Enfermedad tipo influenza en el Hospital Pediátrico de Moa. Enero-agosto 2010 / Influenza-like Illness at the Pediatric Hospital of Moa. January to August 2010

Fundamento: La enfermedad respiratoria producida por el virus de influenza A H1N1, constituyó la primera pandemia de influenza del siglo XXI, provocando gran morbilidad y miles de fallecidos, los daños no fueron mayores gracias a que el virus no mutó a formas más letales, no se desarrolló resistencia al Oseltamivir y la vacuna tuvo una buena compatibilidad con los virus circulantes. Objetivo: Caracterizar los pacientes ingresados por enfermedad tipo influenza (ETI) en el Hospital Pediátrico Universitario de Moa. Métodos: Se realizó un estudio de serie de casos, de 50 pacientes con diagnóstico de ETI, en el periodo comprendido entre el primero de enero y el 31 de agosto del año 2010. Las variables analizadas fueron: edad, sexo, tiempo de comienzo de los síntomas, factores de riesgo, síntomas y signos, comorbilidad asociada, signos radiológicos, evolución y confirmación del virus. Resultados: Existió predominio en el sexo masculino y en el grupo de uno a cuatro años; la fiebre se observó en el 100% de los pacientes; el principal factor de riesgo fue la edad menor de dos años en 27 pacientes (54 %); 39 (78 %) presentaron comorbilidad y/o factores de riesgo, con mayor comorbilidad del asma bronquial en 11 pacientes (22 %). Conclusión: La presencia de comorbilidad y/o factores de riesgo, así como el tiempo de comienzo de los síntomas, se relacionan de forma notable con la aparición de complicaciones en los pacientes con ETI.

Background: The respiratory illness due to the influenza A (H1N1) virus was the first influenza pandemic of the XXI century, causing high morbidity and mortality. The damage was not greater since the virus did not mutate into more lethal strains, no oseltamivir resistance was developed and there was a good match between the vaccine and the circulating viruses. Objective: To characterize patients hospitalized for influenza-like illness (ILI) at the University Pediatric Hospital of Moa. Methods: A case series study including 50 patients diagnosed with ILI was conducted from January 1st to August 31, 2010. The variables analyzed were age, sex, time of onset, risk factors, signs and symptoms, associated comorbidity, radiographic signs as well as virus evolution and confirmation. Results: Predominance of the disease was found in males and in the group aged one to four years; fever was observed in 100% of patients; age under two years was the main risk factor in 27 patients (54 %); 39 patients (78 %) had comorbidity and/or risk factors, with greater comorbidity of bronchial asthma in 11 cases (22 %). Conclusion: Presence of comorbidity and/or risk factors as well as time of onset are significantly related to the occurrence of complications in patients with ILI.

Inhibition of xanthine oxidase by phenolic conjugates of methylated quinic acid.

The caffeoyl conjugates of prenylhydroquinone glucoside and of quinic acid, either in the carboxyl-free or carboxymethyl forms, isolated from Phagnalon rupestre (Asteraceae), showed inhibitory activity on lipid peroxidation induced by Fe 2+/ascorbate and by CCl4/NADPH in rat liver microsomes, with IC50 values ranging from 3 to 11 microM. After having demonstrated their effect on the xanthine oxidase-regulated superoxide production, the active compounds were tested for the direct inhibition of this enzyme. Methylated dicaffeoylquinic conjugates competitively inhibited the enzyme and the highest potency was obtained for the 4,5-diester, with an IC50 value of 3.6 microM, nearly ten times lower than that of the 3,5-analogue. In conclusion, the presence of the caffeoyl moiety is essential for both the antiperoxidative and radical scavenging activities, and the methylation of the quinic carboxyl group enhances the potency on xanthine oxidase inhibitory activity.

Effects of caffeoyl conjugates of isoprenyl-hydroquinone glucoside and quinic acid on leukocyte function.

The activity of three prenylhydroquinone glucosides (1-3) and four caffeoylquinic esters (4-7), obtained from Phagnalon rupestre, on elastase release, myeloperoxidase activity and superoxide and leukotriene B(4) production from polymorphonuclear leukocytes was determined. 4,5-Dicaffeoylquinic acid strongly inhibited elastase release with an IC(50) value of 4.8 microM. Methylated caffeoylquinic derivatives were the most potent inhibitors of myeloperoxidase (IC(50) near 60 microM), whereas both methylated and free carboxyl isomers inhibited superoxide production with similar potency (IC(50) between 27 and 42 microM). The monocaffeoyl conjugate of prenylhydroquinone glucoside (3), the most potent inhibitor of leukotriene B(4) production (IC(50) = 33 microM), possesses a mixed hydroquinone-caffeoyl character that could be considered as a potential anti-inflammatory entity.

Phagnalon rupestre as a source of compounds active on contact hypersensitivity.

The effect of Phagnalon rupestre MeOH extract on dinitrofluorobenzene- and sheep red blood cells-induced hypersensitivity was investigated. Eight compounds were identified: three dimethylallyl-hydroquinone glucosides (1 - 3), 3,5- and 4,5-di-O-caffeoylquinic acid methyl esters (4 and 5), their free carboxyl analogues (6 and 7), and luteolin 7-O-beta-glucoside (8). All were tested for dinitrofluorobenzene-induced contact hypersensitivity inhibitory activity. Flavonoid 8 was the most active (49 % and 79 % inhibition at 24 and 96 h, respectively). The hydroquinones 1, 2 and 3 were effective at 96 h after challenge (62 %, 73 % and 60 % inhibition, respectively), while some of the dicaffeoylquinic derivatives (4 and 7) produced slightly lower reduction of the inflammatory reaction.

Phenolic glycosides from Phagnalon rupestre.

Analysis of the butanol-soluble fraction from the methanolic extract of the aerial parts of Phagnalon rupestre (Asteraceae) has led to the isolation of seven phenolic compounds. Three have been identified on the basis of their NMR spectra as new natural compounds: the lignan 7,7'-bis-(4-hydroxy-3,5-dimethoxyphenyl)-8,8'-dihydroxymethyl-tetrahydrofuran-4-O-beta-glucopyranoside (1), the prenylhydroquinone glycoside 1-O-beta-glucopyranosyl-1,4-dihydroxy-2-(3'-hydroxy-3'-methylbutyl) benzene (2) and the acetophenone glycoside 12-O-beta-glucopyranosyl-9beta,12-dihydroxytremetone (3). The known flavonoids apigenin-7-O-beta-glucoside, luteolin-7-O-beta-glucoside, luteolin-7-O-beta-glucuronide and the acetophenone picein were also isolated.