domingo, 20 de noviembre de 2011

ketorolaco

digemid HA retirado ketorolaco 60 mg endovenoso no sabemos con que criterios. El asunto es que se recomienda para crisis de migraña siendo muy efectivo y mucho mas barato que los triptanos.Sn embargo en casimiro ulloa hay ketorolaco de 30 mg ev.
Y que?  no puede comprar directamente esterptokinasa en el extranjero
 cmori
 
 
 

First page of article

First page of 2008: The Year in Review
 
 

First page of article

First page of 2008: The Year in Review

martes, 15 de noviembre de 2011

levodopa

LEVODOPA

Sinónimos.

Dihidroxifenilalanina. L-Dopa. 3-hidroxi-L-tirosina. Laevo-dopa.

Acción terapéutica.

Antidiscinésico.

Propiedades.

Es un precursor de la dopamina. Al parecer el pequeño porcentual de cada dosis que atraviesa la barrera hematoencefálica se descarboxila a dopamina, que a su vez estimula los receptores dopaminérgicos en los ganglios basales y así mejora el equilibrio entre la actividad colinérgica y la dopaminérgica, con mejoría de la modulación de los impulsos nerviosos voluntarios transmitidos a la corteza motora. Se absorbe en forma rápida en el intestino delgado mediante un sistema de transporte activo de aminoácidos; a la circulación general llega 30% a 50%. Se distribuye en la mayoría de los tejidos corporales, pero no en el SNC, que recibe menos de 1% de la dosis debido al metabolismo intenso de la periferia. La enzima descarboxilasa de aminoácidos L-aromáticos convierte 95% en dopamina en el estómago, intestinos e hígado, por metabolismo de primer paso. Su vida media es de 1 a 3 horas. Se elimina por vía renal; 80% de la dosis se elimina en 24 horas como metabolitos de la dopamina, principalmente ácido dihidroxifenilacético (DOPAC) y ácido homovanílico (HVA).

Indicaciones.

Parkinsonismo idiopático, posencefalítico, sintomático o asociado con arteriosclerosis cerebral.

Dosificación.

En el período inicial, 250mg de 2 a 4 veces al día, con una dosis adicional de 100mg a 750mg al día en intervalos de tres a siete días, según la tolerancia, hasta conseguir la respuesta deseada. Dosis máxima: hasta 8g diarios.

Reacciones adversas.

Pueden aparecer depresión mental, micción dificultosa, mareos, arritmias cardíacas, cambios en el estado de ánimo, náuseas o vómitos; movimientos corporales no habituales e incontrolados. Son de incidencia menos frecuente: hipertensión, debilidad o cansancio no habitual, blefarospasmo; cefaleas y anorexia.

Precauciones y advertencias.

La ingestión de alimentos antes o simultáneamente puede retrasar el efecto de la levodopa. En los diabéticos puede interferir con las pruebas de glucosa y cuerpos cetónicos en orina. Evitar los alimentos o productos vitamínicos que contengan piridoxina (vitamina B 6), puesto que disminuye el efecto de la levodopa. Puede aparecer el fenómeno on-off (alternancia de respuesta positiva y negativa al tratamiento). Pueden oscurecerse la orina o el sudor, pero sin significado clínico. En caso de aparición de trastornos psiquiátricos graves (depresión mental) pudiera ser necesario reducir la dosificación e incluso suspender el tratamiento. Los pacientes geriátricos y posencefalíticos necesitan con frecuencia dosis menores que otros pacientes con parkinsonismo.

Interacciones.

El trihexifenidilo o la amantadina pueden ocasionar un aumento de la eficacia de la levodopa, pero no se recomienda su uso simultáneo si existen antecedentes de psicosis. La administración con anestésicos orgánicos puede producir arritmias cardíacas. Los antiácidos aumentan la absorción de levodopa; los anticonvulsivos, las benzodiazepinas, el haloperidol, la papaverina, las fenotiazinas o alcaloides de la rauwolfia pueden disminuir los efectos terapéuticos de la levodopa. La bromocriptina puede producir efectos aditivos y la metildopa puede alterar los efectos antiparkinsonianos de la levodopa. Los inhibidores de la MAO, en asociación con levodopa, pueden ocasionar una crisis hipertensiva. Los simpaticomiméticos pueden aumentar la posibilidad de arritmias cardíacas. La administración de carbidopa con levodopa reduce la tendencia de los simpaticomiméticos a producir arritmias inducidas por la dopamina.

