[Diagnosis and treatment of imported eosinophilia in travellers and immigrants: Recommendations of the Spanish Society of Tropical Medicine and International Health (SEMTSI)]. / Diagnóstico y tratamiento de la eosinofilia importada en viajeros e inmigrantes: recomendaciones de la Sociedad Española de Medicina Tropical y Salud Internacional (SEMTSI).

According to published data, prevalence of imported eosinophilia among travellers and immigrants is set between 8% and 28.5%. Etiological diagnosis is often troublesome, and depending on the depth of the study and on the population analyzed, a parasitic cause is identified in 17% to 75.9% of the individuals. Among the difficulties encountered to compare studies are the heterogeneity of the studied populations, the type of data collection (prospective/retrospective) and different diagnostic protocols. In this document the recommendations of the expert group of the Spanish Society of Tropical Medicine and International Health (SEMTSI) for the diagnosis and treatment of imported eosinophilia are detailed.

Non-quassinoid constituents from the twigs and thorns of Castela polyandra.

The structures of two new constituents, a beta-glycoside (1) and a steroid (2), isolated from the twigs and thorns of Castela polyandra, were established by a combination of spectroscopic and single-crystal X-ray analysis.

Quassinoids from the twigs and thorns of Castela polyandra.

The structures of six new C20 quassinoids and one new C19 quassinoid, all isolated from the twigs and thorns of Castela polyandra, were established by a combination of spectroscopic and single-crystal X-ray analysis. Five known quassinoids and one known sterol were also identified.

Acute and chronic cocaine exposure can produce myocardial ischemia and infarction in Yucatan swine.

The purpose of this study was to determine whether the acute and chronic administration of cocaine could induce myocardial infarction. Twenty-five minipigs were studied before and 4 months after balloon angioplasty of the left anterior descending artery (LAD) and balloon denudation of the left circumflex artery (LCx). Minipigs received cocaine in the initial and in the 4-month study (0.1, 0.5, and 3 mg/kg i.v.). Minipigs were randomized to group I (high-cholesterol diet + daily cocaine; 500 mg i.m.; n = 8), group II (high-cholesterol diet + no i.v. cocaine; n = 5), group III (chow diet + daily cocaine; 500 mg i.m.; n = 6), group IV (chow diet + no i.v. or i.m. cocaine; n = 6). In vivo, coronary flow significantly decreased and vascular resistance significantly increased after the administration of cocaine. Histamine significantly decreased the luminal diameters (LAD and LCx) in groups I, II and III. There were a total of five acute and 16 chronic infarctions among the three groups that received either short- or long-term cocaine; however, no infarct occurred in group IV. The combination of daily cocaine abuse with a cholesterol-rich diet enhanced coronary vasoreactivity in vivo and in vitro. We conclude that long-term or sporadic cocaine abuse can induce myocardial infarction.

Effects of cocaine on carotid vascular reactivity in swine after balloon vascular injury.

BACKGROUND AND PURPOSE: The use of cocaine has been associated with stroke. To evaluate carotid vasospasm as a potential mechanism of cocaine-induced stroke, we studied 12 swine immediately and 10 weeks after angioplasty. METHODS: We compared the short- and long-term vasoconstrictor responses of normal and injured arterial segments to nitroglycerin, histamine, and cocaine in vivo by carotid angiography. We also compared the isometric contractile force responses to different vasoactive substances in normal and injured vascular rings in vivo, and we tested the direct action of cocaine on both arterial segments. RESULTS: In in vivo studies, immediately after angioplasty, luminal diameter in the control segment decreased by 30% with histamine 30 micrograms/kg and by 23% with cocaine 10 mg/kg (P < .001). In contrast, neither histamine nor cocaine produced vasoconstriction in the angioplasty segment. Thus, a transient loss of vasoconstriction occurred at the angioplasty site. Ten weeks later, histamine 30 micrograms/kg significantly (P < .001) decreased luminal diameter by 34% in the control and by 33% in the angioplasty segment; similarly, cocaine 10 mg/kg significantly (P < .001) decreased luminal diameter by 26% in the control and by 34% in the angioplasty segment. Thus, 10 weeks after angioplasty, the transitory loss of carotid vasoconstriction in response to histamine and cocaine reverted, and a moderate generalized vasoconstriction occurred in both segments without localized vasospasm. In vitro, the maximal isometric tension responses to KCl, acetylcholine, histamine, and phenylephrine were similar in vascular rings from normal and angioplasty segments. The median effective doses to histamine and phenylephrine were similar. In contrast, cocaine in concentrations from 10(-7) to 10(-3) mol/L failed to produce any isometric contraction in vitro. CONCLUSIONS: Cocaine in vivo produced a generalized carotid vasoconstriction without evidence of localized vasospasm; since there was no response to cocaine in vitro, the in vivo effect was most likely mediated by neurohumoral factors rather than by a direct action of cocaine on vascular smooth muscle.

