Efficacy of mometasone furoate microemulsion in the treatment of erosive-ulcerative oral lichen planus: pilot study.

BACKGROUND: Oral lichen planus (OLP) is a frequent immunological chronic disease, having different clinical forms: asymptomatic and symptomatic. Symptomatic OLP has been palliated with topical corticosteroids with different levels of efficacy and safety. The purpose of this pilot phase II clinical trial was to determine the efficacy of mometasone furoate microemulsion upon the symptoms and signs of erosive-ulcerative OLP. METHODS: Forty-nine patients with clinical and histologically confirmed erosive-ulcerative OLP were enrolled in this study (36 women and 13 men). Their average age was 56.4 years (from 28 to 78). The treatment consisted of 0.1% mometasone furoate microemulsion mouthwash three times a day over 30 days. Pain, erythema and ulceration were assessed after 15 and 30 days of treatment. The data was processed and statistically analysed by student's t-test for paired samples. RESULTS: Mometasone caused a statistically significant reduction in pain (3.58 vs. 0.65, P = 0.0000). Treatment significantly reduced the surface area of erythema (155.2 vs. 21.9 mm(2), P = 0.0001) and ulceration (30.7 vs. 7.3 mm(2), P = 0.0000). None of these patients suffered severe adverse effects. CONCLUSIONS: Mometasone furoate microemulsion is a safe and effective therapy in the treatment of symptomatic erosive-ulcerative OLP.

Hipotensión refractaria y sostenida durante una anestesia general asociada al tratamiento crónico con inhibidores de la enzima conversiva de la angiotensina / Sustained, refractory hypotension during general anesthesia of a patient chronically treated with angiotensin-converting enzyme inhibitors

El manejo perioperatorio de los fármacos inhibidores de la enzima conversiva de la angiotensina (IECA) es controvertido por su asociación a episodios hipotensivos durante la inducción y el mantenimiento anestésico.Una paciente de 71 años fue programada para lobectomía tiroidea por nódulo tiroideo no funcionante; tenía antecedentes de hipertensión arterial y estaba en tratamiento crónico con un IECA, que se mantuvo hasta la mañana de la intervención. Tras la inducción anestésica la paciente desarrolló un cuadro de hipotensión arterial que no respondió a fluidoterapia con cristaloides y se fue acentuando, a pesar de la administración de una solución coloide tipo gelatina (Gelafundina®). No hubo respuesta a la efedrina ni a la dopamina, precisando para su estabilización adrenalina en perfusión continua durante 12 h. La evolución de la paciente fue satisfactoria y la recuperación, completa sin secuelas.Se comentan las implicaciones anestésicas del tratamiento crónico con fármacos IECA y la posible repercusión hemodinámica que puede suponer su asociación a soluciones tipo gelatina o albúmina humana (AU)

Mechanisms of gastroprotection by transdermal nitroglycerin in the rat.

Nitric oxide (NO) donors prevent experimentally-induced gastric mucosal damage, but their clinical utility is limited by short duration of action or unsuitability of the pharmaceutical form employed. This study analyses the gastroprotection elicited by a clinically used mode of continuous administration of an NO donor, namely the nitroglycerin patch. Application to rats of a transdermal patch that releases doses of nitroglycerin comparable to those used in man (40, 80, 160 and 400 ng min(-1) rat(-1)) reduced gastric damage induced by indomethacin (25 mg kg(-1), p.o. or s.c.). The nitroglycerin patch (160 ng min(-1) rat(-1)) also diminished damage by oral administration (1 ml) of acidified bile salts (100 mg kg(-1) taurocholic acid in 150 mM HCl) or 50% ethanol. Transdermal nitroglycerin (160 ng min(-1) rat(-1)) did not influence basal gastric blood flow, as measured by lasser-doppler flowmetry, but prevented its reduction by indomethacin. Transdermal nitroglycerin (160 ng min(-1) rat(-1)) prevented in vivo leukocyte rolling and adherence in the rat mesentery microvessels superfused with indomethacin, as evaluated by intravital microscopy. The transdermal nitroglycerin patch protects the gastric mucosa from damage by mechanisms that involve maintenance of mucosal blood flow and reduction of leukocyte-endothelial cell interaction.

Omeprazole and ranitidine in long-term treatment of duodenal ulcer: a double-blind comparison of length of time in remission.

In most patients duodenal ulcer is a chronic relapsing disease. If no active maintenance treatment or eradication therapy is given after healing, around 70-100% of patients have a relapse during the first year. We conducted a double-blind multicenter study in 472 patients with duodenal ulcer. They were treated with omeprazole 20 mg every morning for four or eight weeks and when healed were randomly allocated to maintenance treatment with either omeprazole 20 mg every morning or ranitidine 150 mg at bedtime for up to six months. The patients were assessed by endoscopy at monthly intervals until healing occurred. Thereafter scheduled endoscopy was carried out after 1, 3, and 6 months of maintenance treatment or immediately in the event of a suspected relapse. Healing status (intention to treat approach) was 87% at four weeks and 93% at eight weeks. At six months the estimated remission rate was 90% for omeprazole and 82% for ranitidine (P = 0.03, 95% CI 1-15%). The incidence of adverse events was similar during the two maintenance treatments. Treatment with omeprazole 20 mg every morning maintained significantly more patients in remission than treatment with ranitidine 150 mg at bedtime.

In vitro activity of omeprazole in combination with several antimicrobial agents against clinical isolates of Helicobacter pylori.

