Salivary Urease and ADS Enzymatic Activity as Endogenous Protection against Dental Caries in Children.

UNLABELLED: The aim of this cross sectional study was to evaluate the ureolytic and arginolytic activities of saliva in children and associate them with their caries status. STUDY DESIGN: 65, 8 year old children, were randomly selected. The ureolytic and arginolytic activity of non stimulated saliva was studied and associated with DMFT and dmft index. Saliva of children were sampled under fasting conditions; Children refrained from any oral hygiene procedures during the 12 hours that preceded the sample collection. Caries activity was scored and divided in 3 groups: Group A: Index zero: without lesions; Group B: Moderate Index: 1 to 3 enamel caries lesions; and Group C: High Index: more than 4 dentin caries lesions. RESULTS: DMFT scores were moderate: 0.4(±0.79) and dmft: 2.78(±2.45). Results expressed in µmol/min/mg/protein, for urease activity were statistically significant (p=0.048): Group A= 0.69 (±0.7); Group B= 0.45 (±0.43); and Group C= 0.39 (±0.55). The arginine deiminase activity was not statistically significant (p=0.16): Group A= 2.53 (±1.42), Group B= 2.31 (±1.57) and Group C= 1.97 (±2.0). CONCLUSION: Higher levels of ureolytic (statistically significant) and arginolytic activity (trend) in saliva were associated with lower DMFT/dmft scores in 8 year old children. There was a higher production of ammonia from the arginine deiminase system than the urease enzyme in saliva (p>0.05).

MPTP-induced model of Parkinson's disease in cytochrome P450 2E1 knockout mice.

Evidence for involvement of cytochrome P450 2E1 in the MPTP-induced mouse model of PD has been reported [Vaglini, F., Pardini, C., Viaggi, C., Bartoli, C., Dinucci, D., Corsini, G.U., 2004. Involvement of cytochrome P450 2E1 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease. J. Neurochem. 91, 285-298]. We studied the sensitivity of Cyp2e1(-/-) mice to the acute administration of MPTP in comparison with their wild-type counterparts. In Cyp2e1(-/-) mice, the reduction of striatal DA content was less pronounced 7 days after MPTP treatment compared to treated wild-type mice. Similarly, TH immunoreactivity analysis of the substantia nigra of Cyp2e1(-/-) mice did not show any neuronal lesions after MPTP treatment. In contrast to this, wild-type animals showed a minimal but significant lesioning by the toxin as evaluated also by means of non-stereologic computerized assisted analysis of this brain area. Striatal levels of DA metabolites after 7 days were variably affected by the toxin, but consistent differences between the two animal strains were not observed. We evaluated short-term changes in the levels of striatal DA and its metabolites, and we monitored striatal MPP(+) levels. Striatal MPP(+) was cleared more rapidly in Cyp2e1(-/-) mice than in wild-type animals and, consistently, striatal DA content decreased faster in Cyp2e1(-/-) mice than in wild-type animals, and 3-methoxytyramine and HVA levels showed an early and sharp rise. Our findings suggest that Cyp2e1(-/-) mice are weakly sensitive to MPTP-induced brain lesions, markedly in contrast with a protective role of the enzyme as suggested previously. The differences observed between the knockout mice and their wild-type counterparts are modest and may be due to an efficient compensatory mechanism or genetic drift in the colonies.

Increased susceptibility to kainic acid-induced seizures in Engrailed-2 knockout mice.

The En2 gene, coding for the homeobox-containing transcription factor Engrailed-2 (EN2), has been associated to autism spectrum disorder (ASD). Due to neuroanatomical and behavioral abnormalities, which partly resemble those observed in ASD patients, En2 knockout (En2(-/-)) mice have been proposed as a model for ASD. In the mouse embryo, En2 is involved in the specification of midbrain/hindbrain regions, being predominantly expressed in the developing cerebellum and ventral midbrain, and its expression is maintained in these structures until adulthood. Here we show that in the adult mouse brain, En2 mRNA is expressed also in the hippocampus and cerebral cortex. Hippocampal En2 mRNA content decreased after seizures induced by kainic acid (KA). This suggests that En2 might also influence the functioning of forebrain areas during adulthood and in response to seizures. Indeed, a reduced expression of parvalbumin and somatostatin was detected in the hippocampus of En2(-/-) mice as compared to wild-type (WT) mice, indicating an altered GABAergic innervation of limbic circuits in En2(-/-) mice. In keeping with these results, En2(-/-) mice displayed an increased susceptibility to KA-induced seizures. KA (20 mg/kg) determined more severe and prolonged generalized seizures in En2(-/-) mice, when compared to WT animals. Seizures were accompanied by a widespread c-fos and c-jun mRNA induction in the brain of En2(-/-) but not WT mice. Long-term histopathological changes (CA1 cell loss, upregulation of neuropeptide Y) also occurred in the hippocampus of KA-treated En2(-/-) but not WT mice. These findings suggest that En2(-/-) mice might be used as a novel tool to study the link between epilepsy and ASD.

