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J Montero

Publications and source records attributed to J Montero.

At least 19 recordsLinked to original sources
PubMed2007

Electrophysiological study of ephaptic axono-axonal responses in hemifacial spasm.

One of the classic features of hemifacial spasm (HFS) is spread of the blink reflex responses to muscles other than the orbicularis oculi. The pathophysiological mechanisms underlying the generation of such abnormal responses include lateral spread of activity between neighboring fibers of the facial nerve and hyperexcitability of facial motoneurons. In this report we present evidence for another mechanism that can contribute to the generation of responses in lower facial muscles resembling the R1 response of the blink reflex. In 13 HFS patients, we studied the responses induced in orbicularis oris by electrical stimuli applied at various sites between the supraorbital and zygomatic areas. We identified responses with two different components: an early and very stable component, with an onset latency ranging from 10.5 to 14.8 ms, and a more irregular longer-latency component. Displacement of the stimulation site away from the supraorbital nerve and towards the extracranial origin of the facial nerve caused a progressive shortening of response latency. These features indicate that, in our patients, the shortest latency component of the orbicularis oris response was likely generated by antidromic conduction in facial nerve motor axons followed by axono-axonal activation of the fibers innervating the lower facial muscles. Our results suggest that motor axono-axonal responses are generated by stimulation of facial nerve terminals in HFS.

Adult↗
PubMed2005

Sealant and fluoride varnish in caries: a randomized trial.

Little is known about the effect of discontinuation of sealant or fluoride varnish. The purpose of this study was to compare sealant with fluoride varnish in the prevention of occlusal caries in permanent first molars of children over a nine-year period: 4 yrs for program evaluation plus 5 yrs of discontinuation. A clinical trial was conducted on three groups of six- to eight-year-old schoolchildren: a control group (n = 45); a group (n = 37) in which sealant was applied and reapplied up to 36 mos; and a group (n = 38) in which fluoride varnish was applied and re-applied up to 42 mos. Percent caries reduction was studied in these initially healthy molars with complete occlusal eruption: 129 (control), 113 (sealant), and 129 (varnish) molars met inclusion criteria. Of these, 76.7%, 26.6%, and 55.8% had developed occlusal caries at 9 yrs, which implies caries reductions of 65.4% (SE = 8.5%) for sealants vs. control and 27.3% (SE = 10.2%) for varnish vs. control. Furthermore, the varnish program was not effective during the discontinuation period.

Bisphenol A-Glycidyl Methacrylate↗
PubMed2003

Stimulated single-fiber EMG of the frontalis and orbicularis oculi muscles in ocular myasthenia gravis.

We performed single-fiber electromyography by axonal stimulation (stimulated SFEMG) of the frontalis and orbicularis oculi muscles of 20 patients with ocular myasthenia gravis (OM) and 46 controls. In controls, mean consecutive differences (MCD) ranged from 5 to 55 micros (average, 14.7 +/- 2.8 micros) in the frontalis and from 4 to 56 micros (average, 12.56 +/- 2.19 micros) in orbicularis oculi. The mean MCD of individual muscle potentials (MPs) was 14.6 +/- 6.8 micros in frontalis and 12.68 +/- 6.10 micros in orbicularis oculi. In the OM patients, the mean MCD was 43.85 +/- 25.18 micros in the frontalis and 69.85 +/- 29.55 micros in orbicularis oculi (P < 0.0001), and the number of MPs with altered MCD was 7.15 +/- 4.66 (range, 1-18) and 12.65 +/- 4.90 (range, 6-21), respectively (P < 0.0001). We conclude that stimulated SFEMG of the orbicularis oculi muscle is more sensitive for the diagnosis of OM than of the frontalis muscle.

Adult↗
PubMed2002

Steroidal management and serum cytokine profile of a case of alcoholic hepatitis with leukemoid reaction.

Leukemoid reactions (LRs) are rare in alcoholic hepatitis (AH), but they are a sign of poor prognosis. The treatment of AH with corticosteroids is controversial, though several reports suggest that these should be used in severe cases of AH. We report a case of AH-associated LRs that presented with an increase of the serum concentrations of the proinflammatory cytokines interleukin (IL)-18 (an initiator of inflammation) and IL-1beta (likely responsible for the neutrophilia of the LRs). These findings provided a pathogenic indication for the use of corticosteroids (that block the transcription of IL-1beta), and this approach achieved a clinical and analytical recovery in our patient. This pathogenic mechanism might also underlie other cases of LRs and other complications of AH, thus providing a rationale for the benefits of corticotherapy in these rare but severe conditions.

Adult↗
PubMed2001

Genetic study of patients with dexamethasone-suppressible aldosteronism without the chimeric CYP11B1/CYP11B2 gene.