An agar dilution checkerboard method was used to evaluate the in vitro activity of omeprazole combined with clarithromycin, amoxicillin, and ceftibuten, respectively, against clinical isolates of Helicobacter pylori. Mueller-Hinton agar plus 5% horse blood, an inoculum of 10(6) cfu/ml, and incubation of 72 h in a CO2 atmosphere were used. With the omeprazole and clarithromycin combination, synergism was observed in 51.5% and partial synergism in 39.3% of 33 strains; with omeprazole and amoxicillin, synergism was observed in 3% and partial synergism in 60.6% of 33 strains; and with omeprazole and ceftibuten, synergism was observed in 33.3% and partial synergism in 50% of 24 strains. Antagonism between omeprazole and each antibiotic was exhibited in 0%, 6.1%, and 4.1% of these groups of strains, respectively. Of the antibiotic combinations tested, omeprazole plus clarithromycin exhibited synergism (partial or total) in the highest percentage of strains.

[Omeprazole and maintenance treatment: new concepts for traditional therapies?]. / Omeprazol y el tratamiento de mantenimiento: nuevos conceptos en terapias tradicionales?

Duodenal ulcer and reflux oesophagitis are a chronic diseases characterized by remission and relapses. If no active prophylactic treatment is given after healing around 70-100% of the patients have a relapse during the first year. Various therapeutic strategies have been suggested to maintain the disease in remission. Continuous maintenance treatment with H2 blockers has proved to be effective in reducing the spontaneous recurrence rate of duodenal ulcers but the results are disappointing in reflux oesophagitis. Initials studies on different treatment regimen of omeprazole for maintenance treatment have indicated promising results. The efficacy and safety of this drug have been evaluated in this article.

[Comparative multicentric study of omeprazole versus ranitidine in the treatment of duodenal ulcer]. / Estudio comparativo multicéntrico de omeprazol frente a ranitidina en el tratamiento de la úlcera duodenal.

A total of 158 patients, aged 19-78 years and with endoscopically verified duodenal ulcer of at least 5 mm in maximum diameter were recruited. 79 patients were randomised to treatment with omeprazole, a proton-pump inhibitor of the parietal cell, and 79 patients were treated with ranitidine. This double blind study is the first clinical trial with omeprazole in Spain. Using "intention to treat" analysis there was no difference in healing rates at 2 weeks between the omeprazole group (70%) and the ranitidine group (59%) with p = 0.13. At four weeks, however, omeprazole healed significantly more patients (92%) than ranitidine (76%) with p = 0.005. Using per protocol analysis a similar result was obtained with no significant difference between omeprazole (71%) and ranitidine (63%) at two weeks (p = 0.3) but significantly greater healing on omeprazole at 4 weeks (97%) compared with ranitidine (83%) with p = 0.008. The influence of additional prognostic factors was assessed using a multivariate analysis. At two and four weeks, there was a significant effect of ulcer size on healing rate. At four weeks there was also a significant effect of treatment. Symptom relief was rapid in both treatments but the omeprazole group had significantly fewer days of pain and better patient's overall evaluation than ranitidine group. No serious adverse events were reported. In conclusion omeprazole healed significantly more duodenal ulcers than ranitidine and symptom relief was more rapid during omeprazole therapy.

Late cases of toxic oil syndrome: evidence that the aetiological agent persisted in oil stored for up to one year.

The symptoms of toxic oil syndrome (TOS), an epidemic that occurred in central and north-western Spain, developed in the great majority of patients during May or June 1981. We now describe the clinical and epidemiological data of five patients with TOS whose onset of symptoms was considerably later than the great majority of cases. In June 1982, one person became symptomatic as a result of consuming a suspect oil two months earlier. Four members of a family that started consuming a suspect oil in November 1981 became ill in December 1981. These data indicate that the aetiological agent of TOS persisted in stored oil for periods as long as one year. The apparent stability of the TOS aetiological agent increases the likelihood of its continued presence in significant concentrations in oils that have been stored since 1981. Thus, the use of such oils in further in vivo and in vitro toxicological studies may yet lead to the isolation and identification of the causal agent of TOS.

The association of oil ingestion with toxic oil syndrome in two convents.

The authors studied the pattern of occurrence of toxic oil syndrome, a previously undescribed disease that occurred in Spain in epidemic form in 1981, in two convents in Madrid. In one convent, the disease affected 66% of 35 novices and nuns who ingested oil from a suspect source, but none of 56 laywomen who ate the same meals but used a different type of oil. In the second convent, in which nuns were also exposed but laywomen were not, 98% of 43 nuns developed toxic oil syndrome compared with none of 70 laywomen. These findings support the hypothesis that a food oil transmitted the etiologic agent of toxic oil syndrome.

Toxic-oil syndrome: case reports associated with the ITH oil refinery in Sevilla.

Toxic-oil syndrome (TOS), a new disease that occurred in epidemic form in Spain in 1981, has been associated with the ingestion of unlabelled oil bought principally from travelling salesmen. Chemical analysis of oils taken from ill families has shown them to consist of varying proportions of different vegetable oils and animal fats, often showing chemical evidence of prior treatment with aniline. We investigated the unusual circumstances surrounding the reported occurrence of three TOS cases in two families in Sevilla, a city located far away (approximately 300 km) from the group of 14 provinces in central and northwestern Spain where 99% of the TOS cases occurred. Each case we investigated fitted the clinical picture of TOS and was not consistent with any other diagnosis. Illness apparently occurred as a result of ingestion of oil taken from the ITH oil refinery in Sevilla, a plant in which rapeseed and grapeseed oils were refined for the distributing firm through which oil bearing the causative agent of TOS is thought to have entered the market. These data provide further strong support for the hypothesis that food oil was the vehicle by which the aetiological agent of TOS was transmitted. Because ingestion of refined denatured rapeseed oil was most closely associated with the illness in time, the TOS agent was probably contained initially in this type of oil. The agent very probably entered later oil mixtures through such contaminated rapeseed oil.