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Dipirona
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<p style="text-align: justify;"><span id="more-4682"></span>INTRODUÇÃO<br>
Analgesia por AINEs é explicada pela ação
inibitória da síntese local
de PGE2 (Vane, 1971). Essa ação previne o desenvolvimento
da
hiperalgesia , isto é, a sensibilização dos
receptores de dor para
estímulos químicos e físicos.</p>
<p style="text-align: justify;">Dipirona é um analgésico
e antipirético muito utilizado em diversos países onde
sua propaganda é permitida.</p>
<p style="text-align: justify;">Existe uma impressão entre os
médicos
de que a dipirona tem um efeito clínico diferente dos AINEs.
Existem
muitos artigos e estudos na literatura mostrando que a dipirona tem
efeito analgésico maior que aspirina, que é um
antiinflamatório
inibidor de COX clássico (Mukherjee et Sudha, 1980; Petrova et
al.
1980) ou paracetamol (Daftary et al, 1980), um analgésico do
grupo da
anilina, e por isso o perfil do efeito farmacológico da dipirona
é
certamente diferente do que dos AINEs e também dos
analgésicos de ação
central (Nikolova et al, 1980; Nikolov et al., 1980). No entanto, esse
sítio de ação analgésica é um
mecanismo controverso. A ação central foi
proposta por Von Tomek (1955) e não confirmada por Lorenzetti
(1999)
que, ao aplicar dipirona intra-cerebroventricular de rato, não
conseguiu inibir a hiperalgesia induzida por prostaglandina em pata
trazeira de rato.</p>
<p style="text-align: justify;">2 – O QUE É DIPIRONA</p>
<p style="text-align: justify;">Dipirona é o nome
genérico de ácido
[(2,3-dihidro-1,5-dimetil-3-oxo-2-fenil-1H-pirazol-4-il)metilamino]metanossulfônico,
também chamado de
1-fenil-2,3-dimetil-5-pirazolona-4-metilaminometanossulfonato de
sódio
(ou de magnésio), e ainda denominado de metamizol, um segundo
nome
genérico e muito encontrado na literatura farmacológica
norte-americana
e européia.</p>
<p style="text-align: justify;"><br>
</p>
<p style="text-align: center;"><img class="aligncenter size-full wp-image-12787" title="dipirona" src="http://antonini.med.br/portal/wp-content/uploads/2009/06/dipirona.jpg" alt="" height="151" width="367"></p>
<p style="text-align: justify;">Com peso molecular de 351,36 e uma
distribuição relativa de 44,44% de carbono, 5,16% de
hidrogênio, 11,96%
de nitrogênio, 6,54% de sódio (7,26% se for
magnésio), 22,77% de
oxigênio e 9,13% de enxofre, apresenta fórmula
empírica
C13H16N3NaO4S.H2O (ou C26H32MgN6O8S2. Na dipirona magnesiana ligam-se
duas moléculas de dipirona ao cátion magnésio).
É preparada a partir da
metilação do grupo amino da sulfamipirina, tratada com
aldeído
metanóico (formaldeído ou formol), em
solução de bissulfito de sódio.