Utilización del compuesto MTA en fracturas radiculares verticales producidas por traumatismos sin intervención quirúrgica / Utilization of the compound MTA in fractures radiculares vertical produced by traumatism without surgical intervention

El estudio corresponde a la presentación de 2 casos clínicos con fractura radicular horizontal (tercio apical, tercio 1⁄2), tratadas con el agregado del trióxido mineral (MTA). En ambos casos las piezas sufrieron la fractura por trauma y el MTA se utilizo sin acción quirúrgica, vale decir, se coloco intraconducto. El objetivo del estudio es conocer la viabilidad de la terapia en estos casos, recordando que es necesario realizar nuevas investigaciones para demostrar la efectividad del material.

The study corresponds to the presentation of two clinical cases with horizontally root fractures (apical third, 1⁄2 third) treated with mineral trioxide aggregate (MTA). In both cases the pieces suffered fracture for trauma and the MTA was used without surgical action, is worth saying, its place in root canal. The intention of the study is to know the viability of the therapy in these cases, remembering that it is necessary to realize new investigations to demonstrate the efficiency of the material.

Fractura de fresa gate glidden en un conducto radicular / Gate glidden drill fracture in a root canal

Este articulo corresponde a un caso clínico donde se produjo la fractura de un usual instrumento utilizado en una pieza dentaria que se le estaba realizando un tratamiento endodóntico, una fresa Gate Glidden nº1; pero la extracción de este tipo de instrumento hoy en día se hace dificultoso y además se realiza con instrumental de alto costo, pero en este caso clínico utilizamos materiales de bajo valor y mucho ingenio pudiendo realizar el retiro del instrumento que obviamente podría ser usado en cualquier servicio publico donde los recursos son muy limitados y muchas veces austeros.

This article presents to a clinical case where the fracture of a Gate Glidden drill # 1 ocurred during endodontic therapy. Extraction of this type of instrument nowadays is difficult in addition is performed by instruments expensive, but in this clinical case we used materials of low value, and very innovative, being able to extract the instrument. This obviously could be used in any public service where the resources are very limited and often austere.

Shall we operate? Preoperative assessment in elderly cancer patients (PACE) can help. A SIOG surgical task force prospective study.

BACKGROUND: A number of elderly cancer patients do not receive standard surgery for solid tumors because they are considered unfit for treatment as a consequence of inaccurate estimation of the operative risk. To tailor treatment to onco-geriatric series, oncologists are now beginning to use a comprehensive geriatric assessment (CGA). This study investigates the value of an extended CGA in assessing the suitability of elderly patients for surgical intervention. PATIENTS AND METHODS: Preoperative assessment of cancer in the elderly (PACE) incorporates validated instruments including the CGA, an assessment of fatigue and performance status and an anaesthesiologist's evaluation of operative risk. An international prospective study was conducted using 460 consecutively recruited elderly cancer patients who received PACE prior to elective surgery. Mortality, post-operative complications (morbidity) and length of hospital stay were recorded up to 30 days after surgery. RESULTS: Poor health in relation to disability (assessed using the instrumental activities of daily living (IADL)), fatigue and performance status (PS) were associated with a 50% increase in the relative risk of post-operative complications. Multivariate analysis identified moderate/severe fatigue, a dependent IADL and an abnormal PS as the most important independent predictors of post-surgical complications. Disability assessed by activities of daily living (ADL), IADL and PS were associated with an extended hospital stay. CONCLUSION: PACE represents a valuable tool in enhancing the decision process concerning the candidacy of elderly cancer patients for surgical intervention and can reduce inappropriate age-related inequity in access to surgical intervention. It is recommended that PACE be used routinely in surgical practice.

CYP 2E1 mutant mice are resistant to DDC-induced enhancement of MPTP toxicity.

