Purpose: Loratadine is used as antihistaminic without side effects in nervous systems. This drug is a weak base and it is absorbed from the intestine. The nitrogen of the pyridine ring is protonated in the stomach affecting the oral bioavailability. The aim of this paper was obtaining, characterize and evaluate the release profiles and the stability of a gastroresistant loratadine nanosuspension. Methods: The nanosuspension was prepared by the solvent displacement evaporation method, using three different polymers (Eudragit® L 100 55, Kollicoat® MAE 100P and PEG 4000) and Polysorbate 80. Dynamic Light Scattering was used for evaluating the particle size (PS), zeta potential, and conductivity of the nanosuspension. Loratadine release profiles were evaluated in simulated gastrointestinal fluids. The shelf and accelerated stability were assessed during three months. Results: Nanosuspension particle size was 45.94 ± 0.50 nm, with a low polydispersion index (PdI, 0.300). Kollicoat® MAE 100P produced a hard and flexible coating layer. In simulated intestinal fluids, the 100 percent of loratadine was released in 40 min, while in simulated stomach fluids the release was lesser than 5%. Nanosuspension presented a good physicochemical stability showing a reduction in PS and PdI after three months (43.29 ± 0.16 and 0.250; respectively). Conclusions: A promissory loratadine nanosuspension for loratadine intestinal delivery was obtained, by using a low energy method, which is an advantage for a possible scale up for practical purpose.

The aim of this study was to determine whether loratadine, a selective inverse agonist of peripheral histamine H1 receptors, would reduce emotional blushing. Loratadine (10 mg) or placebo was administered orally one hour before 31 healthy participants sang a children's nursery rhyme to evoke embarrassment and blushing. Skin blood flow was monitored via a laser Doppler probe attached to the cheek. Increases in facial blood flow while participants sang were greater in the loratadine than the placebo group (mean increase ± standard deviation 71 ± 52% in the loratadine group versus 35 ± 37%, p = .036). However, perceptions of blushing were similar in both groups. These findings suggest that loratadine augmented blushing rather than inhibiting it. Thus, histamine released during blushing may inhibit acute increases in facial blood flow by evoking H1 receptor-mediated vasoconstriction.

We report a rare case of dermatophyte infection of the glabrous skin (Tinea corporis) caused by Nannizzia gypsea (formerly Microsporum gypseum). A 22-year-old Malagasy female who reported close contact reportedly with cats, presented a single round lesion with a peripheral, active, squamous and pruriginous inflammatory bead. Morphologic species identification was confirmed by sequencing the internal transcribed spacer (ITS) region of the genome. Specific treatment with oral loratadine and topical miconazole cream was effective.

Fixed drug eruption is a delayed type hypersensitivity reaction to a drug seen most frequently with antibiotics such as tetracyclines, sulfonamides, and NSAIDs such as naproxen and ibuprofen. Although H1-antihistamines rarely elicit cutaneous adverse effects, there have been a few reports in the literature implicating them in causing fixed drug eruption, particularly the piperazine derivatives (hydroxyzine, cetirizine, levocetirizine), and loratadine. However, cutaneous drug reactions with the alkylamine derivatives like pheniramine maleate are extremely uncommon and fixed drug eruptions have not been reported with any of the alkylamine antihistamines to date. We herein report a case of multifocal bullous fixed drug eruption following ingestion of pheniramine maleate.

A validation for the use of model-based melt viscosity in hot-melt extrusion numerical simulations was presented. Here, the melt viscosity of an amorphous solid dispersion (ASD) was calculated by using its glass transition temperature (Tg) and the rheological flow profile of the pure polymeric matrix. All further required physical properties were taken from the pure polymer. For forming the ASDs, four active pharmaceutical ingredients (APIs), that had not been considered in first place to establish the correlation between Tg and melt viscosity were examined. The ASDs were characterized in terms of density, specific heat capacity, melt rheology, API solubility in the polymeric matrix, and deviation from the Couchman⁻Karasz fit to, identify the influencing factors of the accuracy of the simulation using model-based melt viscosity. Furthermore, the energy consumption of the hot-melt extrusion (HME) experiments, conventional simulation, and simulation using model-based melt viscosity were compared. It was shown, with few exceptions, that the use of model-based melt viscosity in terms of the HME simulation did not reduce the accuracy of the computation outcome. The commercial one-dimensional (1D) simulation software Ludovic® was used to conduct all of the numerical computation. As model excipients, vinylpyrrolidone-vinyl acetate copolymer (COP) in combination with four APIs (celecoxib, loratadine, naproxen, and praziquantel) were investigated to form the ASDs.