Glucocorticoid-remediable aldosteronism is an inherited disorder caused by a chimeric gene duplication between the CYP11B1 (11beta-hydroxylase) and CYP11B2 (aldosterone synthase) genes. The disorder is characterized by hyperaldosteronism and high levels of 18-hydroxycortisol and 18-oxocortisol, which are under ACTH control. The diagnosis of glucocorticoid-remediable aldosteronism had been traditionally made using the dexamethasone suppression test; however, recent studies have shown that several patients with primary aldosteronism and a positive dexamethasone suppression test do not have the chimeric CYP11B1/CYP11B2 gene. The aim of this work was to evaluate whether other genetic alterations exist in CYP11B genes (gene conversion in the coding region of CYP11B1 or in the promoter of CYP11B2) that could explain a positive dexamethasone suppression test and to determine another genetic cause of glucocorticoid-remediable aldosteronism. We also evaluated the role of 18-hydroxycortisol as a specific biochemical marker of glucocorticoid-remediable aldosteronism. We studied eight patients with idiopathic hyperaldosteronism, a positive dexamethasone suppression test, and a negative genetic test for the chimeric gene. In all patients we amplified the CYP11B1 gene by PCR and sequenced exons 3-9 of CYP11B1 and a specific region (-138 to -284) of CYP11B2 promoter. We also measured the levels of 18-hydroxycortisol, and we compared the results with those found in four subjects with the chimeric gene. None of eight cases showed abnormalities in exons 3-9 of CYP11B1, disproving a gene conversion phenomenon. In all patients a fragment of 393 bp corresponding to a specific region of the promoter of CYP11B2 gene was amplified. The sequence of the fragment did not differ from that of the wild-type promoter of the CYP11B2 gene. The 18-hydroxycortisol levels in the eight idiopathic hyperaldosteronism patients and four controls with chimeric gene were 3.9 +/- 2.3 and 21.9 +/- 3.5 nmol/liter, respectively (P < 0.01). In summary, we did not find other genetic alterations or high levels of 18-hydroxycortisol that could explain a positive dexamethasone suppression test in idiopathic hyperaldosteronism. We suggest that the dexamethasone suppression test could lead to an incorrect diagnosis of glucocorticoid-remediable aldosteronism.

Adult↗
PubMed2001

[High prevalence of subclinical thyroidal disease among individuals attended in health control].

BACKGROUND: There is no information about the prevalence of thyroidal diseases in the general Chilean population. AIM: To assess the prevalence of thyroidal diseases in individuals attended in occupational health examinations. SUBJECTS AND METHODS: Four hundred seventy two individuals were examined between 1998 and 1999. In all, serum levels of thyroid hormones, TSH and anti thyroidal antibodies (anti microsomal, anti thyroid peroxidase and anti thyroglobulin) were measured. RESULTS: Forty four subjects were excluded from the study due to an incomplete medical record and 18 due to a personal history of thyroidal disease. Abnormal serum levels of thyroid hormones or TSH were detected in 28 subjects (6.8%). Four (1%) had hypothyroidism, 23 a subclinical hypothyroidism (5.6%) and one (0.2%) had hyperthyroidism. In 87 subjects (21.2%) at least one of the antibodies was positive. Positive anti thyroid antibodies were found in 14 of 28 subjects (50%) with abnormal thyroid hormone levels, compared with 73 of 382 subjects (19.1%) with normal thyroid hormone levels. Thyroid dysfunction was twice as frequent in women than in men. CONCLUSIONS: In this sample, a 6.8% prevalence of abnormal thyroid function tests was detected.

Adolescent↗
PubMed2000

Stimulated single fiber EMG of the frontalis muscle in the diagnosis of ocular myasthenia.

We performed single fiber electromyography by axonal stimulation (SFEMG-AS) of the frontalis muscle of 16 patients with ocular myasthenia gravis (OM) and 33 controls. In the controls, values of mean consecutive differences (MCD) ranged from 5 to 55 micros (average, 14.7 +/- 2.8 micros) and mean MCD of individual MPs was 14. 6 +/- 6.8 micros. All the OM patients showed abnormal SFEMG-AS jitter before prostigmine was administered (mean MCD: 49.19 +/- 21. 82 micros, percentage of blocks: 20.97 +/- 18.53). Twenty or 30 min after prostigmine had been administered, we saw a significant improvement in jitter: mean MCD was 36.38 +/- 22.49 micros (P = 0. 005), and percentage of blocks was 10.16 +/- 18.87 (P = 0.008). The method was well tolerated. We conclude that SFEMG-AS of the frontalis muscle is a sensitive technique for the diagnosis of OM and is easy to carry out.

Adult↗
PubMed2000

Primary hyperaldosteronism in essential hypertensives: prevalence, biochemical profile, and molecular biology.