In order to reach a deeper insight into the mechanism of diethyldithiocarbamate (DDC)-induced enhancement of MPTP toxicity in mice, we showed that CYP450 (2E1) inhibitors, such as diallyl sulfide (DAS) or phenylethylisothiocyanate (PIC), also potentiate the selective DA neuron degeneration in C57/bl mice. Furthermore we showed that CYP 2E1 is present in the brain and in the basal ganglia of mice (Vaglini et al., 2004). However, because DAS and PIC are not selective CYP 2E1 inhibitors and in order to provide direct evidence for CYP 2E1 involvement in the enhancement of MPTP toxicity, CYP 2E1 knockout mice (GONZ) and wild type animals (SVI) of the same genetic background were treated with MPTP or the combined DDC + MPTP treatment. In CYP 2E1 knockout mice, DDC pretreatment completely fails to enhance MPTP toxicity, although enhancement of MPTP toxicity was regularly present in the SVI control animals. The immunohistochemical study confirms our results and suggests that CYP 2E1 may have a detoxifying role.

Cytochrome P450 and Parkinson's disease: protective role of neuronal CYP 2E1 from MPTP toxicity.

Elucidation of the biochemical steps leading to the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP)-induced degeneration of the nigro-striatal dopamine (DA) pathway has provided new clues to the pathophysiology of Parkinson's Disease (PD). In line with the enhancement of MPTP toxicity by diethyldithiocarbamate (DDC), here we demonstrate how other CYP450 (2E1) inhibitors, such as diallyl sulfide (DAS) or phenylethylisothiocyanate (PIC), also potentiate the selective DA neuron degeneration in C57/bl mice. In order to provide direct evidence for this isozyme involvement, CYP 2E1 knockout mice were challenged with MPTP or the combined treatment. Here we show that these transgenic mice have a low sensitivity to MPTP alone, similarly to the wild type SVI, suggesting that it is likely that transgenic mice compensate for the missing enzyme. However, in these CYP 2E1 knockout mice, DDC pretreatment completely fails to enhance MPTP toxicity; this enhancement is instead regularly present in the SVI control animals. This study indicates that the occurrence of CYP 2E1 in C57/bl mouse brain is relevant for MPTP toxicity, and suggests that this isozyme may have a detoxificant role related to the efflux transporter of the toxin.

Assessing neuroprotection in Parkinson's disease: from the animal models to molecular neuroimaging in vivo.

An important goal in Parkinson's Disease research is to identify neuroprotective therapy, and the interaction between basic science and clinical research is needed to discover drugs that can slow or halt the disorder progression. At present there is not a perfect animal model of PD to test neuroprotective strategies, however the models that portray the basic characteristics needed are toxin-induced and gene-based models. The first group comprehends 6-OHDA e MPTP and recently rotenone, paraquat and epoxomicin treated animals that shows some of human disease characteristics. Gene-based models are various and, even if with limits, they seem suitable models to test neuroprotection in PD since they present replicable lesions, a predictable pattern of neurodegeneration and a well-characterized behavior, biochemistry and morphology to assist in the understanding of induced changes. In clinical trials researchers have first used as marker of disease progression clinical scores and motor tasks which are limited by the potential symptomatic effect of tested drugs and are not useful in the pre-clinical phases of PD. Recently has emerged the important role of neuroimaging (Dopamine Transporter SPECT, 18FDopa-PET) as surrogate biomarker of PD progression. Even if there are still concerns about the influence of regulatory effects of tested drugs, neuroimaging features could represent a good outcome measure to evaluate PD progression and putative neuroprotective effect of pharmacological and non-pharmacological manipulations.

Pre-operative assessment of cancer in the elderly (PACE): a comprehensive assessment of underlying characteristics of elderly cancer patients prior to elective surgery.