Contraindicaciones.

Debe evaluarse la relación riesgo-beneficio en presencia de asma bronquial, enfisema, antecedentes de trastornos convulsivos, diabetes mellitus, glaucoma de ángulo cerrado, úlcera péptica, disfunción hepática o renal, estados psicóticos y melanoma.


P.R. VADEMÉCUM 2009
P.R. VADEMÉCUM.

martes, 18 de octubre de 2011

vildagliptina (galvus) nobartis

Vildagliptina

De Wikipedia, la enciclopedia libre
Vildagliptina
Nombre (IUPAC) sistemático
2S)-1-[N-(3-hidroxi-1-adamantil)glicil]pirrolidin-2-carbonitrilo
Identificadores
Código ATC  ?
Datos químicos
Fórmula  ?
Datos clínicos
Cat. embarazo  ?
Estado legal  ?

Wikipedia NO es un consultorio médico Aviso médico

Vildagliptina (2S)-1-[N-(3-hidroxi-1-adamantil)glicil]pirrolidin-2-carbonitrilo CAS 274901-16-5[1] (previamente identificada como LAF237, Galvus®) es un agente hipoglicemiante nuevo (Antidiabético) de la clase nueva inhibidores de DPP4 (DPP-4).[2] Vildagliptina inhibe la inactivación del GLP-1 por DPP-4, permitiendo que GLP-1 y GIP potencien la secreción de insulina por las celulas beta y suprimiendo la liberación de glucagon por las células alfa en los islotes de Langerhans pancreáticos.[3] Uno de los tres inhibidores sitagliptina, saxagliptina, y vildagliptina que se puede emplear asociado a metformina[4] [5]

  1. http://chem.sis.nlm.nih.gov/chemidplus/ProxyServlet?objectHandle=DBMaint&actionHandle=default&nextPage=jsp/chemidlite/ResultScreen.jsp&TXTSUPERLISTID=0274901165
  2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769847/pdf/dst-03-0068.pdf
  3. Matthieu C. 2009 The scientific evidence: vildagliptin and the benefits of islet enhancement Diabetes, Obesity and Metabolism, 11 (Suppl. 2), 2009, 9–17
  4. http://www.ncbi.nlm.nih.gov/pubmed/19748066
  5. Joshua J. Neumiller Differential chemistry (structure),mechanism of action, and pharmacology of GLP-1 receptor agonists and DPP-4 inhibitors J Am Pharm Assoc. 2009;49(suppl 1):S16–S29.

miércoles, 29 de junio de 2011

PRASUGREL

 

se abre Trial con prasugrel en casimiro en colaboracion con clinica INCA de Dr Mogrovejo

 

Prasugrel

 
Prasugrel
Systematic (IUPAC) name
(RS)-5-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4,5,6,7-
tetrahydrothieno[3,2-c]pyridin-2-yl acetate
Clinical data
Licence data EMA:LinkUS FDA:link
Pregnancy cat. B(US) B
Legal status POM (UK) -only (US)
Routes Oral
Pharmacokinetic data
Bioavailability ≥79%
Protein binding Active metabolite: ~98%
Metabolism Rapid intestinal and serum metabolism via esterase-mediated hydrolysis to a thiolactone (inactive), which is then converted, via CYP450-mediated (primarily CYP3A4 and CYP2B6) oxidation, to an active metabolite (R-138727)
Half-life ~7 hours (range 2-15 hours)
Excretion Urine (~68% inactive metabolites); feces (27% inactive metabolites)
Identifiers
CAS number 150322-43-3
ATC code B01AC22
PubChem CID 6918456
ChemSpider 5293653 YesY
ChEMBL CHEMBL1201772 N
Chemical data
Formula C20H20FNO3S 
Mol. mass 373.442 g/mol
SMILES eMolecules & PubChem
 N(what is this?)  [1]

Prasugrel (marketing name Effient in the US, Efient in the EU and Prasita in India) is a novel platelet inhibitor developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). Prasugrel was approved for use in Europe in February 2009, and is currently available in the UK. On July 10, 2009, the US Food and Drug Administration approved the use of prasugrel for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome who are to be managed with PCI.[1]

[edit] Pharmacology

Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Compared to clopidogrel, "prasugrel(trade name apagrel) inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI".[2] Clopidogrel, unlike prasugrel, was issued a black box warning from the FDA on March 12, 2010, as the estimated 2-14% of the US population that have low levels of the CYP 2C19 liver enzyme needed to activate clopidogrel may not get the full effect. Tests are available to predict if a patient would be susceptible to this problem or not.[3][4] Prasugrel has not been shown to carry those same limitations.