Muito solúvel em água (1g/1,5ml), é pouco
solúvel em etanol e
praticamente insolúvel em éter, acetona, benzeno e
clorofórmio, sendo
um complicador quando é necessário fazer uma
cromatografia de camada
delgada para diferenciação da dipirona de outros
tóxicos e barbitúricos
em processos jucidiais onde é pedido a
identificação toxicológica com
fins forenses, pois os melhores carreadores de moléculas em
cromatografia de camada delgada são justamente o benzeno, o
éter, o
etanol, o hexano e a acetona, sendo o metanol muito pouco utilizado
devido à sua toxicidade e a água não ser usada por
dissolver a camada
de sílica da placa.</p>
<p style="text-align: justify;">Observando a molécula da
dipirona, é
possível identificar duas estruturas ligantes que tem
papéis
importantes no mecanismo de ação deste fármaco. O
primeiro é o
grupamento benzoil, que tem atividade anestésica comprovada,
tanto que
a maior contribuição da cocaína para a
farmacológia foi a identificação
dos componentes de sua fórmula estrutural e a descoberta de que,
retirando-se o radical benzoil, a cocaína perdia sua
ação anestésica
(Cavazzani, 1994).</p>
<p style="text-align: center;"><img class="aligncenter size-full wp-image-12790" title="benzoil" src="http://antonini.med.br/portal/wp-content/uploads/2009/06/benzoil.jpg" alt="" height="84" width="108"></p>
<p style="text-align: justify;">Outro ligante de importância na
estrutura da dipirona é o grupamento sulfato, responsável
por sua alta
solubilidade em água e pela sua facilidade de
absorção, é
potencilamente agressivo para a medula óssea, podendo causar
desde
neutropenias, agranilocitoses, até aplasia de medula
óssea, uma
patologia hematopoiética muito severa que só tem um
tratamento, o
transplante de medula óssea que, se não realizado em
tempo, pode levar
o indivíduo ao óbito.</p>
<p style="text-align: justify;">Grupamento sulfato:</p>
<p style="text-align: center;"><img class="aligncenter size-full wp-image-12792" title="sulfato" src="http://antonini.med.br/portal/wp-content/uploads/2009/06/sulfato.jpg" alt="" height="120" width="104"></p>
<p style="text-align: justify;">Foi patentetada sob nº 254, pelo
Laboratório Hoechst em 1911, na Alemanha com o nome de
Metamizol® que
hoje acabou virando nome genérico, como aconteceu com a
Aspirina®, que
é marca registrada de ácido acetilsalicílico,
desenvolvido pela Bayer e
que se consagrou, tornando-se um nome genérico.</p>
<p style="text-align: justify;">3 – MECANISMO DE
AÇÃO</p>
<p style="text-align: justify;">Apesar de todas as pesquisas já
realizadas apontarem para uma ação bloqueadora da
hiperalgesia exercida
pela ligação a um receptor periférico, combinado
com ação espinal da
dipirona e com poucos efeitos antiedematosos e/ou
antiiflmatórios,
alguns bancos de dados insistem em continuar afirmando que a
ação da
dipirona atua unicamente por inibição de cicloxigenase,
inibindo a
síntese de prostaglandinas (Abbate et al, 1990; Anon, 1973;
Reynolds,
1994; Gladtke, 1983; Arellano et Sacristan, 1990).</p>
<p style="text-align: justify;">No volume 116, de setembro de 2000 do
banco de dados Drugdex (Micromedex) aparece a citação
feita no
parágrafo anteiror, ignorando os trabalhos realizados entre 1996
e 1999
por Aleksander Zampronio, Berenice B. Lorenzetti e Sérgio H.
Ferreira,
que apontam para a ação periférica da dipirona
sobre um receptor
sináptico com estimulação epinhal via
ativação da arginina/cGMP em
neurônios sensoriais primários.</p>
<p style="text-align: justify;">A ação antitérmica
da dipirona pode ser
explicada pelo antagonismo direto de cininas pirogênicas em
receptores
do centro termo-regulador, localizado no tálamo.</p>
<p style="text-align: justify;">4 – FARMACOCINÉTICA</p>
<p style="text-align: justify;">4.1 – INÍCIO DA
AÇÃO</p>
<p style="text-align: justify;">Na hipertermia (febre), após
administração oral, o efeito hipotermiante começa
a aparecer entre 30
minutos e no máximo em uma hora (Ajgaonkar et al, 1988;
Giovannini et
al, 1986; Reiner et al, 1984). O pico máximo de resposta ficam