BACKGROUND: Cancer is a disease that particularly affects the elderly and, although surgery is the first treatment choice, many elderly cancer patients do not receive standard surgery because they are considered unfit for treatment due to an inaccurate estimation of operative risk. Pre-operative Assessment of Cancer in the Elderly (PACE) was developed in order to address the need to provide detailed information about the functional reserve of the elderly cancer patient to aid individualised management. METHODS: PACE incorporates a battery of validated instruments including the Comprehensive Geriatric Assessment (CGA), Brief Fatigue Inventory (BFI), Eastern Cooperative Oncology Group Performance Status (ECOG-PS), and American Society Anesthesiologists (ASA) grade. An international prospective study was conducted with 460 consecutive elderly cancer patients (216 breast, 146 GIT, 71 GUT, 27 other) receiving PACE prior to receiving elective surgery. RESULTS: Three hundred and eighty four patients (83.4%) were observed to have at least one co-morbidity; the most common being hypertension (n=246, 53.5%). More than two thirds of the patients had good functional and mental status according to PACE. After adjusting for age, sex and type of cancer, six of the seven items of PACE were found to be significantly associated with co-morbidities (according to the Satariano's Index of Co-morbidities (SIC)). A multivariate analysis identified IADL, BFI and ASA to be the most important instruments in explaining SIC. DISCUSSION: PACE has been effectively used to describe the functional capacity and health status in an international cohort of elderly cancer patients. The majority of PACE instruments have been found to be significantly associated with co-morbidities (SIC) and can distinguish between type and severity of cancer. PACE represents a useful tool in evaluating onco-geriatric fitness for surgery.

Structure, organization and characterization of the gene cluster involved in the production of microcin E492, a channel-forming bacteriocin.

Microcin E492 is a low-molecular-weight, channel-forming bacteriocin produced and excreted by Klebsiella pneumoniae RYC492. A 13 kb chromosomal DNA fragment from K. pneumoniae RYC492 was sequenced, and it was demonstrated by random Tn5 mutagenesis that most of this segment, which has at least 10 cistrons, is needed for the production of active microcin and its immunity protein. Genes mceG and mceH correspond to an ABC exporter and its accessory protein, respectively, and they are closely related to the colicin V ABC export system. The microcin E492 system also requires the product of gene mceF as an additional factor for export. Despite the fact that this bacteriocin lacks post-translational modifications, genes mceC, mceI and mceJ are needed for the production of active microcin. Genes mceC and mceI are homologous to a glycosyl transferase and acyltransferase, respectively, whereas mceJ has no known homologue. Mutants in these three genes secrete an inactive form of microcin, able to form ion channels in a phospholipidic bilayer, indicating that the mutation of these microcin genes does not alter the process of membrane insertion. On the other hand, microcin isolated from mutants in genes mceC and mceJ has a lethal effect when incubated with spheroplasts of sensitive cells, indicating that the microcin defects in these mutants are likely to alter receptor recognition at the outer membrane. A model for synthesis and export is proposed as well as a novel maturation pathway that would involve conformational changes to explain the production of active microcin E492.

Twenty-four-hour endothelin-1 secretory pattern in stroke patients.

Endothelin-1 (ET-1) is a potent and long-acting vasoconstrictor peptide, which may play a role in the pathophysiology of a number of diseases. Controversial data exist on its role in human ischemic stroke. In order to ascertain whether changes in ET-1 plasma levels occur in ischemic stroke, plasma ET-1 levels and mean arterial pressure were determined in 15 patients at their first ischemic cerebral infarction and in 15 control subjects, over a 24-hour period. In stroke patients, mean 24-hour plasma ET-1 levels (4.9+/-0.5 ng/L) were higher (P< 0.05) than in control subjects (3.2+/-0.3 ng/L), and correlated with the mean size of the lesion, but not with the severity score of the neurological deficit. These results support the hypothesis that ET-1 levels reflect an indicator function for the amount of damaged cerebral tissue rather than a pathophysiological role.

D2/D3 dopamine receptor heterodimers exhibit unique functional properties.

