Pressure ulcer (PU) remains a common worldwide problem in all health care settings, it is synonymous with suffering. PU is a complex disease that is dependent on a number of interrelated factors. It involves multiple mechanisms such as physiological risk factors, chronic inflammation, oxidant–antioxidant imbalance and proteolytic attack on extracellular matrix by matrix metalloproteinases (MMP). Therefore, we propose that these wounds lead to molecular variations that can be detected by assessing biomarkers. In this study, we aimed to evaluate the major clinical elements and biological scars in Tunisian patients suffering from PU. Consistently, non-healing wound remains a challenging clinical problem. The complex challenges of the wound environment, involving nutrient deficiencies, bacterial infection, as well as the critical role played by inflammatory cells, should be considered because of their negative impact on wound healing. In addition, an imbalance between pro-oxidants and antioxidant systems seems to be more aggravated in patients with PU compared to healthy subjects. Of interest, this study provides further evidence to support a core role of the biological activity of MMP-9 in the pathogenesis of PU and indicates that the MMP9-1562 C/T (rs 3918242) functional polymorphism is associated with protection against this disease.
BackgroundAcute aortic dissection is an extreme emergency that is generally manifested by violent chest pain irradiating to a patient’s back and abdomen. Paraplegia due to spinal cord ischemia and infarction as a presenting manifestation of aortic dissection has been found in 2 to 5 % of patients. However, painless paraplegia is exceedingly rare and limited to a few case reports in the literature. We describe a new case with this unusual presentation of aortic dissection and here we emphasize that this condition must be considered in all patients with painless paraplegia.Case presentationA 70-year-old Arab man with no previous known medical or surgical conditions was hospitalized for brutal heaviness of his lower limbs associated to urinary retention. A neurological examination revealed flaccid paraplegia without sensory disorder. His blood pressure and his pulse were in normal ranges. He was afebrile. His peripheral pulses were not checked. Laboratory investigations eliminated multiple organ failure. Spinal magnetic resonance imaging realized in emergency was normal. He had a cardiopulmonary arrest 1 day after his hospitalization. His autopsy report concluded a type A aortic dissection with an intimal tear at his aortic isthmus with intrapericardial rupture and extension to his intercostal and lumbar arteries.ConclusionsAcute aortic dissection is an extreme emergency that can lead to death unless there is an early diagnosis. It must be considered in any patient with paraplegia even painless. Clinical examination has a major role to play in diagnosing this condition. Apart from the neurological examination, palpation of peripheral pulses and blood pressure measurements in all four limbs is of paramount importance. Then further investigations must be carried out consisting of aortic angiography by computed tomography or by magnetic resonance imaging.
Woodhouse-Sakati syndrome (WSS) is an infrequent autosomal recessive condition characterized by progressive extrapyramidal signs, mental retardation, hypogonadism, alopecia, and diabetes mellitus. This syndrome belongs to a heterogeneous group of inherited neurodegenerative disorders characterized iron accumulation in the brain, and it is caused by mutations of the C2orf37 gene. We report the first Tunisian family with two affected sisters presenting with a phenotype suggestive of WSS. We examined the index patient presenting with movement disorders and mental retardation and then searched for similar cases in her family, which identified a sister with similar signs. We performed a genetic study that confirmed the diagnosis and revealed a c.436delC mutation of the C2orf37 gene. Therefore, WSS is an important consideration in patients presenting with movement disorders and intellectual disability. A high consanguinity contributes to the clustering of such rare autosomal recessive syndromes.
This study aimed to investigate whether the single nucleotide polymorphism C677T (rs1801133) of the methylene-tetrahydrofolate reductase (MTHFR) gene was associated with the risk of coronary artery disease (CAD) and circulating homocysteine (Hcy) levels in Tunisian population. 310 angiografically diagnosed CAD patients and 210 controls were enrolled in this study. The MTHFR C677T (rs1801133) polymorphism was genotyped, and the Hcy concentrations were measured. The severity of CAD was evaluated using the Gensini scoring system. Compared to the CC genotype, the TT genotype confers a higher risk for CAD severity with an OR = 9.07 and 95% CI = 3.78–21.8. The T allele was the predisposing allele for CAD and that it was probably associated with CAD severity. The area under the ROC curve for Hcy was 0.764 (95% CI 0.660 to 0.868, p = 0.001). The receiver operating characteristics curve (ROC) for Hcy showed its useful prediction of CAD. Hcy levels were not significantly associated with CAD severity expressed by Gensini Score (GS). The MTHFR C677T (rs1801133) polymorphism influences circulating Hcy levels. The MTHFR C677T polymorphism and hyperhomocysteinemia could have an important role in the prediction of the presence and not the severity expressed by GS of CAD.
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