entre 4
e 6 horas (Ajgaonkar et al, 1988; Giovannini et al, 1986; Reiner et al,
1984).</p>
<p style="text-align: justify;">4.2 – NÍVEL MÁXIMO
DE CONCENTRAÇÃO PLASMÁTICA</p>
<p style="text-align: justify;">Após administração
oral, pode ser
encontrado um nível máximo de concentração
após 1 a 2 horas (Vlahov et
al, 1990; Flusser et al, 1988; Volz et Kellner, 1980). O nível
máximo
de concentração plasmática do metabólito
ativo 4-MAA encontrado foi de
11, 21 e 41 mcg/ml, após administração oral de
750, 1500 e 3000mg de
dipirona, respectivamente (Vlahov et al, 1990). Na realidade e dipirona
é uma pro-droga que é metabolizada no trato intestinal em
4-metilaminoantipirina (4-MAA), o metabólito ativo (Vlahov et
al, 1990;
Flusser et al, 1988; Brune, 1988; Levy, 1986; Volz et Kellner, 1980). O
4-MAA é metabolizado no fígado em 4-aminoantipirina
(4-AA), um segundo
metabólito ativo (Brune, 1988; Flusser et al, 1988).</p>
<p style="text-align: justify;">A dipirona não apresenta
interações
conhecidas com alimentos ou então são clinicametne
insignificantes
(Levy et al, 1995; Flusser et al, 1988).</p>
<p style="text-align: justify;">4.3 – SÍTIOS DE
DISTRIBUIÇÃO</p>
<p style="text-align: justify;">Cerca de 58% do 4-MAA e 48% do 4-AA
são
distribuidos ligados às proteínas plasmáticas
(Zylber-Katz et al,
1985). Os metabólitos da dipirona tem sido encontrados no
líquido
céfalo-raquidiano. Em estudo controlado, 28 pacientes com
indicação
terapêutica de dipirona, tomando 1g por via oral (dois
comprimidos de
500mg) em tempos diversos (6 em 6 horas) foram submetidos a
punção
lombar em vários intervalos de tempo e colhido cerca de 2ml de
líquor
sendo detectada a presença dos metabólitos em
concentração menor que no
plasma, mas guardando uma proporção líquor/plasma
de ambos os
metabólitos (Cohen et al, 1998).</p>
<p style="text-align: justify;">4.4 – VOLUME DE
DISTRIBUIÇÃO</p>
<p style="text-align: justify;">O volume de distribuição
do 4-MAA é de 40 litros (Vlahov et al, 1990).</p>
<p style="text-align: justify;">4.5 – METABOLISMO</p>
<p style="text-align: justify;">4.5.1 – PAREDE INTESTINAL</p>
<p style="text-align: justify;">A metabolização da
dipirona na parede
intestinal é extensa (Vlahov et al, 1990; Flusser et al, 1988;
Brune,
1988; Levy, 1986; Volz et Kellner, 1980).</p>
<p style="text-align: justify;">O metabolismo é feito
monoenzimaticamene por hidrólise no trato intestinal formando o
4-MAA,
um dos seus metabólitos ativos (Vlahov et al, 1990; Flusser et
al,
1988; Brune, 1988; Levy, 1986; Volz et Kellner, 1980).</p>
<p style="text-align: justify;">4.5.2 – FÍGADO</p>
<p style="text-align: justify;">No fígado o metabolismo
também é grande
(Flusser et al, 1988; Brune, 1988; Volz et Kellner, 1980). O 4-MAA
é
transformado em 4-AA (Brune, 1988; Flusser et al, 1988; Volz et
Kellner, 1980) e outros metabólitos inativos e de pouca
importância. Em
portadores assintomáticos de hepatite B, com
função hepática normal,
testes demonstraram prejuízo no metabolismo oxidativo da
dipirona
quando comparado com sujeitos não portadores (Levy et al, 1997).</p>
<p style="text-align: justify;">4.5.3 – METABÓLITOS</p>
<p style="text-align: justify;">1. 4-Metilaminoantipirina, é um
metabólito ativo (Flusser et al, 1988; Brune, 1988).</p>
<p style="text-align: justify;">2. 4-Aminoantipirina, também
é um metabólito ativo (Brune, 1988; Flusser et al, 1988;
Volz et Kellner, 1980).</p>
<p style="text-align: justify;">3. 4-Formil-aminoantipirina (4-FAA),
é um metabólito inativo (Vlahov et al, 1990; Volz et
Kellner, 1980).</p>
<p style="text-align: justify;">4. 4-acetilaminoantipirina (4-AcAA),
também é inativo (Vlahov et al, 1990; Volz et Kellner,
1980).</p>
<p style="text-align: justify;">4.5.4 – EXCREÇÃO</p>
<p style="text-align: justify;">4.5.4.1 – Leite Materno</p>
<p style="text-align: justify;">Os metabólitos ativos da
dipirona,
tanto o 4-MAA, quanto o 4-AA podem ser encontrados em altos
níveis no
leite materno. Estão em concentração igual ou
até maior que no plasma.
