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M Recasens

Publications and source records attributed to M Recasens.

At least 19 recordsLinked to original sources
PubMed2003

Macrovascular events after kidney-pancreas transplantation in type 1 diabetic patients.

BACKGROUND: There are few studies concerning the effect of kidney-pancreas transplantation (KPTx) on the progression of macrovascular disease in type 1 diabetic patients. The aim of our study was to retrospectively evaluate the incidence of macrovascular events after functioning KPTx. MATERIALS AND METHODS: We studied 146 patients (96 men and 50 women) who had undergone KPTx from February 1983 to September 2001, with more than 1 year of evolution of both grafts functioning normally. The mean follow-up of the patients after KPTx was 5+/-3 years. RESULTS: Before KPTx, 29 patients displayed 42 macrovascular events. During the follow-up after transplantation, intermittent claudication remained in 25 patients (86.2%) with 11 new macrovascular events (1 stroke, 1 angina pectoris, 1 myocardial infarction, and 8 minor amputations) in 10 patients (34%). Among the 117 patients without antecedent macrovascular events prior to KPTx, 38 (32.5%) experienced a total of 63 macrovascular events (26 intermittent claudication, 4 stroke, 8 angina pectoris, 7 myocardial infarction, 11 minor amputations, and 7 major amputations). Before transplantation, 88.4% of the patients presented with hypertension, 42.5% a history of smoking, and 14.4% previous treatment for dyslipidmia. After transplantation, we observed an important reduction in the percentage of patients with hypertension (48.6%) and smoking (25.5%), without a change in the prevalence of dyslipemia (19.9%). Hypertension after transplantation was clearly associated with the appearance or persistence of macrovascular events. CONCLUSION: In our experience, 43% of the transplant recipients present with macrovascular events. It is important to note the elevated prevalence of cardiovascular risk factors in the patients who underwent KPTx.

Female↗
PubMed2001

Abrupt onset of diabetes during interferon-alpha therapy in patients with chronic hepatitis C.

INTRODUCTION: Interferon-alpha (IFN-alpha) is now widely used in the treatment of chronic hepatitis C. Few patients have been reported as developing impaired glucose tolerance or diabetes mellitus (DM) using this therapy. The explanation for the development of DM in chronic hepatitis C treated with IFN-alpha is unclear. We report two patients who developed an abrupt onset of diabetes during IFN-alpha for chronic hepatitis C. CASE REPORTS: Two male middle-aged patients were admitted to our hospital for an abrupt onset of diabetes, in diabetic ketoacidosis, with a very short duration of hyperglycaemic symptoms. Their clinical course was similar. Case 1 never demonstrated any markers of pancreatic immunogenicity. Case 2 had high levels of decarboxylase glutamic acid autoantibodies (GADAb), before the IFN-alpha treatment that persisted. We compared initial beta-cell function and metabolic control with a group of middle-aged patients from our hospital who had recently been diagnosed with Type 1 diabetes mellitus (DM1). In contrast to these, the onset of the disease was particularly severe with beta-cell function substantially impaired and displaying unstable short-term metabolic control. CONCLUSIONS: Type 1 diabetes should be considered as a potential complication if IFN is administered to patients with chronic hepatitis C. Its onset may be severe and result in short-term difficulties in metabolic control.

Adult↗
PubMed2001

Prevalence of coeliac disease in unexplained chronic hypertransaminasemia.

OBJECTIVE: To determine the prevalence of coeliac disease amongst the population with unexplained chronic hypertransaminasemia in our region. PATIENTS AND METHODS: A prospective study was carried out on 147 consecutive patients with chronic hypertransaminasemia, having previously discarded alcoholic cause, hepatotoxic drugs, B, C and Delta viral infections, autoimmune hepatitis, primary biliary cirrhosis, Jemochromatosis, alfal-antitrypsin deficiency, Wilson's disease, congestive liver and illicit drug use. Serum Ig A to gliadin and endomysium antibodies were determined. Intestinal biopsy was carried out in cases those positive for one or both antibodies. RESULTS: One patient was positive for both IgA to gliadin and to endonisyum antibodies, whereas another three patients were positive to IgA to gliadin only. A duodenal biopsy proved normal in two, a total villous atrophy in one and subtotal atrophy in other. CONCLUSIONS: 1. The prevalence of coeliac disease amongst the population with unexplained chronic hypertransaminasemia in our region is 1.4%. 2. In our region, screening for coeliac disease in unexplained chronic hypransaminasemia should take a secondary place.

Adolescent↗
PubMed2000

White coat hypertension in type 1 diabetic patients without nephropathy.

