Necrotising sinusitis with orbital complication in patient with macrophage activation syndrome (MAS)

Background: Macrophage activation syndrome (MAC) is a potentially fatal clinical-laboratory syndrome of uncontrolled hyperinflammation arising as a result of hereditary or acquired immune-mediated processes of cellular overactivation and nonmalignant proliferation of tissue macrophages/histiocytes, which can cause multiorgan failure.Case report: We present a clinical case of 15-years old child, who was diagnosed with juvenile idiopathic arthritis in 2019. The disease started with macrophage activation syndrome. In the next years the child had multiple hospitalizations in the Pediatrics clinic, but in the course of the disease it developed the picture of severe necrotic pansinuitis with an orbital complication, which required an immediate surgical intervention. Ever since the child had an ongoing necrotizing process in the area of the nasal passages, sinuses, upper jaw and hard palate. Other complications were breakthrough of the hard palate, loss of healthy teeth from the upper dentition and creation of direct communication between the oral cavity and the left maxillary sinus.Conclusions: The diagnosis of MAS is difficult to make, but increased awareness of this disease is an essential for its recognition. The struggle with autoimmune diseases often lasts for years with periods of exacerbation and remission of symptoms. Complications related to them can affect different organs and systems and require interdisciplinary approach

Structure-Activity Relationships of N-Cinnamoyl and Hydroxycinnamoyl Amides on α-Glucosidase Inhibition

Currently, there is an increasing interest towards α-glucosidase inhibition of various diseases including diabetes mellitus type 2, cancer, HIV, and B- and C-type viral hepatitis. Cinnamic acid derivatives have been shown to be potentially valuable as a new group of α-glucosidase inhibitors. Therefore, herein, the α-glucosidase inhibitory activity of trans-N-cinnamoyl and hydroxycinnamoyl amides was studied in vitro. Results revealed that the tested hydroxycinnamoyl amides (1–16) inhibited a-glucosidase with IC50s ranging between 0.76 and 355.1 μg/ml. Compounds 1, 2, 5, 6, 9, 14, and 15 showed significant inhibition of yeast α-glucosidase, being even more potent ones than the used positive inhibitor acarbose (IC50=2.50±0.21 μg/ml)

Central Nervous System Involvement in Henoch-Schonlein Purpura in Children and Adolescents

Central nervous system (CNS) involvement in Henoch-Schonlein purpura (HSP) is rare but poses diagnostic difficulties. The aim of the study was to establish the frequency of CNS involvement in HSP, to analyze its clinical characteristics and do a literature review. Medical files of patients with HSP admitted at the Department of Pediatrics, Plovdiv, were studied retrospectively for a five-year period (2009–2013). Diagnosis was based on the American College of Rheumatology criteria. Out of 112 children with HSP 1 case (0.9%) had CNS involvement presenting as Posterior Reversible Encephalopathy Syndrome (PRES), which may be a result of CNS vasculitis or arterial hypertension. It was an 8-year-old girl with atypical HSP which started with abdominal pain requiring surgery. On the third day after the operation a transient macular rash and arterial hypertension appeared, followed by visual disturbances, hemiconvulsive epileptic seizures, postictal hemiparesis, and confusion. Head CT showed occipital hypodense lesions and MRT-T2 hyperintense lesion in the left occipital lobe. The patient experienced a second similar episode after 2 weeks when palpable purpura had also appeared. Neurological symptoms and MRI resolved completely. HSP can be an etiological factor for PRES in childhood. Although PRES is a rare complication of HSP, clinicians must be aware of it and avoid diagnostic and therapeutic delays

Synthesis, molecular docking, and neuroprotective effect of 2-methylcinnamic acid amide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) - an induced Parkinson’s disease model

Parkinson’s disease (PD) has emerged as the second most common form of human neurodegenerative disorders. However, due to the severe side effects of the current antiparkinsonian drugs, the design of novel and safe compounds is a hot topic amongst the medicinal chemistry community. Herein, a convenient peptide method, TBTU (O-(benzotriazole-1-yl)-N,N,N′,N′-tetramethyluronium tetrafluoroborate), was used for the synthesis of the amide (E)-N-(2-methylcinnamoyl)-amantadine (CA(2-Me)-Am3)) derived from amantadine and 2-methylcinnamic acid. The obtained hybrid was studied for its antiparkinsonian activity in an experimental model of PD induced by MPTP. Mice (C57BL/6,male, 8 weeks old) were divided into four groups as follows: (1) the control, treated with normal saline (i.p.) for 12 consecutive days(2) MPTP (30 mg/kg/day, i.p.), applied daily for 5 consecutive days(3) MPTP + CA(2-Me)-Am, applied for 12 consecutive days, 5 days simultaneously with MPTP and 7 days after MPTP(4) CA(2-Me)-Am +oleanoic acid (OA), applied daily for 12 consecutive days. Neurobehavioral parameters in all experimental groups of mice were evaluated by rotarod test and passive avoidance test. Our experimental data showed that CA(2-Me)-Am in parkinsonian mice significantly restored memory performance, while neuromuscular coordination approached the control level, indicating the ameliorating effects of the new compound. In conclusion, the newly synthesized hybrid might be a promising agent for treating motor disturbances and cognitive impairment in experimental PD

Synthesis, Molecular Docking, and Neuroprotective Effect of 2-Methylcinnamic Acid Amide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)—An Induced Parkinson’s Disease Model

Parkinson’s disease (PD) has emerged as the second most common form of human neurodegenerative disorders. However, due to the severe side effects of the current antiparkinsonian drugs, the design of novel and safe compounds is a hot topic amongst the medicinal chemistry community. Herein, a convenient peptide method, TBTU (O-(benzotriazole-1-yl)-N,N,N′,N′-tetramethyluronium tetrafluoroborate), was used for the synthesis of the amide (E)-N-(2-methylcinnamoyl)-amantadine (CA(2-Me)-Am; 3)) derived from amantadine and 2-methylcinnamic acid. The obtained hybrid was studied for its antiparkinsonian activity in an experimental model of PD induced by MPTP. Mice (C57BL/6,male, 8 weeks old) were divided into four groups as follows: (1) the control, treated with normal saline (i.p.) for 12 consecutive days; (2) MPTP (30 mg/kg/day, i.p.), applied daily for 5 consecutive days; (3) MPTP + CA(2-Me)-Am, applied for 12 consecutive days, 5 days simultaneously with MPTP and 7 days after MPTP; (4) CA(2-Me)-Am +oleanoic acid (OA), applied daily for 12 consecutive days. Neurobehavioral parameters in all experimental groups of mice were evaluated by rotarod test and passive avoidance test. Our experimental data showed that CA(2-Me)-Am in parkinsonian mice significantly restored memory performance, while neuromuscular coordination approached the control level, indicating the ameliorating effects of the new compound. In conclusion, the newly synthesized hybrid might be a promising agent for treating motor disturbances and cognitive impairment in experimental PD