No entanto, os metabólitos foram encontrados no leite até
48 horas após
administração única de dipirona por via oral ,
devendo o uso de
dipirona ser evitado durante o aleitamento materno (Zylber-Katz et al,
1986).</p>
<p style="text-align: justify;">4.5.4.2 – Rins</p>
<p style="text-align: justify;">A excreção renal é
intensa, sendo a
maior via de eliminação (Vlahov et al, 1990; Volz et
Kellner, 1980). Os
metabólitos 4-FAA e 4-AcAA são excretados primeiramente
na urina
(Vlahov et al, 1990; Volz et Kellner, 1980).</p>
<p style="text-align: justify;">4.5.5 – MEIA VIDA</p>
<p style="text-align: justify;">O metabólito 4-MAA tem uma meia
vida de
2 a 3 horas (Vlahov et al, 1990; Volz et Kellner, 1980). O tempo de
eliminação médio do metabólito 4-MAA
é significativamente aumentado nos
portadores assintomáticos de hepatite B, quando comparado com
indivíduos sadios. (Levy et al, 1997), enquanto o tempo de
meia-vida de
eliminação do 4-FAA está significativamente
diminuido em portadores de
hepatite B em comparação com sujeitos não
portadores. Os tempos de
meia-vida de eliminação dos metabólitos 4-MAA e
4-AcAA não apresentam
diferenças estatísticas significantes entre os dois
grupos. (Levy et
al, 1997).</p>
<p style="text-align: justify;">O metabólito 4-AA tem uma
meia-vida de eliminação de 4 a 5 hoas (Vlahov et al,
1990; Volz et Kellner, 1980).</p>
<p style="text-align: justify;">5 – Diluição e
Estabilidade</p>
<p style="text-align: justify;">A Dipirona é compatível
com solução glicosada a 5%, solução de NaCl
a 0,9%<br>
e Ringer lactato*.<br>
A administração deve ser imediata em “bolus”
(ou em bolo) já que a estabilidade é limitada nas<br>
três soluções, devendo ser evitada a infusão
contínua*.</p>
<p style="text-align: justify;">* Informações do
fabricante Aventispharma (fabricante da Novalgina®).<br>
6 – RESTRIÇÕES AO USO</p>
<p style="text-align: justify;">6.1 –
CONTRA-INDICAÇÕES</p>
<p style="text-align: justify;">Discrasias sanguíneas ou
depressão da
medula óssea, hipersensibilidade, rinite, urticária, asma
e reações
alérgicas à aspirina ou outros agentes
antiinflamatórios.</p>
<p style="text-align: justify;">6.2 – PRECAUÇÕES</p>
<p style="text-align: justify;">História de úlceras
gastrointestinais,
hemorragias gástricas ou perfurações da mucosa;
disfuções renais;
hipertensão cardíaca (sobrecarga ventricular esquerda) ou
disfunções
cardíacas agravadas por retenção de fluidos e
edema; disfução hepática;
infecções pré-existentes; porfíria;
deficiencia de glicose-6-fosfato
desidrogenase e uso concomitante com clorpormazina.</p>
<p style="text-align: justify;">6.3 – REAÇÕES
ADVERSAS</p>
<p style="text-align: justify;">Anemia hemolítica e aplasia de
medula
óssea tem sido reportada durante o uso de dipirona (Anon, 1986;
Sansone
et al, 1984; Lay, 1966). Agranulocitose é a ocorrência
mais frequente
durante a administração de dipirona e pode ser fatal
(Arellano et
Sacristan, 1990; Hargis et al, 1989; Kiatboonsri et Richter, 1989;
Anon, 1986; Gladtke, 1983; Anon, 1973; Bottiger et Westerholm, 1973;
Sadusk, 1965; Huguley, 1964), tendo muitos casos acontecidos durante 20
anos de uso de dipirona na Holanda (van der Klauw et al, 1998). A
incidência da indução de agranulocitose tem
variação geográfica.
Aparece em altas frequências em Barcelona e Berlim e em pequnos
índices
em Budapest, Tel-Aviv e Sofia (Anon, 1986; Arellano et Sacristan, 1990;
Anon, 1973; Vlahov et Bacracheva, 1989) e varia de estudo para estudo.
Diferenças regionais são muito provavelmente relatadas
pela avaliação e
uso em modelos em vários países. A incidência de
agranulocitose varia
em 1,1 por milhão, durante a primeira semana de
administração (Anon,
1986) e um caso para cada 3000 usuários (Bottiger et Westerholm,
1973).
