50 research outputs found
Analgesic drug taking: Beliefs and behavior among headache patients
No full textObjective.-To explore beliefs and behavior with respect to analgesic drug taking in headache patients. To compare episodic headache to chronic headache sufferers. Methods.-A consecutive series of 280 headache patients, newly admitted to the Headache Center of the University of Modena, all referred by their general practitioner, were asked to fill out a brief questionnaire, specially compiled for this survey. The questionnaire invited patients to indicate how they themselves thought they should best cope with their headache, and how they actually did so in practice. Results.-The majority of our patients had a positive attitude towards over-the-counter analgesics, which they believed to be more adequate than prescription drugs for acute treatment of their headache. They handled analgesics very carefully, believing it correct to take the drug only when the pain became unbearable, if it was not possible for them to stop work. Chronic headache patients tended to consume more prescription drugs than episodic headache sufferers. Furthermore, the majority of chronic sufferers, as opposed to episodic sufferers, took the analgesic even when not at work. Conclusions.-The use of over-the-counter drugs is considered the best way to treat acute headache even by subjects suffering from severe idiopathic headache and seeking professional care in specialized clinics. Prescribed analgesics are underused by patients with serious episodic headache, which is precisely the group for which they are principally intended
Headache patients’ attitude toward analgesic drugs
No full textThe majority of our patients had a positive attitude towards over-the-counter analgesics, which they believed to be more adequate than prescription drugs for acute treatment of their headache. They handled analgesics very carefully, believing it correct to take the drug only when the pain became unbearable, if it was not possible for them to stop work. Chronic headache patients tended to consume more prescription drugs than episodic headache sufferers. Furthermore, the majority of chronic sufferers, as opposed to episodic sufferers, took the analgesic even when not at work.
The use of over-the-counter drugs is considered the best way to treat acute headache even by subjects suffering from severe idiopathic headache and seeking professional care in specialized clinics. Prescribed analgesics are underused by patients with serious episodic headache, which is precisely the group for which they are principally intended
Il ripristino della funzione meccanica atriale dopo cardioversione della fibrillazione atriale: fattori predittivi clinici ed ecocardiografici.
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L’uso quotidiano di analgesici è causa od effetto della cronicizzazione di una cefalea?
No full textGli analgesici sono i farmaci più utilizzati nel mondo (1). Escludendo i morfinici sono oggetto d’abuso e/o inducono dipendenza unicamente su base iatrogena, in soggetti con dolore cronico quando vengono mal curati (2). L’uso di analgesici e’ tipico di chi soffre di cefalea (3) mentre l’uso eccessivo si associa invariabilmente ad una cefalea cronica, quotidiana o quasi. Le forme croniche rappresentano uno dei capitoli più complessi nell’ambito della diagnosi e della terapia delle cefalee. Nonostante l’importanza pero’ non hanno ancora trovato una sistemazione nosologica definitiva e sono di difficile inserimento anche nell’ambito della classificazione dell’IHS (4, Silberstein,1994, 51). Le cefalee croniche gravi e disabilitanti, comportano un costo notevole sul piano individuale e sociale (5, 6), impegnano il maggior numero di risorse sanitarie (7) e spesso sono refrattarie alle terapie efficaci nelle forme episodiche (8). Quando alla cefalea cronica si associa un uso frequente, regolare, eccessivo, improprio, o un vero abuso di analgesici (che può portare alla dipendenza) i due fenomeni si sovrappongono e si intrecciano in un tutto quasi inestricabile.