There is evidence that primary aldosteronism (PA) may be common in patients with essential hypertension (EH) when determinations of serum aldosterone (SA), plasma renin activity (PRA), and the SA/PRA ratio are used as screening. An inherited form of primary hyperaldosteronism is the glucocorticoid-remediable aldosteronism (GRA) caused by an unequal crossing over between the CYP11B1 and CYP11B2 genes that results in a chimeric gene, which has aldosterone synthase activity regulated by ACTH. The aim of this study was to evaluate the prevalence of PA and the GRA in 305 EH patients and 205 normotensive controls. We measured SA (1-16 ng/dL) and PRA (1-2.5 ng/mL x h) and calculated the SA/PRA ratio in all patients. A SA/PRA ratio level greater than 25 was defined as being elevated. PA was diagnosed in the presence of high SA levels (>16 ng/dL), low PRA levels (<0.5 ng/mL x h), and very high SA/PRA ratio (>50). Probable PA was diagnosed when the SA/PRA ratio was more than 25 but the other criteria were not present. A Fludrocortisone test was done to confirm the diagnosis. GRA was differentiated from other forms of PA by: the aldosterone suppression test with dexamethasone, the high levels of 18-hydroxycortisol, and the genetic detection of the chimeric gene. In EH patients, 29 of 305 (9.5%) had PA, 13 of 29 met all the criteria for PA, and 16 of 29 were initially diagnosed as having a probable PA and confirmed by the fludrocortisone test. Plasma potassium was normal in all patients. The dexamethasone suppression test was positive for GRA in 10 of 29 and 18-hydroxycortisol levels were high in 2 of 29 patients who had also a chimeric gene. In normotensive subjects, 3 of 205 (1.46%) had PA, and 1 of 205 had a GRA. In summary, we found a high frequency of normokalemic PA in EH patients. A high proportion of PA suppressed SA with dexamethasone, but only a few had a chimeric gene or high levels of 18-hydroxycortisol. These results emphasize the need to further investigate EH patients.

Aldosterone↗
PubMed2000

[Excess of mineralocorticoids in essential hypertension: clinical-diagnostic approach].

BACKGROUND: Primary hyperaldosteronism is more frequent among subjects with essential hypertension than previously thought. The prevalence, according to local and international evidence could fluctuate between 9 and 10%. AIM: To investigate if subjects with essential hypertension have different aldosterone and renin plasma levels than normotensive subjects. PATIENTS AND METHODS: One hundred twenty five subjects with essential hypertension, not receiving medications for at least two weeks prior to the study and 168 age and sex matched normotensive controls were studied. Blood was drawn between 9 and 10 AM during a sodium free diet to determine plasma aldosterone, plasma renin activity and potassium. RESULTS: Plasma aldosterone was higher in hypertensive subjects than controls (11.6 +/- 7.6 and 9.9 +/- 5.1 ng/dl respectively; p = 0.04). Plasma renin activity was lower in hypertensives than controls (1.42 +/- 1.28 and 1.88 +/- 1.39 ng/ml/b respectively; p < 0.001). Thus, plasma aldosterone/plasma renin activity ratio was higher in hypertensives (13.8 +/- 13.5 and 8.3 +/- 7.8; p < 0.001). A pathological ratio was defined as over 25, corresponding to the mean plus two standard deviations of the control group. Primary hyperaldosteronism was found in 5/125 hypertensives (4%) and 1/168 normotensive subject (0.6%). None had hypokalemia. CONCLUSIONS: Subjects with essential hypertension have higher plasma aldosterone and lower plasma renin activity than normal controls. A plasma aldosterone/plasma renin activity over 25 was defined as abnormal.

Adult↗
PubMed1999

A(-6)G variant of angiotensinogen gene and aldosterone levels in hypertensives.

Recently, a novel mutation in the promoter region of the angiotensinogen gene that involves the presence of an adenine instead of a guanine 6 bp upstream from the transcription initiation site (A(-6)G) has been shown to induce an increase in gene transcription. The aim of this study was to determine the prevalence of the A(-6)G mutation in essential hypertensive patients and to correlate it with aldosterone and renin activity levels. We studied 191 hypertensives. We measured levels of aldosterone (plasma and urinary) and plasma renin activity. We determined the variants A and G using a mutagenically separated polymerase chain reaction technique. In 191 hypertensives, the A variant was detected in 266 of 382 (69.6%) and the G variant in 116 of 382 alleles (30.4%). Plasma aldosterone was significantly higher in patients homozygous for AA than in those homozygous for GG (369+/-208 versus 246+/-142 pmol/L). Urinary aldosterone was significantly higher in homozygous AA than in AG or GG patients (62.4+/-39.4 versus 50.8+/-25.2 and 37.4+/-22.3 nmol/d, respectively). When the patients were grouped according to the presence or absence of the A allele, the aldosterone levels and the plasma aldosterone/plasma renin activity ratio were significantly higher in patients with the A allele. The presence of the A variant was associated with higher levels of aldosterone. These results suggest that the presence of the A variant could determine the appearance of arterial hypertension through higher transcription activity of the angiotensinogen gene and concomitant aldosterone production.

Aged↗
PubMed1999

[Pericarditis secondary to the rupture of a hydatid cyst].

Cardiac hydatic cysts are rare and represent 0.5 to 2% of all hydatic cysts in humans, but usually associated with fatal complications. We report a case of a male 27 years old with a hydatid cyst located in left ventricle asymptomatic until rupture. It was diagnosed by two-dimensional echocardiogram in a control.

Adult↗