[edit] Pharmacodynamics

Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.[5] Following a 60-mg loading dose of Effient, approximately 90% of patients had at least 50% inhibition of platelet aggregation by 1 hour. Maximum platelet inhibition was about 80% (Figure 2). Mean steady-state inhibition of platelet aggregation was about 70% following 3 to 5 days of dosing at 10 mg daily after a 60-mg loading dose of Effient. Platelet aggregation gradually returns to baseline values over 5–9 days after discontinuation of prasugrel, this time course being a reflection of new platelet production rather than pharmacokinetics of prasugrel. Discontinuing clopidogrel 75 mg and initiating prasugrel 10 mg with the next dose resulted in increased inhibition of platelet aggregation, but not greater than that typically produced by a 10 mg maintenance dose of prasugrel alone. It should also be noted that increasing platelet inhibition could increase bleeding risk. The relationship between inhibition of platelet aggregation and clinical activity has not been established. [2]

[edit] Pharmacokinetics

Prasugrel is a prodrug and is rapidly metabolized to a pharmacologically active metabolite and inactive metabolites. The active metabolite has an elimination half-life of about 7 hours (range 2–15 hours). Healthy subjects, patients with stable atherosclerosis, and patients undergoing PCI show similar pharmacokinetics.

[edit] TRITON-TIMI 38 study

As published in the New England Journal of Medicine's online edition, the TRITON-TIMI 38 study of 13,608 patients with acute coronary syndromes compared prasugrel against clopidogrel, both in combination with aspirin, and found that, as a more potent anti-platelet agent, prasugrel reduced the combined rate of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke (12.1% for clopidogrel vs. 9.9% for prasugrel). This difference in the primary endpoint was mainly driven by the reduction of non-fatal myocardial infarctions. However, an increased rate of serious bleedings (1.4%, vs. 0.9% in the clopidogrel group) and fatal bleedings (0.4% vs. 0.1%) was also observed.[6] Overall mortality did not differ between the two treatment groups.

From the editorial in the NEJM, "In TRITON–TIMI 38, for each death from cardiovascular causes prevented by the use of prasugrel as compared with clopidogrel, approximately one additional episode of fatal bleeding was caused by prasugrel".[7]

In patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI), prasugrel was associated with a significantly lower incidence of ischemic events than clopidogrel, and was particularly effective in specific subgroups of patients, such as those with diabetes mellitus. In this sub-group there is a 30% relative risk reduction (4.2% ARR for unstable angina/NSTEMI and 5% AAR for STEMI) compared to the clopidogrel group without significant increased risk for major bleeding(2.2% vs. 2.3%). However, the efficacy of prasugrel was offset by a higher risk of bleeding than clopidogrel, with patients aged ≥75 years, those weighing <60 kg and those with a history of stroke or transient ischemic attack at the greatest risk. A lower dose of prasugrel in patients aged ≥75 years and those weighing <60 kg may help to minimize the bleeding risk, although more data are needed to establish this; prasugrel is contraindicated in patients with a history of stroke or transient ischemic attack.[8] The estimated number of patients needed to be treated with prasugrel at the dosage studied, as compared with standard-dose clopidogrel, to prevent one primary efficacy end point during a 15-month period was 46. The number of patients who would have to be treated to result in an excess non–CABG-related TIMI major hemorrhage was 167.[9]

Furthermore, data from a pharmacodynamic study suggests that acute coronary syndrome (ACS) patients can be safely switched from clopidogrel to prasugrel and that doing so results in a further reduction in platelet function after one week.[10] When patients receive a loading dose of prasugrel prior to switching from clopidogrel, the reduction in platelet function occurs within two hours.[11]