Calculos baseados em dados levantados, sugerem que o uso da dipirona
está associado a menos de 7000 casos por ano no mundo todo
(Kiatboonsri
et Richter, 1989).</p>
<p style="text-align: justify;">Os efeitos cardiovasculares incluem
hipotensão de moderada até severa (Hoigne et al, 1986;
Sanahuja et al,
1990). Evidencias de hipotensão com doses orais também
tem sido
descritas (Giovannini et al, 1986; Paeile et Gallardo, 1974).</p>
<p style="text-align: justify;">Efeitos centrais mais significativos
são sonolência, astenia e cefaléia (Lehtonen et al,
1983; Paeile et Gallardo, 1974).</p>
<p style="text-align: justify;">Efeitos gastrointestinais incluem
náusea, vômitos, irritação gástrica e
xerotomia, que tem sido relatadas
com a administração parenteral de dipirona (Marthak et
al, 1991;
Lehtonen et al, 1983; Paeile et Gallardo, 1974; von Szeged et Michos,
1986).</p>
<p style="text-align: justify;">Broncoespasmo também tem sido
descrito em administrações contínuas de dipirona
(Arellano et Sacristan, 1990).</p>
<p style="text-align: justify;">Entre as reações
cutâneas pode ser
encontrado necrose epidermal tóxica, urticária,
“rash” cutâneo (Anon,
1973; Arellano et Sacristan, 1990; Pandhi et al, 1984; Pasricha, 1979;
Lehtonen et al, 1983; Saban et al, 1991).</p>
<p style="text-align: justify;">Choque anafilático também
pode
acontecer, com uma incidência de 1 caso em 5000
administrações (Fosseus
et Straughan, 1983; Arellano et Sacristan, 1990; Kiatboonsri et
Richter, 1988).</p>
<p style="text-align: justify;">6.4 – TERATOGÊNESE</p>
<p style="text-align: justify;">Em estudo controlado, com
administração
de dipirona via oral durante a gravidez, mostrou que o desenvolvimento
de tumor de Wilms foi da ordem de 10,9% (com p<0,05). Esse estudo
incluiu 109 casos de tumor de Wilms e 218 controles. A idade
significante dos casos ao tempo do diagnóstico foi de 41,1
meses. As
mães foram questionadas sobre o uso de medicamentos durante a
gravidez
para se determinar a correlação do desenvolvimento do
tumor e o uso de
medicamentos e a dipirona foi a mais utilizada durante a gravidez de
mulheres cujos filhos apresentaram o tumor, possivelmente devido a
facilidade de acesso à droga. Sem dados de estudos prospectivos,
o
aumento na indicencia de tumor de Wilms em crianças expostas
à dipirona
não pode ser atribuida definitivamente ao fármaco, no
entanto, baseado
nesses estudos o uso de dipirona durante a gravidez deve ser evitado
(Sharpe et Franco, 1996).</p>
<p style="text-align: justify;">6.5 – INTERAÇÕES
MEDICAMENTOSAS</p>
<p style="text-align: justify;">6.5.1 – ACENOCOUMAROL</p>
<p style="text-align: justify;">Não foram observados efeitos
significantes nos tempos de coagulação durante uso
concomitante com a
dipirona (Zylber-Katz et al, 1985), porém sempre é
indicado o máximo de
cuidado e monitorização do paciente em uso concomitante
de dipirona com
anticoagulantes orais, especialmente se houver necessidade da
adição de
um antiinflamatório não esteróide ao tratamento. O
efeito adverso mais
comum é o aumento do risco de hemorragias.</p>
<p style="text-align: justify;">6.5.2 – ALENDRONATO</p>
<p style="text-align: justify;">Durante três anos de estudo
clínico
controlado, envolvendo 2027 pacientes que recebiam
antiinflamatórios
não esteroidais, a incidência de efeitos adversos
gastrointestinais foi
similar entre os pacientes recebendo alendronato e pacientes recebendo
placebo. No entanto, quando administrado alendronato com AINEs, e
dipirona, a incidencia aumentava, especialmente a
irritação gástrica,
efeito também observado com a dipirona (Prod Info
FosamaxÒ , 1999).</p>
<p style="text-align: justify;">6.5.3 – INIBIDORES DA ECA</p>