Evidence for heterodimerization has recently been provided for dopamine D(1) and adenosine A(1) receptors as well as for dopamine D(2) and somatostatin SSTR(5) receptors. In this paper, we have studied the possibility that D(2) and D(3) receptors interact functionally by forming receptor heterodimers. Initially, we split the two receptors at the level of the third cytoplasmic loop into two fragments. The first, containing transmembrane domains (TM) I to V and the N-terminal part of the third cytoplasmic loop, was named D(2trunk) or D(3trunk), and the second, containing the C-terminal part of the third cytoplasmic loop, TMVI and TMVII, and the C-terminal tail, was named D(2tail) or D(3tail). Then we defined the pharmacological profiles of the homologous (D(2trunk)/D(2tail) and D(3trunk)/D(3tail)) as well as of the heterologous (D(2trunk)/D(3tail) and D(3trunk)/D(2tail)) cotransfected receptor fragments. The pharmacological profile of the cross-cotransfected fragments was different from that of the native D(2) or D(3) receptors. In most cases, the D(3trunk)/D(2tail) was the one with the highest affinity for most agonists and antagonists. Moreover, we observed that all of these receptor fragments reduced the expression of the wild type dopamine D(2) and D(3) receptors, suggesting that D(2) and D(3) receptors can form complexes with these fragments and that these complexes bind [(3)H]nemonapride less efficiently or are not correctly targeted to the membrane. In a second set of experiments, we tested the ability of the split and the wild type receptors to inhibit adenylyl cyclase (AC) types V and VI. All of the native and split receptors inhibited AC-V and AC-VI, with the exception of D(3), which was unable to inhibit AC-VI. We therefore studied the ability of D(2) and D(3) to interact functionally with one another to inhibit AC-VI. We found that with D(2) alone, R-(+)-7-hydroxydypropylaminotetralin hydrobromide inhibited AC-VI with an IC(50) of 2.05 +/- 0.15 nm, while in the presence of D(2) and D(3) it inhibited AC-VI with an IC(50) of 0.083 +/- 0.011 nm. Similar results were obtained with a chimeric cyclase made from AC-V and AC-VI. Coimmunoprecipitation experiments indicate that D(2) and D(3) receptors are capable of physical interaction.

Evaluation of the secretory pattern of plasma arginine vasopressin in stroke patients.

Arginine vasopressin (AVP) may play a role in the development of ischemic brain edema and/or cerebral vasospasm. Data available on AVP plasma levels in ischemic stroke are few and discordant. In order to ascertain whether changes in AVP plasma levels occur in ischemic stroke, plasma AVP levels, plasma osmolality and mean arterial pressure were determined in 24 patients with unprecedented ischemic cerebral infarction and in 15 controls over a 24-hour period. In stroke patients, mean 24-hour plasma AVP levels (7.2 +/- 0.8 ng/l) were higher (p < 0.05) than in control subjects (2.4 +/- 0.3 ng/l), and correlated with the severity score of the neurologic deficit and the mean size of the lesion. In patients with a more severe neurologic deficit, the mean 24-hour plasma AVP levels (8.7 +/- 1.0 ng/l) were higher than in patients with a less severe neurologic deficit (5.2 +/- 0.8 ng/l). Data indicate that in ischemic stroke an increased AVP secretion occurs independently of osmotic or baroreceptorial mechanisms. The possibility that AVP may play a role in neuronal cell damage following cerebral ischemia warrants further attention.

[Effectiveness and side effects of the treatment with propafenone and flecainide for recent-onset atrial fibrillation]. / Efficacia ed effetti collaterali del trattamento con propafenone e flecainide della fibrillazione atriale di recente insorgenza.

BACKGROUND: The authors report their experience in recent-onset atrial fibrillation treated with intravenous flecainide and propafenone, in comparison with the placebo group. METHODS: We randomized 352 (138 in the flecainide group, 164 in the propafenone group and 50 in the control group) consecutive patients (167 males, 185 females, mean age 59 +/- 12 years) with recent-onset atrial fibrillation. The electrocardiogram of all patients was monitored for at least 24 hours. RESULTS: The restoration of sinus rhythm occurred in 72.5, 80.4, 86.2 and 89.8% of patients in the flecainide group; in 54.3, 68.3, 75 and 92.1% in the propafenone group; in 22.2, 27.8, 35.2 and 46.3% in the control group, at 1, 3, 6 and 24 hours respectively. The occurrence of side effects was the same in all treatment groups, and occurred in about 10% of patients in the flecainide and propafenone groups, and in 4% in the control group. In our study population the treatment of recent-onset atrial fibrillation with flecainide was faster in converting the arrhythmia to sinus rhythm (p < 0.005 at 1 hour, p < 0.05 at 3 hours, p = 0.05 at 6 hours). However within 24 hours the efficacy of either flecainide or propafenone was the same (p = NS at 24 hours). CONCLUSIONS: Side effects were similar in both treatment groups. In particular malignant arrhythmias did not occur in the treatment groups and in the control group.

Stimulatory role of dopamine on fibroblast growth factor-2 expression in rat striatum.