Sebbene le prime prove dell’esistenza di cefalee croniche correlate ad un uso eccessivo di analgesici siano state suggerite sin dagli anni ’50 (8) la responsabilità della cronicizzazione fu attribuita con forza ai farmaci analgesici solo negli anni ’80 (10-12) osservando che quando si riesce ad interrompere stabilmente l’assunzione dell’analgesico si assiste anche ad un miglioramento della cefalea. Da allora le stesse osservazioni sono state ripetute ed ampliate: che i farmaci analgesici rappresentino il principale fattore di cronicizzazione di una cefalea inizialmente episodica e’ pertanto una conoscenza considerata acquisita (13). L’inter- relazione tra farmaci analgesici e cefalea cronica viene di norma descritta come se i primi fossero la causa della seconda: il paziente assumeva analgesici tutti i giorni e soffriva di una grave cefalea; sospendendo l’uso di analgesici la sua cefalea e’ migliorata; ne deriva che gli analgesici erano la causa del suo star male. La stessa realtà clinica può pero’ essere descritta anche nel modo seguente: il paziente soffriva di una grave cefalea e doveva assumere analgesici tutti i giorni; trovando finalmente una soluzione efficace e diversa dall’uso dell’analgesico sta molto meglio e non ha più bisogno di assumere tanti analgesici. Tra i controlli ed un gruppo di soggetti con cefalea cronica non c’era nessuna differenza nel consumo di analgesici sintomatici prima che insorgesse la cronicità (Baldrati et al, 1985) Allora l’assunzione dei farmaci analgesici era la causa della cefalea cronica oppure una sua logica conseguenza? Per tentare di rispondere a questa domanda abbiamo analizzato la letteratura di lingua inglese dal 1988 ad oggi sulle cefalee croniche e l’uso di analgesici, focalizzando la ricerca sugli elementi a favore e/o contro ciascuna delle due interpretazioni della stessa realtà clinica. L’obiettivo era quello di farne una valutazione critica, orientata a capire se nei soggetti che soffrono di cefalea cronica e fanno un uso eccessivo di analgesici l’intervento terapeutico deve puntare primariamente a trattare l’abuso per curare la cefalea o a trattare la cefalea per prevenire l’abuso
Heparin-induced thrombocytopenia in patients treated with unfractionated heparin: Prevalence of thrombosis in a 1 year follow-up
No full textBACKGROUND: Patients with unstable angina are usually treated with unfractionated heparin and aspirin, but very little is known about the prevalence of heparin-induced antibodies and their relation to thrombotic complications some time after the acute phase of unstable angina. The aim of the present study was to establish the prevalence of heparin-induced thrombocytopenia and the prevalence of heparin-dependent platelet-reactive antibodies in patients treated with unfractionated heparin and the occurrence of thrombosis in a 1 year follow-up. METHODS: Patient population included 124 consecutive patients with unstable angina treated with unfractionated heparin for almost 5 days. The prevalence of heparin-dependent platelet-reactive antibodies using an ELISA assay was measured before the beginning of heparin therapy and after 7 and 40 days. The platelet count was measured at the same time and the presence of thrombotic occurrences was checked. Clinical follow-up lasted 1 year. RESULTS: At baseline no one patient was positive for heparin-induced antibodies. On day 6, 38 patients (30%) produced a positive heparin-induced antibody result and 30 patients (24%) had an intermediate result. The majority of patients (74%) who developed antibodies became positive after 6 days of heparin therapy. The combined incidence of death, myocardial infarction, recurrent angina, urgent revascularization and stroke was 66% in patients with antibodies and 44% in patients without antibodies during a 1 year follow-up. The incidence of combined primary end points was statistically higher in patients positive for antibodies. The log-rank test was statistically significant (chi2 = 4.39, p < 0.01). CONCLUSIONS: No one patient developed a clinical evidence of thrombocytopenia. Nevertheless thrombotic events during follow-up were more common in patients who developed heparin-induced antibodies. These patients need a more accurate evaluation and surveillance after hospital discharge.Background. Patients with unstable angina are usually treated with unfractionated heparin and aspirin, but very little is known about the prevalence of heparin-induced antibodies and their relation to thrombotic complications some time after the acute phase of unstable angina. The aim of the present study was to establish the prevalence of heparin-induced thrombocytopenia and the prevalence of heparin-dependent platelet-reactive antibodies in patients treated with unfractionated heparin and the occurrence of thrombosis in a 1 year follow-up. Methods. Patient population included 124 consecutive patients with unstable angina treated with unfractionated heparin for almost 5 days. The prevalence of heparin-dependent platelet-reactive antibodies using an ELISA assay was measured before the beginning of heparin therapy and after 7 and 40 days. The platelet