The aim of our study was to determine the prevalence of white coat hypertension (WCH) in type 1 diabetic patients. Therefore, ambulatory blood pressure monitoring (ABPM) and 24-h urinary albumin excretion (UAE) were determined in 47 patients with type 1 diabetes mellitus (27 with new diagnosis of hypertension by office blood pressure (BP) measurement and 20 with normotension). WCH was diagnosed in 20 patients (74%). Patients with WCH presented higher values of systolic and diastolic BP and UAE than normotensive patients. The results indicate that in type 1 diabetes mellitus WCH is very frequent. Thus, WCH may represent a potential risk for the development of diabetic complications, mainly diabetic nephropathy.

Adult↗
PubMed2000

Adult celiac disease and hypertransaminasemia.

OBJECTIVE: to determine the incidence of hypertransaminasemia in adult patients with celiac disease with or without relevant chronic liver disease, and to evaluate the response after a gluten-free diet. PATIENTS AND METHODS: retrospective study of 20 cases of adult celiac disease (> 14 years old at diagnosis). Patients were included in the study if they fulfilled the revised EPSGAN criteria. If laboratory tests of liver function revealed alterations, hepatitis B and C viral serology, thyroid hormones, and use of alcohol and drugs were investigated, and liver ultrasound scans were done. Liver biopsy and endoscopic retrograde cholangiopancreatography were done only in patients for whom these studies were considered necessary. RESULTS: ten patients had hypertransaminasemia (50%), ascribed to benzodiazepine use in 1 patient, chronic HCV hepatitis in 1, and celiac disease in 8. In all of these last patients except 1 (benzodiazepine use), laboratory values returned to normal after 4-10 months on a gluten-free diet. CONCLUSIONS: celiac disease was frequently associated with hypertransaminasemia. In most patients transaminase levels returned to normal within 1 year after dietary gluten intake was restricted. If alterations in laboratory values persist, other causes that may be related (e.g., autoimmunity or tumors) or unrelated to celiac disease (e.g., virus) must be ruled out.

Adult↗
PubMed1999

Potentiation of glutamatergic agonist-induced inositol phosphate formation by basic fibroblast growth factor is related to developmental features in hippocampal cultures: neuronal survival and glial cell proliferation.

We investigated the modulation by growth factors of phospholipase C (PLC)-linked glutamate receptors during in vitro development of hippocampal cultures. In defined medium, glial cells represent between 3 and 14% of total cell number. When we added basic fibroblast growth factor (bFGF) 2 h after plating, we found: (i) a neuroprotection from naturally occurring death for up to 5 days; (ii) a proliferation of glial cells from day 3; and (iii) a potentiation of quisqualate (QA)-induced inositol phosphate (IP) formation from 1 to 10 days in vitro (DIV) and 1S, 3R-amino-cyclopentane-1,3-dicarboxylate (ACPD) response from 3 to 10 DIV. The antimitotic cytosine-beta,D-arabinofuranoside (AraC) blocked glial cell proliferation induced by bFGF, but not neuroprotection. Under these conditions, the early potentiation of the QA response (1-3 DIV) was not changed, while the ACPD and late QA response potentiations were prevented (5-10 DIV). Epidermal growth factor was not neuroprotective but it induced both glial cell proliferation and late QA or ACPD potentiation. Surprisingly, the early bFGF-potentiated QA-induced IP response was blocked by 6, 7-dinitro-quinoxaline-2,3-dione (DNQX), suggesting the participation of ionotropic (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptors. The delayed bFGF-potentiated ACPD-induced IP response is inhibited by (S)-alpha-methyl-4-carboxyphenylglycine (MCPG), indicating possible activation of glial metabotropic receptors. These results suggest that, in hippocampal cultures, bFGF modulates AMPA and metabotropic glutamate receptors linked to the IP cascade, possibly in relation to the regulation of neuronal survival and glial cell proliferation, respectively.

Animals↗
PubMed1999

Intravitreal tPA and SF6 promote clearing of premacular subhyaloid hemorrhages in shaken and battered baby syndrome.

BACKGROUND AND OBJECTIVE: Child abuse is a serious problem in many cultures. The ocular signs of shaken baby include intraretinal, subretinal, and preretinal hemorrhages. The hemorrhages may be unilateral or bilateral and are seen in 50% to 80% of patients. Previous treatment was limited to observation or vitrectomy, but some observed eyes develop amblyopia, and pediatric vitrectomy has many complications. PATIENTS: We report 4 eyes in 2 children with shaken baby syndrome in whom we administered intravitreal tissue plasminogen activator (tPA) in an attempt to resolve preretinal hemorrhages earlier than observation alone without the complications of vitrectomy. The tPA dose ranged from 12.5-25 microg per injection. Eyes were injected once weekly for 3 consecutive weeks. Each time 0.25 cc of sulfur hexafluoride gas was also injected. RESULTS: Within 1 week following the last tPA administration, complete resolution of the preretinal hemorrhage was seen. There were no associated ophthalmic complications. CONCLUSION: Intravitreal tPA with an expansive gas is an alternative method to observation or vitrectomy for resolution of preretinal hemorrhages in battered babies and may allow faster resolution of hemorrhages without the complications of vitrectomy.