<p style="text-align: justify;">É conhecida a
interação entre os
inibidores da ECA e a dipirona, podendo surgir bradicardia,
frequentemente induzida por hipercalemia (Shionori, 1993). Esse
distúrbio pode levar a paradas cardíacas (Kurata et al,
1999).</p>
<p style="text-align: justify;">6.5.4 – BLOQUEADORES
BETA-ADRENÉRGICOS</p>
<p style="text-align: justify;">Em uso concomitante de dipirona com
beta-bloqueadores, tem sido reportado aumento na tensão arterial
e
interferência no controle da pressão sanguínea
(Radack et al, 1987;
Webster et al, 1984; Abate et al, 1990; Chalmers et al, 1984; Durao et
al, 1977; Salvetti et al, 1984; Watkins et al, 1980).</p>
<p style="text-align: justify;">6.5.5 – BLOQUEADORES DE CANAIS DE
CÁLCIO</p>
<p style="text-align: justify;">O uso de dipirona com bloqueadores de
canais de cálcio (nifedipina), aumenta o risco de hemorragia
gastrintestinal (Pahor et al, 1996).<br>
7 – EFICÁCIA COMPARATIVA</p>
<p style="text-align: justify;">7.1 – ACETAMINOFENO (Paracetamol)</p>
<p style="text-align: justify;">7.1.1 – FEBRE</p>
<p style="text-align: justify;">Dipirona na dose de 0,5g oral
demonstrou efeitos antipiréticos mais acentuados que o
paracetamol na
mesma dose em pacientes com febre tifóide e estudo controlado. A
redução da temperatura retal foi muito mais significativa
com dipirona
do que com paracetamol até uma ou duas horas após a
administração.
Existe uma tendência da dipirona para um efeito prolongado, em
torno de
6 horas ou mais (Ajgaonkar et al, 1988).</p>
<p style="text-align: justify;">7.2 – ÁCIDO
ACETILSALICÍLICO (Aspirina)</p>
<p style="text-align: justify;">7.2.1 – FEBRE</p>
<p style="text-align: justify;">Em um estudo pequeno, duplo-cego, o
efeito de 500mg de dipirona “per-ós” foi superior
à mesma dose de ácido
acetilsalicílico no tratamento de febre (Reiner et al, 1984).</p>
<p style="text-align: justify;">7.2.2 – DOR
PÓS-OPERATÓRIA</p>
<p style="text-align: justify;">O efeito de 500mg de dipirona 500mg
“per-ós” é consideravelmente superior ao do
ácido acetilsalicílico na
mesma dose no tratamento de dor, em estudo controlado (Arellano et
Sacristan, 1990).</p>
<p style="text-align: justify;">7.3 – N-METIL-BUTIL-ESCOPOLAMINA
(Hioscina)</p>
<p style="text-align: justify;">7.3.1 – NA CÓLICA RENAL</p>
<p style="text-align: justify;">Em estudo controlado com n=96 pacientes
com cólica renal, a hioscina em dose 20mg intravenosa foi
inefetiva na
remissão dos sintomas dolorosos, enquanto a dipirona na dose de
1 grama
intravenosa apresentou efeito menor que 2,5 gramas pela mesma via. 61%
dos pacientes tratados com hioscina precisaram da
adminstração conjunta
de analgésicos narcóticos (petidina, nalbufina, tramadol
ou morfina)
para controlar a dor, enquanto 17% e 0%, respectivamente, dos pacientes
em uso de dipirona precisaram da adição de
analgésico opióide (Lloret
et al, 1987).</p>
<p style="text-align: justify;">7.4 – CLONIXINA</p>
<p style="text-align: justify;">7.4.1 – DOR NA
PÓS-HISTERECTOMIA</p>
<p style="text-align: justify;">Em estudo randomizado, duplo-cego com
n=160 pacientes divididos em 4 grupos de 40 pacientes cada, foi
administrado 30mg em bolus 15 minutos antes da cirurgia e 15mg em bolus
de clonixina após a cirurgia, ou 660mg de dipirona em bolus
antes e
330mg após a histerectomia. 4,4% das pacientes tratadas com
dipirona
necessitaram de doses adicionais de dipirina para controlar a dor no
pós-operatório contra 11% das pacientes tratadas com
clonixina
(Rodriguez et al, 1993).</p>
<p style="text-align: justify;">7.5 – DEXTROCETOPROFENO</p>
<p style="text-align: justify;">7.5.1 – DOR NO
PÓS-OPERATÓRIO ODONTOLÓGICO</p>