count was measured at the same time and the presence of thrombotic occurrences was checked. Clinical follow-up lasted 1 year. Results. At baseline no one patient was positive for heparin-induced antibodies. On day 6, 38 patients (30%) produced a positive heparin-induced antibody result and 30 patients (24%) had an intermediate result. The majority of patients (74%) who developed antibodies became positive after 6 days of heparin therapy. The combined incidence of death, myocardial infarction, recurrent angina, urgent revascularization and stroke was 66% in patients with antibodies and 44% in patients without antibodies during a 1 year follow-up. The incidence of combined primary end points was statistically higher in patients positive for antibodies. The log-rank test was statistically significant (x2= 4.39, p < 0.01). Conclusions. No one patient developed a clinical evidence of thrombocytopenia. Nevertheless thrombotic events during follow-up were more common in patients who developed heparin-induced antibodies. These patients need a more accurate evaluation and surveillance after hospital discharge
Azioni, interazioni, controindicazioni, tossicità dei farmaci utilizzati nella terapia dell'emicrania
No full textL'emicrania è un disturbo diverso da latri stati dolorosi che riconoscono una causa organica ed ha una sintomatologia così tipica da indirizzare la diagnosi. I farmaci antiemicranici eliminano il dolore soltanto in una percentuale di pazienti mentre gi altri on rispondono al trattamento pur essendo apparentemente emicranici quanto i responders. Nel valutare gli effetti a lungo termine di un trattamento farmacologico siamo di solito approssimativi. Per esempio quando dopo una terapia preventiva dimostratasi efficace ricompaioni gli attacchi di emicrania non abbiamo modo di capire quanto questo sia dovuto al ripresentarsi di eventi scatenanti oppure sia correlato alle proprietà dinamiche e cinetiche del farmaco usat
L’evoluzione clinica dell’emicrania può essere modificata dalla modulazione della terapia
No full textL’emicrania cronica complicata da medication-overuse è un disturbo disabilitante, che causa un’enorme sofferenza, costi sociali altissimi ed è difficile da trattare. E’ quindi indispensabile tentare di prevenirla. A questo fine si raccomanda che i pazienti emicranici con attacchi gravi e frequenti ricevano, oltre alla diagnosi: 1.un trattamento efficace dell’attacco; 2. l’inizio precoce di una terapia di profilassi adeguata per dosaggio e durata; l’individuazione e la terapia di eventuali comorbidità e fattori modificabili di rischio di progressione.
Teoricamente un’inizio precoce, aggressivo della terapia di profilassi dovrebbe essere l’intervento decisivo per prevenire la cronicizzazione. I farmaci per la profilassi dell’emicrania, anche quelli di prima scelta, hanno una efficacia limitata. Circa il 50% dei pazienti può aspettarsi una riduzione del 50% degli attacchi. L’altro 50% sperimenta gli effetti collaterali del farmaco in assenza di benefici significativi. Tutti i trattamenti di profilassi agiscono poco o nulla sulle caratteristiche intrinseche degli attacchi, non modificano in modo significativo gravità e durata degli attacchi. Inoltre la scelta è empirica in quanto non ci sono elementi predittivi di efficacia
La Cefalea da abuso di analgesici” analizzata alla luce della “evidence based medicine"
No full textIn conclusione ci sono diverse interpretazioni “dell’abuso” e della “dipendenza da farmaci”. Esiste confusione perche’ anche l’uso corretto dei farmaci, secondo prescrizione medica, se non e’ limitato nel tempo, puo’ determinare tolleranza e dipendenza. Queste condizioni sono il risultato di adattamenti fisiologici dell’organismo chiaramente individuabili nell’ambito della farmacologia sperimentale e nell’attivita’ clinica.
Analizzando la letteratura sulle cefalee croniche associate ad uso di farmaci emergono i seguenti punti critici:
1°) non esistono dati certi sul dosaggio dei differenti farmaci necessario per produrre la “cefalea da farmaci”
2°) non e’ chiaro se l’elemento chiave per la genesi della cefalea da farmaci e’ la dose della sostanza, la durata dell’assunzione o se entrambi questi fattori sono importanti
3°) farmaci appartenenti a classi farmacologiche completamente diverse (FANS, paracetamolo, codeina, barbiturici, ergotaminici, benzodiazepine) sembrano provocare cefalee simili, quasi identiche. Sono realmente identiche o non sono state studiate con attenzione?
4°) non esistono dati certi sulla patogenesi della cefalea da analgesici, morfinici, barbiturici. E’ stato unicamente ipotizzato il meccanismo della cefalea da ergotaminici.
Per tentare di chiarire questi punti occorrerebbe descrivere la cefalea associata all’assunzione di sostanze di una specifica classe farmacologica precisando la dose, la durata dell’assunzione, con quali sintomi si manifesta, con quale frequenza e quali provvedimenti terapeutici possono alleviarla. Sarebbe inoltre utile definire che cosa si intende per sindrome da sospensione, come si manifesta, con che frequenza, quanto dura, quali interventi terapeutici possono ridurla o prevenirla.