[edit] Adverse Effects

Cardiovascular: Hypertension (8%), hypotension (4%), atrial fibrillation (3%), bradycardia (3%), noncardiac chest pain (3%), peripheral edema (3%) Central nervous system: Headache (6%), dizziness (4%), fatigue (4%), fever (3%), extremity pain (3%) Dermatologic: Rash (3%) Endocrine & metabolic: Hypercholesterolemia/hyperlipidemia (7%) Gastrointestinal: Nausea (5%), diarrhea (2%), gastrointestinal hemorrhage (2%) Hematologic: Leukopenia (3%), anemia (2%) Neuromuscular & skeletal: Back pain (5%) Respiratory: Epistaxis (6%), dyspnea (5%), cough (4%)

[edit] References

  1. ^ Baker WL, White CM. Role of Prasugrel, a Novel P2Y12 Receptor Antagonist, in the Management of Acute Coronary Syndromes. American Journal of Cardiovascular Drugs Aug 1, 2009; 9 (4): 213-229. Link text
  2. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  3. ^ Food and Drug Administration (United States) (March 12, 2010). "FDA Announces New Boxed Warning on Plavix: Alerts patients, health care professionals to potential for reduced effectiveness". Press release. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm204253.htm. Retrieved March 13, 2010. 
  4. ^ "FDA Drug Safety Communication: Reduced effectiveness of Plavix (clopidogrel) in patients who are poor metabolizers of the drug". Drug Safety and Availability. Food and Drug Administration (United States). March 12, 2010. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm203888.htm. Retrieved March 13, 2010. 
  5. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function" (in English). http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011. 
  6. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  7. ^ Bhatt DL (2007). "Intensifying Platelet Inhibition — Navigating between Scylla and Charybdis". N Engl J Med 357 (20): 2078–81. doi:10.1056/NEJMe0706859. PMID 17982183. http://content.nejm.org/cgi/content/full/NEJMe0706859?query=TOC. 
  8. ^ Duggan ST, Keating GM. Prasugrel: A Review of its Use in Patients with Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention. Drugs Aug 20, 2009; 69 (12): 1707-26 Link text
  9. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  10. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". 1.Angiolillo DJ, Saucedo JF, DeRaad R, et al. Increased platelet inhibition after switching from maintenance clopidogrel to prasugrel in patients with acute coronary syndromes. J Am Coll Cardiol 2010; 56: 1017-23.. http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011. 
  11. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". http://www.theheart.org. http://www.theheart.org/article/1123367.do#bib_1. Retrieved 1 April 2011. 

[edit] External links

domingo, 26 de junio de 2011

DONECIL

 

DONECIL - ABL PHARMA

Terapéutica del Alzheimer.

Composición.

Cada comprimido contiene: donepecilo clorhidrato 5,0mg y 10,0mg, excipientes cs.

Presentación.

Caja por 30 comprimidos de 5mg y 10mg.

carencil

 

CARENCIL - DRUGTECH

Terapéutica del Alzheimer.

Composición.

Donepecilo.

Presentación.

5mg: caja tabletas x 30. 10mg: caja tabletas x 30.


miércoles, 15 de junio de 2011

redex

REDEX - MAGMA

Antiinflamatorio. Relajante muscular.

Composición.

Diclofenaco sódico. Clorzoxazona.

Presentación.

Tabletas recubiertas: 250mg en caja x 20 y 60.


P.R. VADEMÉCUM 2009
P.R. VADEMÉCUM.

redex

REDEX - MAGMA

Antiinflamatorio. Relajante muscular.

Composición.

Diclofenaco sódico. Clorzoxazona.

Presentación.

Tabletas recubiertas: 250mg en caja x 20 y 60.


P.R. VADEMÉCUM 2009
P.R. VADEMÉCUM.

lunes, 13 de junio de 2011

valaciclovir

BAGOVIR - BAGO

Antiviral

Composición.

Valaciclovir.

Presentación.

500mg: caja x 10 comprimidos recubiertos.


P.R. VADEMÉCUM 2009
P.R. VADEMÉCUM.

viernes, 10 de junio de 2011

supracalm paracetamol 1 gr

SUPRACALM - TECNOFARMA

Analgésico.

Composición.

Cada comprimido contiene: paracetamol CD 90% 1.112mg (equivalente a 1.000mg de paracetamol).

