challenges remain, both in the understanding of its pathophysiology and diagnosis, evaluation of its activity and prognosis, and its treatment. Possible solutions involve the sharing of data for relapsing polychondritis from worldwide reference centers. Thus, we would be able to evolve toward a better knowledge of its pathophysiology, the publication of new diagnosis criteria, which will include biological markers and imaging findings, the prediction of life-threatening or organ-threatening situations, and the publication of therapeutic evidence-based guidelines after performing at randomized controlled trials.


Saudi Journal of Kidney Diseases and Transplantation | 2017

Prevalence and risk factors of chronic kidney disease in newly diagnosed and untreated hypertensive patients in cameroon: A cross-sectional study

Félicité Kamdem; Fernando Kemta Lekpa; Marie Solange Doualla; Yvette Ngo Nouga; Olivier Donfack Sontsa; Elvis Temfack; Samuel Kingue

Chronic kidney disease (CKD) has emerged as a worldwide problem and is a major cause for comorbidity in hypertensive patients. In an attempt to enhance awareness and to help in establishing preventive measures and care, it is necessary to describe CKD among newly diagnosed and untreated hypertensive patients. We conducted a cross-sectional study to describe the characteristics of CKD among newly diagnosed, treatment naïve, hypertensive patients in four health-care centers in the city of Douala, Cameroon. Sociodemographic and biological data were collected and serum creatinine was measured by enzymatic - colorimetric methods. We calculated estimated glomerular filtration rate (eGFR) by the Modification of Diet in Renal Disease equation and described CKD as eGFR <60 mL/min/1.73 m2. Logistic regression was further used to develop early clues of association. We included 839 newly diagnosed hypertensive treatment naïve patients, among which 412 (49.1%) men. The mean [±standard deviation (SD)] age was 51 (±11) years and was higher among those with CKD. Seventy-six had a family history of hypertension and 65 were known diabetic patients. Mean (±SD) eGFR was 94.4 (±33.3) mL/min and the prevalence of CKD was 12.4% (104/839). From multivariate logistic regression, age >55 years [OR: 5.29 (3.33-8.42)], obesity [OR: 0.15 (0.10-0.26)], kalemia [OR: 1.33 (1.03-1.72)] were independently associated to CKD. CKD is a common condition in newly diagnosed and untreated hypertensive patients in Cameroon. Individuals with hypertension should be carefully evaluated for the presence of CKD, especially those with decreased GFR.


Archives of Cardiovascular Diseases | 2016

Prevalence and factors associated with hyperuricaemia in newly diagnosed and untreated hypertensives in a sub-Saharan African setting

Félicité Kamdem; M.S. Doualla; Fernando Kemta Lekpa; Elvis Temfack; Yvette Ngo Nouga; Olivier Sontsa Donfack; Anastase Dzudie; Samuel Kingue

BACKGROUND Few studies have evaluated the link between hyperuricaemia and cardiovascular disease in sub-Saharan Africa. AIMS To assess the prevalence of and factors associated with hyperuricaemia among newly diagnosed treatment-naïve hypertensive patients in sub-Saharan Africa. METHODS We performed a community-based cross-sectional study from January to December 2012 in Douala, Cameroon (Central Africa). We enrolled newly diagnosed treatment-naïve hypertensive patients, and excluded those with gout or a history of gout. Serum uric acid concentrations were measured by enzymatic colourimetric methods, and hyperuricaemia was defined as a serum uric acid concentration>70IU/mL. Fasting blood sugar concentrations, serum creatinine concentrations and lipid profiles were also measured. Logistic regression was used to study factors associated with hyperuricaemia. RESULTS We included 839 newly diagnosed treatment-naïve hypertensive patients (427 women and 412 men; mean age 51±11 years; mean serum uric acid concentration 60.5±16.5IU/L). The prevalence of hyperuricaemia was 31.8% (95% confidence interval [CI] 28.7-34.9) and did not differ by sex (132 women vs. 135 men; P=0.56). Multivariable logistic regression identified age>55 years (adjusted odds ratio [AOR] 1.65, 95% CI 1.12-2.29), family history of hypertension (AOR 1.65, 95% CI 1.01-2.67), waist circumference>102cm in men or>88cm in women (AOR 1.60, 95% CI 1.12-2.29), low-density lipoprotein cholesterol>1g/L (AOR 1.33, 95% CI 0.97-1.82) and triglycerides>1.5g/L (AOR 1.63, 95% CI 1.01-2.65) as independently associated with hyperuricaemia. CONCLUSION Hyperuricaemia is common among newly diagnosed treatment-naïve hypertensive patients in sub-Saharan Africa and is associated with some components of the metabolic syndrome.


Diabetes and Metabolic Syndrome: Clinical Research and Reviews | 2018

Prevalence and characteristics of metabolic syndrome in gout patients in a hospital setting in sub-Saharan Africa

Marie Doualla-Bija; Yonathan Lobe Batchama; Jude Moutchia-Suh; Vicky Joceline Ama Moor; Félicité Kamdem; Fernando Kemta Lekpa; Henry Luma Namme

BACKGROUND Evidence from epidemiological studies suggests an important association between gout and the metabolic syndrome (MetS). However, to the best of our knowledge, prevalence of metabolic syndrome in gout has not been reported in sub-Saharan African (SSA) settings. OBJECTIVES The aim of this study was to determine the prevalence and characteristics of MetS in gout in a SSA population. METHOD After prior ethical clearance, we carried out a cross-sectional study involving gout patients in a referral hospital in Douala-Cameroon. Metabolic syndrome was defined using International Diabetes Foundation criteria. Associations between variables were assessed using logistic regression.p <  0.05 was considered significant. RESULTS On 174 gout patients (48.3% females) who consented to participate in the study, the median (IQR) age was 55.00 (14.25) years, and the median (IQR) duration of gout was 7.5 (10.0) years. Prevalence of metabolic syndrome was 54.6% (95% CI: 47.9%-62.8%). One hundred and forty-seven (84.5%) participants had central obesity, 62 (35.6%) raised triglycerides, 79 (45.4%) reduced HDL-C, 129 (74.1%) raised blood pressure, and 85 (48.9%) had raised fasting plasma glucose. On logistic regression analyses, gout patients with metabolic syndrome significantly had a higher body mass index (OR: 1.09, 95% CI: 1.02-1.17), and higher levels of serum uric acid (OR: 1.02, 95% CI: 1.01-1.04). CONCLUSIONS About 1 out of every 2 gout patients in this population have metabolic syndrome. These gout patients with metabolic syndrome significantly have a higher body mass index, and higher levels of serum uric acid. Cohort studies are required to clearly establish the direction of the relationship between gout and metabolic syndrome.


Clinical Case Reports | 2018

Multiple cerebral infarction revealing Takayasu's disease: a case report in a 32‐year‐old man from Cameroon, sub‐Saharan Africa

Félicité Kamdem; Caroline Kenmegne; Ba Hamadou; Yacouba Njankouo Mapoure; Fernando Kemta Lekpa; Sidicki Mouliom; Ahmadou Musa Jingi; Henry Namme Luma; Marie Solange Doualla

This case suggests that young patients with few vascular risk factors, and who present with acute stroke syndrome involving more than one vascular territory should be screened for an inflammatory or infectious cause.

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Elvis Temfack

Paris Descartes University

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Daniel Wendling

University of Franche-Comté

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Ba Hamadou

University of Yaoundé

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Henry Luma

University of Yaoundé I

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