Cocaine-induced microvascular spasm in Yucatan miniature swine. In vivo and in vitro evidence of spasm.

The purpose of the present study was to determine the maximal coronary flow reserve (CFR) before and after the administration of successive cocaine doses (0.1, 0.5, 3, and 7 mg/kg IV) for 2 minutes at 10-minute intervals in eight miniature swine. CFR was assessed by the administration of adenosine (0.03, 0.3, and 3 mg IC). Hemodynamic and flow measurements were performed 3 minutes after each dose. Coronary flow (CF) was measured with a Doppler-tipped wire in the proximal left anterior descending coronary artery (LAD). Also, microvessels were dissected, and vessel diameters were measured by a videoelectronic dimension analyzer. In vivo, LAD CF increased fourfold, CFR increased twofold, and coronary vascular resistance (CVR) decreased fourfold after the administration of adenosine. In contrast, LAD CF decreased threefold, CFR decreased onefold, and CVR increased sixfold 3 minutes after the administration of cocaine. Adenosine (3 mg) was repeated 4 minutes after the administration of cocaine, and LAD CF increased 1.4-fold, CVR increased 2.5-fold, and CFR decreased onefold. Thus, adenosine partially reversed the potent cocaine constrictor effect. In vitro, 10(-9) mol/L cocaine decreased the diameter of the coronary microvessels from 129 +/- 12 to 127 +/- 12 microns, and 10(-4) mol/L cocaine decreased coronary microvessel diameter to 114 +/- 15 microns (P < .05). In conclusion, cocaine in vivo decreases CFR, and consistent with the in vivo effect, cocaine in vitro produced constriction of vessels < 200 microns. These results indicate that cocaine can produce profound microvascular spasm. This may contribute to the ischemia/infarction reported in patients who abuse cocaine and who are subsequently found to have normal epicardial coronary arteries.

Hypertension and sudden death. Disparate effects of calcium entry blocker and diuretic therapy on cardiac dysrhythmias.

This study was designed to evaluate the impact of antihypertensive therapy on cardiac dysrhythmias in 13 hypertensive patients who received calcium entry blockers and in 10 hypertensive patients who received hydrochlorothiazide. Mean arterial pressure fell to a similar extent in both treatment groups; however, left ventricular mass index decreased (from 102 +/- 4 to 95 +/- 2 g/m2) only in patients receiving calcium entry blockers, but not in those taking hydrochlorothiazide. The prevalence of premature ventricular contractions decreased 74% from 21 +/- 14/h to 5.7 +/- 6/h in the calcium entry blocker group, but did not change in the hydrochlorothiazide group (15 +/- 17/h to 16 +/- 13/h). Couplets, multiform contractions, ventricular tachycardia, and supraventricular tachycardia were completely abolished after calcium entry blocker therapy, whereas the prevalence of these arrhythmias remained unchanged during treatment with hydrochlorothiazide. We conclude that antihypertensive therapy with calcium entry blockers (but not with thiazide diuretics) reduces left ventricular mass and the prevalence and severity of ventricular dysrhythmias. Whether this reduction will improve the ominous prognosis of left ventricular hypertrophy and diminish the risk of sudden death remains unknown.

Serum uric acid in renovascular hypertension: reduction following surgical correction.

Mild hyperuricemia in patients with essential hypertension reflects early renal vascular involvement. This report describes a retrospective analysis of 28 patients with unilateral renal arterial disease and hypertension who underwent surgical treatment. Following surgical repair of the arterial lesion: systolic pressure decreased from 188 +/- 25 to 146 +/- 21 mm Hg (p less than 0.001); diastolic pressure decreased from 108 +/- 4 to 87 +/- 6 mm Hg (p less than 0.001), and serum uric acid and creatinine concentrations decreased from 7.0 +/- 1.1 to 6.1 +/- 1.4 mg/dL and from 1.3 +/- 0.3 to 1.0 +/- 0.3 (p less than 0.02 and p less than 0.03, respectively). The reduced serum potassium levels, reflecting hyperaldosteronism, increased after surgical treatment (p less than 0.003). The 28 patients were classified in three groups according to previous therapy: group I (14 patients) had been treated with a centrally active adrenergic agonist or a beta adrenergic receptor blocking agent; group II (7 patients) had been treated with a diuretic, and group III (7 patients) had never received antihypertensive therapy. Serum uric acid concentrations were similar in each of the three groups and decreased significantly in each group after correction of the renal artery stenosis. These data strengthen our previous observations and further suggest that serum uric acid concentration may be useful as an index of renal vascular involvement in hypertension.