We have previously shown that systemic injection of (-)nicotine produces a selective up-regulation of fibroblast growth factor (FGF)-2 mRNA levels in rat striatum. Because (-)nicotine can increase striatal release of dopamine and glutamate, in the present study we have investigated the contribution of these neurotransmitters in the modulation of FGF-2 expression. We found that coinjection of dopaminergic D1 (SCH23390) or D2 (haloperidol) receptor antagonists prevents nicotine-induced elevation of FGF-2 expression. However, injection of the NMDA receptor antagonist MK-801 produced a significant increment of FGF-2 mRNA and protein levels in rat striatum similar to the effect produced by (-)nicotine alone. Interestingly this effect of MK-801 could also be prevented by D1 or D2 receptor antagonists, suggesting that an elevation of dopamine levels may be required for the regulation of the trophic molecule. Accordingly we found that the non-selective dopaminergic agonist apomorphine can similarly increase striatal FGF-2 mRNA levels. Despite the observation that both D1 and D2 receptors appear to contribute to the modulation of FGF-2 expression, only a direct activation of D2 receptors, through quinpirole administration, was able to mimic the effect of apomorphine. On the basis of FGF-2 neurotrophic activity, these results suggest that direct or indirect activation of dopaminergic system can be neuroprotective and might reduce cell vulnerability in degenerative disorders.

Apomorphine, dopamine and phenylethylamine reduce the proportion of phosphorylated insulin receptor substrate 1.

We tested the ability of dopamine, apomorphine, phenylethylamine and pergolide to inhibit the proliferation of fetal calf serum-stimulated human breast cancer (MCF)-7 cells. While the first three compounds were able to block the proliferation of MCF-7 cells, pergolide failed to do so (up to 100 microM). The inhibitory effect of dopamine, apomorphine and phenylethylamine was also evident in serum-starved insulin-stimulated MCF-7 cells. Apomorphine also inhibited the proliferation of the human oestrogen receptor-negative breast cancer (MDA-MB231) and prostate carcinoma (LNCaP) cell lines. In a second set of experiments, we measured the ability of dopamine, apomorphine, phenylethylamine and pergolide to inhibit the phosphorylation (or increase the dephosphorylation) of the insulin receptor substrate (IRS)-1, a major intracellular substrate of the insulin-like growth factor (IGF)-1 receptor. Dopamine, apomorphine and phenylethylamine all reduced to zero the level of phosphorylated IRS-1 with potencies ranging between 0.01 and 1 microM. Finally, we found that fibroblasts from IRS-1 null (-/-) mice were less sensitive to the anti-proliferative effect of apomorphine compared to fibroblasts from wild type-mice, suggesting that the inhibition of IRS-1 phosphorylation by apomorphine is an important aspect of the activity of this compound.

[Assessment of plasma lipid profile in acute coronary syndromes. The use of fibrinolytics and heparin do not affect it significantly]. / Andamento del profilo lipidico plasmatico nelle sindromi coronariche acute. L'uso di fibrinolitici ed eparina non lo modificano significativamente.

BACKGROUND: Neurohormonal and metabolic responses to acute ischemic events associated with thrombolysis and heparin induce substantial changes in the lipid profile (acute phase response). The aim of this study was to assess changes in total cholesterol and triglycerides in patients with acute coronary syndrome, admitted to our Intensive Coronary Care Unit (ICCU). METHODS: The study included 1051 consecutive patients, 316 with unstable angina, 583 with Q wave acute myocardial infarction (AMI) and 152 with non-Q wave AMI. Total cholesterol and triglycerides were measured in all patients at time 0 (admission), at time 1 (the morning following admission), at time 2 (the morning after discontinuation of heparin treatment). RESULTS: The mean value of total cholesterol at admission was 235, 210 and 197 mg% at admission, time 1 and time 2, respectively. Triglyceride levels were 234, 178 and 189 mg%, respectively. In the subgroup of thrombolized AMI the reduction in total cholesterol at time 1 and time 2 resulted similar in comparison with non-thrombolized AMI (p = NS). The decrease in triglycerides showed a similar pattern in the different subgroups. Comparison was also done according to sex, age, and complications. CONCLUSIONS: These data confirm that mean total cholesterol and triglycerides at admission are sharply higher than values considered normal in the literature. Within 24 hours of admission there is a 10.7% drop in total cholesterol which increases to 16.2% after a few days (mean 3.4 days). Total cholesterol determination upon admission in patients with acute coronary syndromes is necessary in order to know the true concomitant lipid profile during the precipitating ischemic events. The decision of initiating early therapy with statins would then appear more justified.