Presentación.

SUPRACALM 1g: caja con 10 comprimidos en blíster.


P.R. VADEMÉCUM 2009
P.R. VADEMÉCUM.

domingo, 6 de marzo de 2011

El topiramato o topamax muy usado en España...

Octavio Huerta de Mora posted in cibermedicos.Octavio Huerta de Mora4:41pm Mar 5

El topiramato o topamax muy usado en España tendría relación con defectos de nacimiento como labio leporino o paladar Hendido según nuevo informe de la FDA. A tomar en cuenta en sus prescripciones colegas!
Topiramate Linked to Birth Defects

topirol topamac topictal
www.medscape.com

: New human data show that the prevalence of cleft lips and palates in infants born to women taking topiramate was roughly 3 times higher than that for women taking other antiepileptic drugs

 

Topiramate Linked to Birth Defects

Robert Lowes

Posted: 03/04/2011

Physician Rating:  5 stars   ( 37 Votes )            
Rate This Article:
 
0 stars
 

processing....

 

March 4, 2011 — Pregnant women taking topiramate (Topamax, Ortho-McNeil Janssen) to treat epileptic seizures or prevent migraine headaches have an increased risk of bearing children with a cleft lip or palate, the US Food and Drug Administration (FDA) announced today.

Consequently, clinicians should warn women of childbearing age about the possibility of these birth defects if they become pregnant while taking the medication.

"Health care professionals should carefully consider the benefits and risks of topiramate when prescribing it to women of childbearing age," said Russell Katz, MD, director of the Division of Neurology Products in the FDA's Center for Drug Evaluation and Research, in a statement from the FDA. "Alternative medications that have a lower risk of birth defects should be considered."

Pregnant women prescribed the medication should continue to take it unless advised not to by a clinician.

Topiramate, an anticonvulsant, is approved for treating certain seizures in patients with epilepsy and preventing migraine headaches. However, it is not indicated for treating the pain of such headaches when they occur. The drug also is used on an off-label basis to treat weight loss, alcohol dependence, and psychiatric illnesses such as bipolar disorder.

According to new data from the North American Antiepileptic Drug Pregnancy Registry, infants exposed to topiramate as a single therapy in the first trimester of pregnancy had a 1.4% prevalence of oral clefts compared with 0.38% to 0.55% for infants exposed to other antiepileptic drugs. The prevalence rate was even lower — 0.07% — for infants of mothers who did not have epilepsy and were not being treated with other AEDs.

These findings have prompted the agency to strengthen the label warning for topiramate by changing its pregnancy classification to category D. This category means that there are human data showing positive evidence of human fetal risk, but that the drug's benefits in pregnant women may outweigh the risks in some situations. The drug's pregnancy category previously had been a lower category C because of the absence of human data.

The FDA also will update the patient medication guide and prescribing information for the brand name and generic versions of topiramate.

More information about today's announcement is available on the FDA Web site.

To report adverse events related to topiramate, contact MedWatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.

Authors and Disclosures

Journalist

Robert Lowes

Freelance writer, St. Louis, Missouri

Disclosure: Robert L. Lowes has disclosed no relevant financial relationships.

 
 
---------- Mensaje reenviado ----------
De: Octavio Huerta de Mora <notification+yfo6tzj9@facebookmail.com>
Fecha: 5 de marzo de 2011 16:41
Asunto: [cibermedicos] El topiramato o topamax muy usado en España...
Para: Claudio Mori Gonzales <clagui57@gmail.com>


Octavio Huerta de Mora posted in cibermedicos.
El topiramato o topamax muy usado en España tendría relación con defectos de nacimiento como labio leporino o paladar Hendido según nuevo informe de la FDA. A tomar en cuenta en sus prescripciones colegas!
Octavio Huerta de Mora 4:41pm Mar 5
El topiramato o topamax muy usado en España tendría relación con defectos de nacimiento como labio leporino o paladar Hendido según nuevo informe de la FDA. A tomar en cuenta en sus prescripciones colegas!
: New human data show that the prevalence of cleft lips and palates in infants born to women taking topiramate was roughly 3 times higher than that for women taking other antiepileptic drugs.

View Post on Facebook · Edit Email Settings · Reply to this email to add a comment.