Peritoneal dialysis (PD)-related peritonitis is recognized as a common complication of peritoneal dialysis. Eosinophilic peritonitis is a rare type of non-infection PD-related peritonitis. Eosinophilic peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients was first reported in 1967. The cause of eosinophilic peritonitis is obscure, however it may be related to some etiologies: (1) hypersensitivity to PD materials, including catheter or dialysate; (2) bacteria, fungal or mycobacterium tuberculosis infection. Clinical investigations include asymptomatic cloudy PD effluent, fever, abdominal pain and eosinophil count elevate in PD effluent. Eosinophilic peritonitis is usually mild and self-limited. With the development of PD, more eosinophilic peritonitis cases and researches were reported. Here, we report a patient on CAPD with eosinophilic peritonitis. A 71-year-old female patient developed end-stage renal disease for 4 years and underwent CAPD (2 000 mL of 1.5% dialysis solution with four exchanges daily) for 5 months. With a history of unclean food, she was hospitalized for complaints of diarrhea, fever and cloudy peritoneal effluent for 10 days. Dialysis effluent showed an elevated white blood cell (WBC) count of 1 980 cell/mm3, with 60% polymorphonuclear cells. She was diagnosed as PD-related peritonitis, and therapy was initiated with intraperitoneal ceftazidime 1 g once a day and vancomycin 500 mg every other day. She was admitted to the hospital as the symptoms were not relieved. Her peripheral blood cell count showed a total WBC count of 6 940 cells/mm3, 36.8% eosinophil. Her PD effluent analysis showed turbidity, total WBC count of 1 480 cells/mm3, and 83% polymorphonuclear cells. Her dialysate bacteria culture, fungus culture, polymerase chain reaction for Mycobacterium tuberculosis (TB-PCR), acid-fast stain were all negative. On admission day 4, the treatments were changed to levofloxacin 200 mg once a day and vancomycin 500 mg every other day. After two weeks of antibiotics treatment, patient's symptoms were not completely improved and her dialysis effluent remained cloudy. Her blood eosinophil count elevated to 36.8%，eosinophil proportion in PD effluent>90% and PD effluent pathological findings showed eosinophil>90%. Eosinophilic peritonitis was diagnosed and a decision was made to give loratadine daily dose of 10 mg orally. The possible reasons might be the patient's allergy to some components of PD solution or connection systems in the beginning of PD, and this bacterial peritonitis episode, as well as the application of vancomycin, might lead to the fact that eosinophilic peritonitis acutely developed. For there was no improvement in clinical symptoms, loratadine was stopped, and the patient was discharged 18 days later, and received follow-up closely. Two months later, eosinophil count in blood and PD fluid decreased to normal range with no symptom. This case reminds us that in any PD-related peritonitis patient with prolonged symptoms after appropriate antibiotic therapy, and typical clinical symptoms, the diagnosis of eosinophilic peritonitis should be considered. For the count and percentage of eosinophils are not routinely reported in most laboratories, doctors need to contact the department of laboratory and the department of pathology, to confirm the cell count and proportion of eosinophils in dialysis effluent, so as to make the definite diagnosis, which can not only avoid antibiotics overuse, but also avoid antibiotics-induced eosinophilic peritonitis (such as vancomycin).

Oxidized LDL (ox-LDL) is one of the major risk factors of atherosclerosis. Endothelial dysfunction caused by ox-LDL is an early event in the pathogenesis of cardiovascular diseases. Preclinical studies have been performed to explore efficient means of preventing endothelial abnormalities. In this study, we revealed that loratadine, a histamine H1 type receptor specific antagonist, possesses a protective effect by relieving ox-LDL-induced endothelial inflammation. Treatment of endothelial cells with ox-LDL induces expression of the H1 receptor. The presence of loratadine in endothelial culture efficiently suppressed ox-LDL-induced attachment of monocytes to endothelial cells, production of ROS and vascular adhesion molecules, and induction cytokines including VCAM-1, E-selectin, TNF-α, IL-6 and IL-8. Mechanistically, we show that loratadine potently blocks ox-LDL-induced JNK activation as well as the AP-1 and NF-κB signaling pathways. Collectively, our data disclose a new role for loratadine in endothelial protection.

Bacteriocinogenic Enterococcus hirae ST57ACC and Pediococcus pentosaceus ST65ACC strains, previously isolated from artisanal cheese, were evaluated for their safety with the aim to determine whether they could be used as beneficial strains, especially in the control of Listeria monocytogenes. Both isolates survived simulated gastrointestinal conditions and showed high levels of auto- and co-aggregation with L. monocytogenes, although the hydrophobicity of cells varied. Using the agar-spot test with 33 commercial drugs from different groups, only anti-inflammatory drugs and drugs containing loratadine and propranolol hydrochloride were able to affect the growth of the tested strains. Both strains were resistant to 3 out of 11 antibiotics tested by the disc diffusion method, and low frequencies of antibiotic resistance-encoding genes were observed by PCR analysis. Tested strains neither presented biogenic amine-related genes nor produced these substances. Aside from some antibiotic resistance characteristics, the tested strains were considered safe as they lack other virulence-related genes. E. hirae ST57ACC and P. pentosaceus ST65ACC both presented beneficial properties, particularly their ability to survive gastrointestinal conditions and to aggregate with L. monocytogenes, which can facilitate the elimination of this pathogen. Further studies should be conducted to better understand these interactions.

Loratadine, an over-the-counter antihistamine medication, has two known monotropically related polymorphs, both of which feature disorder. A combined experimental and computational approach using variable temperature single crystal X-ray diffraction (VT-SCXRD) analysis and dispersion corrected density functional theory (DFT-D) reveals that the nature of the disorder in each form is markedly different and cannot be described by a simple isolated-site model with thermally populated conformations in either of the two cases. In Form I, the ethyl carbamate functionality adopts two different configurations, with adjacent moieties interacting along one-dimensional chains. The most stable arrangement features alternating configurations, but because of the low energetic cost of stacking faults, the domain sizes are short and an average crystal structure is observed experimentally. The configurational free energy of the disordered structure is lower than the energy of the two corresponding ordered crystal structures, but the energy decrease is dominated by the lower lattice energy of the alternating arrangement with a small entropic contribution. In Form II, the flexible cycloheptane bridge adopts two different configurations. The disorder is not an equilibrium property but is instead frozen-in during the crystallisation process. The configurational free energy of the disordered structure falls in between the lattice energies of the two corresponding ordered structures. The two ordered components of each disordered structure are all found in a crystal structure prediction (CSP) study with the GRACE programme. However, the experimentally observed stability relationship is only reproduced when the energy contribution of disorder is taken into account. The disordered model of Form I is found to be lower in energy than all the other predicted structures and there is no indication of a missing, thermodynamically more stable, form. The case of loratadine demonstrates that experimentally observed disorder close to 50/50 does not necessarily correspond to a free energy decrease by kT ln 2.