Battered Child Syndrome↗
PubMed1995

Protein kinase C differently regulates quisqualate- and 1S,3R-trans aminocyclopentane dicarboxylate-induced phosphoinositide hydrolysis during in vitro development of hippocampal neurons.

Transient peaks of quisqualate (QA)-, but not 1S,3R-1-amino-3-cyclopentane dicarboxylate (1S,3R-ACPD)- and carbachol-induced inositol phosphate formation occur between 2 and 5 days in vitro (DIV) in hippocampal neurons in culture. In order to elucidate the putative origin of such developmental activity differences, the effect of PKC on metabotropic glutamate receptor (mGluR) and muscarinic receptor responses was investigated at 3 and 10 DIV. (i) Stimulation of PKC by phorbol-12,13-dibutyrate inhibited QA, 1S,3R-ACPD and carbachol responses at 3 DIV. At 10 DIV, only 1S,3R-ACPD response was still inhibited by phorbol esters. (ii) Inhibition of PKC by staurosporine at 3 DIV potentiated 1S,3R-ACPD-induced inositol phosphate formation, but had no effect on QA and carbachol responses. At 10 DIV, all responses were potentiated by staurosporine. These data strongly suggest that PKC differently modulates 1S,3R-ACPD- and QA-induced inositol phosphate accumulations during in vitro development. The specific activity of mGluRs during development, vs that of muscarinic receptor, and the peculiar modes of regulation by PKC of these two mGluR activities further suggest their particular involvement in the maturation of neuronal culture.

Alkaloids↗
PubMed1992

Dithiotreitol specifically inhibits metabotropic responses of glutamate and depolarizing agents in rat brain synaptoneurosomes.

Dithiotreitol (DTT), a sulfhydryl reducing agent inhibits in a dose-dependent manner the inositol phosphates (IPs) accumulation responses evoked by glutamate and potassium without affecting that of carbachol in rat forebrain synaptoneurosomes. Furthermore, DTT neither provokes a depolarization of the membrane, nor increases the internal calcium concentration. Depolarization and internal calcium rise are known to stimulate IPs production. Moreover, DTT does not modify the depolarizing effect and the calcium rise elicited by glutamate and potassium. In addition, the antioxidant compounds 2-aminoethylisothiouronium bromide (AET) and ascorbic acid have no effect on the basal and stimulated IPs accumulation. Thus, it is concluded that: (1) two distinct transduction pathways exist, one stimulated by glutamate and depolarizing agents and the other one by cholinergic agonists; (2) DTT produces its inhibition by reducing disulfide bridges likely at the level of proteins of the phosphoinositide transduction mechanism.

Animals↗
PubMed1990

Glutamate neurotoxicity in the cochlea: a possible consequence of ischaemic or anoxic conditions occurring in ageing.

Glutamate is considered to be one of the most common neurotransmitters in the fast excitatory synapses in the central nervous system. On the other hand, its excitotoxic properties are increasingly cited to explain some of the brain damage linked with hypoxia and ischaemia: i.e., those that occur frequently in ageing. An excess release of glutamate could, either directly or indirectly, activate receptors on the postsynaptic neuron, causing ion influxes accompanied by a massive entry of water, which would lead to an acute swelling of dendrites. In addition, calcium influx deregulates calcium homeostasis, which could lead to cell death. In the cochlea, glutamate is now considered to be one of the best candidates to mediate neurotransmission between inner hair cells (IHCs) and the auditory nerve dendrites. Among the variety of anatomical and physiological findings supporting the glutamate hypothesis, is the striking similarity of acute damage in the organ of Corti caused by exposure to a glutamate analogue (kainic acid), or by hypoxia, or even by an intense loud noise. In all cases an immediate swelling is observed, specifically affecting the radial afferents below the IHCs. The best explanation for this swelling is related to glutamate (or glutamate analogue) excitotoxicity. Thus, some of the cochlear damage that occur with ageing, especially the loss of the radial afferent fibres and type I ganglion cells, might well be attributed to glutamate excitotoxicity linked to vascular atrophy. The present paper discusses this hypothesis.