<p style="text-align: justify;">A dipirona é tão eficaz
quanto do cetoprofeno em analgesia no pós-operatório
odontológico (Bagan et al, 1998).</p>
<p style="text-align: justify;">7.6 – DICLOFENACO</p>
<p style="text-align: justify;">7.6.1 – NA CÓLICA RENAL</p>
<p style="text-align: justify;">injeção intravenosa de
2,5 gramas de
dipirona combinada com pitofenona (um espasmolítico semelhante
à
atropina) e fempiverinium (um espasmolítico homólogo da
papaverina) tem
efeito similar ao diclofenaco na dose 75mg por via intramuscular. Ou
seja, o diclofenaco em monoterapia é mais efetivo que a dipirona
em
monoterapia (Sanahuja et al, 1990).</p>
<p style="text-align: justify;">7.6.2 – NA CIATALGIA</p>
<p style="text-align: justify;">No tratamento da ciatalgia (dor do
nervo ciático), 2,5 gramas de dipirona intramuscular foi mais
efetivo
que 75 miligramas de diclofenaco pela mesma via em tratamento
controlado, randomizado, duplo-cego de 260 pacientes que receberam
dipirona, diclofenado ou placebo por via intramuscular. A dipirona foi
mais efetiva que o diclofenaco com início do efeito após
uma hora da
aplicação e prolongando-se por cerca de 48 horas
(Babej-Dolle et al,
1994).</p>
<p style="text-align: justify;">7.7 – IBUPROFENO</p>
<p style="text-align: justify;">7.7.1 – NA DOR
PÓS-CIRÚRGICA</p>
<p style="text-align: justify;">Em estudo comparado entre dipirona
magnesiana intramuscular, ibuprofeno e placebo por via oral, a espectro
analgésico e o tempo de duração da
ação entre a dipirona e o ibuprofeno
foram semelhantes e superiores ao placebo (de Miguel Rivero et al,
1997).</p>
<p style="text-align: justify;">7.8 – INDOMETACINA</p>
<p style="text-align: justify;">7.8.1 – NA CÓLICA RENAL</p>
<p style="text-align: justify;">Injeção intravenosa de
2,5g de dipirona
tem mostrado efeito maior que 50mg de indometacina pela mesma via, no
tratamento da cólica ureteral em litíases
(cálculos) renais (Lehtonen
et al, 1983).</p>
<p style="text-align: justify;">7.9 – KETORALAC</p>
<p style="text-align: justify;">7.9.1 – EM ANALGESIA</p>
<p style="text-align: justify;">Em estudo randomizado, comparando
aplicação de 30mg de ketorolac por via intramuscular (um
AINE derivado
da pirazolona) com 2g de dipirona pela mesma via cada 12 horas em n=60
pacientes com dor de severa à moderada após cirurgia
ortopédica,
encontrou-se uma eficácia similar entre o ketorolac e a dipirona
no
controle da dor nas primeiras 6 horas do pós-operatório.
Após os três
dias seguintes, a redução da intensidade da dor foi
melhor conseguida
com o ketorolac, demonstrando uma eficácia maior deste
analgésico em
relação à dipirona (Fernandez-Sabate et al, 1991).</p>
<p style="text-align: justify;">7.10 – MEPERIDINA (Petidina)</p>
<p style="text-align: justify;">7.10.1 – NA DOR
PÓS-CIRÚRGICA</p>
<p style="text-align: justify;">Dipirona na dose 2,5g intramuscular ou
intravenosa tem sido tão efetivo quanto 50 ou 100mg de petidina
intravenosa no tratamento da dor pós-cirúrgica (Patel et
al, 1980; Lal
et al, 1973; Arellano et Sacristan, 1990).</p>
<p style="text-align: justify;">7.10.2 – NA CÓLICA RENAL</p>
<p style="text-align: justify;">Doses de 2,5g de dipirona intravenosa
tem se mostrado tão efetivo quanto 50mg de petidina intravenosa
no
tratamento da cólica renal em cólica ureteral em um
estudo randomizado
(Lehtonen et al, 1983).</p>
<p style="text-align: justify;">7.11 – NIMESULIDE</p>
<p style="text-align: justify;">7.11.1 – NA FEBRE</p>
<p style="text-align: justify;">Em um pequeno estudo duplo-cego, 500mg
de dipirona por via oral foi comparada em eficácia com o
nimesulide (um
novo AINE) na dose 100mg pela mesma via, no tratamento da febre