Purtroppo molti contributi della letteratura si limitano a presentare casistiche di soggetti con cefalea cronica che consumano naturalmente piu’ farmaci e a dosaggio piu’ elevato, evidentemente come logica conseguenza della maggiore durata, frequenza ed intensita’ degli episodi dolorosi, rispetto a quanti soffrono di una cefalea episodica.
Le spiegazioni sono in genere limitate a questo: poiche’ questo tipo di cefalea migliora drammaticamente con la sospensione dell’assunzione dei farmaci analgesici se ne deduce che la cefalea cronica e’ causata dall’abuso di farmac
Assessment of the efficacy and tolerability of triptans in clinical practice
No full textIn most cases a triptan is prescribed to a patient suffering from
migraine who has been taking OTCAs for years, alone or combined
with caffeine, antiemetics, barbiturates, etc.
A proper use of triptans is therefore indispensable to correctly assess
whether they are efficacious and/or toxic in a completely different setting
from the one in which controlled clinical trials are conducted.
Patient’s judgments on the treatment are therefore fundamental to
assess if it is ineffective and/or causes toxic effects.
The physician knows that the efficacy and toxicity among triptans are
similar in clinical practice and that the response is individual and closely
connected to the patient’s compliance and expectations. Most side
effects of triptans appear the first time they are taken and their efficacy
is rarely the same each time they are taken. It is therefore advisable to
agree with the patient upon the use of the triptans: triptans are indispensable
drugs to treat migraine, but they are not miraculous. To prevent
the patient from stopping treatment or from trying different triptans
and then returning to self-medication, the patient must agree to fill
out a form on the efficacy and toxicity of the drug being taken.
Naturally, before preparing this form, the physician has to decide
whether to use the same parameters of efficacy and tolerability in clinical
practice and controlled clinical trials.
Whatever instruments are used to assess the drug, there are some key
elements to consider: time when the migraine attack started; time when
the drug was taken; presence of autonomic symptoms or aura; intensity
of the pain when it started and at the moment when the drug was
taken; duration of attack; should there be any relapse, at what time it
appeared; should there be any side effects, their intensity and duration.
The information gathered must then be discussed with the patient to
decide whether to continue or modify the treatment. Data on the efficacy
and tolerability of triptans, also if combined with other drugs,
could help to identify sub-groups of patients suffering from migraine
who are non-responders to triptans and/or prone to toxic effects
Pharmacoepidemiology of drug abuse in headache patients: comparison between sufferers of medication-overuse headache and migraine
No full textChronic headache patients often overuse symptomatic drugs while episodic headache patients usually take drugs in a very cautious way. It is unknown if the differences between the two groups of headache sufferers concern only the amount or also the type of drug used. Our aim was to compare the pharmacological habit between medication-overuse headache (MOH) and migraine patients. Methods We compared a) all drugs that 138 MOH patients (F/M=5.3; mean age +DS: + years) consecutively admitted at the in-patient ward of the Headache Centre of the University of Modena and Reggio Emilia, were taking and b) all drugs that 78 migraine patients (F/M= 2.3; mean age +DS: + years) consecutively referred at the out-patient ward of the Centre. Data were collected by means a standardized clinical chart and recorded in an apposite database. The study was carried out between June 2004 and March 2005. Results There were great differences in the type of symptomatic medications used between MOH and migraine patients. In particular MOH patients used concomitantly more than one type of symptomatic: triptans 43.5%, NSAIDs 42%, association of indomethacin, prochlorperazine and caffeine (IPC) 14.5%, and weak opioid 10%. Migraine patients took: NSAIDs 56%, triptans 30%, IPC 5%, and other analgesic combinations 2.6%. In both groups most used drugs, respectively among NSAIDs and triptans, were nimesulide and sumatriptan. Fifty-eight per cent of MOH but only 20% of migraine patients were taking prophylactic treatments. More than 71% of MOH patients were using other medications, too: antihypertensive agents 27.5%, benzodiazepines 27%, antidepressants 23%, hormones 23%, antilipemic agents 7%, antiplatelet agents 6%. Among migraine patients 54% were using other medications, too: hormones 33%, antihypertensive agents 8%, antidepressants 10%, benzodiazepines 5%. Conclusions Even if MOH often evolves from migraine, our study indicates that pharmacoepidemiology of drug use was different between the two headache forms: MOH overused triptans more than NSAIDs and were poli-medicated; migraine patients for acute treatment took mainly NSAIDs, did not use weak opioid and overall took few other medications