Aging↗
PubMed1990

[Laparoscopic findings in liver fascioliasis. Study of 13 cases].

The laparoscopic findings in 13 patients with liver fasciolasis are described. Diagnosis was made in three cases in base of the presence of ova Fasciola Hepatica in the patient's faeces and in 10 cases, because they fulfilled the following conditions: ingestion of fresh watercress, eosinophilic count exceeding 30%, positive serologic tests, eosinophilic granulomas with Charcot-Leyden crystals in liver biopsy and good response to treatment with dihidroemetine or bithionol. Nine cases (68.2%) showed hepatomegaly. In 12 of 13 (92.3%) lesions suggestive of hepatic distomatosis were found. Hepatic nodules of different sizes and shapes could be seen in 10 patients (76.9%), Glisson capsule was involved in five cases (38.4%) and peritoneum in three (23%). The latter was always affected with the liver but, on the other hand, liver capsule was found affected alone in two cases. In our experience, laparoscopy with liver biopsy is an important method for diagnosis of abdominal fasciolasis.

Adult↗
PubMed1989

K+ differentially affects the excitatory amino acids- and carbachol-elicited inositol phosphate formation in rat brain synaptoneurosomes.

K+, excitatory amino acids (EAAs) and carbachol (Carb) were tested separately or in pairs for their ability to stimulate inositol phosphate (IPs) formation in rat forebrain synaptoneurosomes. K+ ions per se, stimulate IPs synthesis (158% of the control value) as well as EAAs and Carb. The glutamate (Glu)- and quisqualate (QA)-elicited IPs formation is not additive with that evoked by K+. Inversely, K+ ions (up to 30 mM) potentiate the Carb-induced IPs accumulation. These results indicate that QA (or Glu) and Carb enhance IPs formation independently and that QA- and K+ -induced IPs responses are interdependent. This suggests that they share a 'common intermediate' step in the multistep mechanism which leads from receptor activation to the IPs synthesis. This 'common intermediate' step may be depolarization and/or Na+ influx.

Amino Acids↗
PubMed1989

Developmental changes in the chemosensitivity of rat brain synaptoneurosomes to excitatory amino acids, estimated by inositol phosphate formation.

The evolution of excitatory amino acids-(EAA) stimulated inositol phosphates (IPs) turnover during postnatal development was investigated in synaptoneurosomes prepared from rat forebrains. The two main EAA agonists which induce the IPs synthesis were quisqualate (QA) and N-methyl-D-aspartate (NMDA). The QA and NMDA stimulations of IPs formation present a particular developmental pattern, characterized by an active phase during rat synaptogenesis. The QA-evoked IPs accumulation peaked in synaptoneurosomes prepared from 8-day-old rat forebrains while that evoked by NMDA peaked in synaptoneurosomes from 12-day-old rats. These two developmental patterns are specific of the EAA agonists since the other various neuroactive substances tested (carbachol (Carb), noradrenaline, and high concentrations of potassium) induced an IPs accumulation, which increases during development and reaches a maximum in synaptoneurosomes of adult animals. Aging leads to a decrease in the capability of EAAs and muscarinic agonists to stimulate IPs formation in synaptoneurosomes, whereas the stimulation of IPs turnover by noradrenaline remains constant. Taken together, these results suggest that EAAs play a key role during brain development by sequentially activating two receptor subtypes, a new QA receptor, and a NMDA receptor, linked to the phosphoinositide metabolism. They may also indicate that these EAA-induced IPs responses are related to neuronal plastic events, the amplitude of which decreases with aging.

Aging↗
PubMed1987

Chloride transport blockers inhibit the chloride-dependent glutamate binding to rat brain membranes.

The effects of a series of chloride transport blockers (ethacrynate, furosemide, torasemide, 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene and diphenylcarboxylate) on Cl(-)-dependent L-[3H]glutamate (Glu) binding were tested in rat brain membranes, Cl-transport blockers inhibit the Ca2+/Cl(-)-induced increase in L-[3H]Glu binding, some of them without affecting the Ca2+/Cl(-)-independent L-[3H]Glu binding. Increasing the medium osmolarity by augmenting the sucrose concentration also inhibited the Ca2+/Cl(-)-induced increase in L-[3H]Glu binding. The effects of both sucrose and Cl-transport blockers were not additive, suggesting that they acted on the same type of mechanism. We recently suggested that L-[3H]Glu binding to brain membranes corresponds to Glu uptake in membrane vesicles. Therefore we propose that the Cl-transport blockers inhibit a Cl(-)-dependent Glu accumulation into these vesicles.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