frequentemente produzida por diversos fatores. Ambas as drogas
apresentaram o mesmo escore de efetividade e foram superioras ao
ácido
acetilsalicílico, que também foi utilizado no estudo, em
efeito (Reiner
et al, 1984).</p>
<p style="text-align: justify;">7.11.2 – NA DOR
PÓS-CIRÚRGICA</p>
<p style="text-align: justify;">Em estudo duplo-cego em crianças
com
dor pós-operatória foram utilizados supositórios
de 100mg de nimesulide
e 300mg de dipirona a cada 6 horas e ambas as drogas apresentaram a
mesma eficácia no tratamento da dor inflamatório no
pós-operatório das
crianças (Scharli et al, 1990).</p>
<p style="text-align: justify;">7.12 – PENTAZOCINE</p>
<p style="text-align: justify;">7.12.1 – NA DOR DO
PÓS-CIRÚRGICO BUCO-MAXILO-FACIL</p>
<p style="text-align: justify;">Administrações orais de
dipirona na
dose 300mg e pentazocine na dose 50mg a cada 4 horas mostraram
eficácia
semelhante em tratamento da dor no pós-cirúrgico de
procedimentos
bucais, maxilares e faciais, em estudo duplo-cego. Neste estudo
encontrou-se efeitos adversos maiores causados pelo pentazocine em
relação à dipirona (Paeile et Gallardo, 1974).</p>
<p style="text-align: justify;">7.13 – SUPROFENO</p>
<p style="text-align: justify;">7.13.1 – NEURALGIAS CRÔNICAS</p>
<p style="text-align: justify;">Suprofeno oral na dose 200mg 3 à
4
vezes ao dia foi tão efetivo quanto a dipirona na dose 500mg 3 a
4
vezes ao dia no tratamento de neuralgias cronicas de moderada a severa
em estudo controlado envolvendo 60 pacientes hospitalizados (von Szeged
et Michos, 1986).</p>
<p style="text-align: justify;">7.14 – TRAMADOL</p>
<p style="text-align: justify;">7.14.1 – NA CÓLICA BILIAR
AGUDA</p>
<p style="text-align: justify;">Um estudo multicêntrico e
randomizado,
um grupo de 74 pacientes com cólica aguda severa de
vesícula biliar,
induzida por litíase biliar, foram comparados dipirona, 2,5g,
hioscina
20mg e tramadol 100mg, todos por via intravenosa. O temp início
da
redução da dor foi significativamente menor com a
dipirona (10,9
minutos), em comparação com o tramadol (15,8 minutos) e
hioscina (25,6
minutos). No grupo tratado com dipirona, 3 pacientes necessitaram de
doses adicionais da droga após 20 minutos, enquanto no grupo da
hioscina 8 pacientes necessitaram de outra dose do fármaco e no
grupo
tratado com tramadol apenas 1 paciente necessitou de outra dose do
analgésico (Schmieder et al, 1993).</p>
<p style="text-align: justify;">7.14.2 – NAS ODONTALGIAS</p>
<p style="text-align: justify;">Tramadol na dose 50mg por via oral e
dipirona na dose 100mg pela mesma via foram considerados equipotentes
no tratamento da dor de dente em tratamento experimental de dor
induzida, em estudo controlado envolvendo 10 indivíduos sadios
(Rohdewald et al, 1988).</p>
<p style="text-align: justify;">7.14.3 – NA DOR
PÓS-CIRÚRGICA</p>
<p style="text-align: justify;">A eficácia do efeito
analgésico do
tramado (100mg intramuscular) foi comparado com uma
associação de
dipirona 500mg com difenidramina 12,5mg, drofenina 25mg e benzetilio
2,5mg, para o tratamento da dor pós-operatória em um
estudo controlado,
randomizado com 60 pacientes que sofreram cirurgia abdominal. Ambas as
drogas foram administradas a cada 8 horas por 3 dias. A intensidade da
dor foi reduzida mais efetivamente com tramadol após a primeria
dose e
durante os três dias de tratamento (p<0,05) e a qualidade do
sono
dos pacientes foi significativamente melhor com o tramadol do que com a
dipirona associada (p<0,001). Efeitos adversos apareceram em 3
pacientes do grupo com tramadol e apenas em um paciente no grupo com
dipirona associada (Canepa et al, 1993).</p>
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