Estudos

http://aformulabr.com.br/qrcode/cimetidinafv01.pdf
 CIMETIDINA
Antagonista histamínico que reduz acidez estomacal

DESCRIÇÃO
Antagonista de receptores H2 da classe dos anti-histamínicos que reduz a secreção ácida no estômago.

MECANISMO DE AÇÃO

A cimetidina inibe a secreção gástrica ácida basal e noturna por competição com a histamina nos receptores H2 das
células parietais; na urticária funciona como adjuvante bloqueando os receptores H2 responsáveis pela resposta
inflamatória nos vasos sanguíneos cutâneos. Outros efeitos são observados como: inibidor enzimático dos
citocromos P450 e P448 hepáticos antagoniza a diidrotestosterona, ocorrendo aumento da defesa da mucosa
gástrica.

INDICAÇÕES

 Antagonista dos receptores H2 da histamina;

 Antiulceroso;
 Inibidor da secreção ácida gástrica (refluxo, etc).

DOSE USUAL

Recomendação oral de 200 a 1.000mg de Cimetidina ao dia em adultos, 20mg/kg ao dia em crianças menores de 1
ano, 25 a 30mg/kg ao dia em crianças maiores de 1 ano.

SUGESTÕES DE FÓRMULAS

Cimetidina......................................................... 400mg Cimetidina..................................................... 20mg/kg

Brometo de propantelina....................................... 5mg Suspensão qsp...................................................... 5ml

Modo de uso: 1 dose 2 vezes ao dia. Modo de uso: 20mg/kg/dia, em doses divididas, para
Indicação: antiulceroso. crianças até 1 ano de idade.
Indicação: antiácido infantil.

PRINCIPAIS REFERÊNCIAS

BATISTUZZO, J. A O; ITAYA, M.; ETO, Y. Formulário Médico-Farmacêutico. 5 ed. São Paulo: Pharmabooks, 2015.

LACY F.C.; ARMSTRONG L.L.; GOLDMAN M.P.; LANCE L.L. Drug Information Handbook. American Pharmacists Association. Lexi-Comp. 23ª
edição, 2014-2015.
 CIMETIDINA
ESTUDOS CLÍNICOS

Cimetidine as a novel adjunctive treatment for early stage Lyme disease.

Lyme disease, caused by the spirochete Borrelia burgdorferi (Bb), is the most common vector-borne illness in the
United States. It is a complex disease which may affect the skin, joints, heart, eyes, and central nervous system.
Prompt diagnosis and treatment is curative in most instances. However, a significant percentage of patients
experience ongoing symptoms after treatment. Currently, there is much controversy regarding the diagnosis,
pathophysiology, and treatment of Lyme disease. Pathogen persistence despite treatment lies at the heart of this
debate. Many believe that the ongoing symptoms are due to factors such as autoimmunity or permanent damage that
is incurred during the active infection. However, there is an emerging school of thought that states that ongoing
symptoms are due to a persistent infection that is able to survive both the immune response and antibiotic therapy.
Numerous studies have shown that Bb can indeed persist within the host despite treatment and several mechanisms
have been proposed to explain Bb's persistence capabilities. These include: polymorphism, antigenic variance, biofilm
formation, persister cells, and immunomodulation. There is evidence that Bb is able to alter cytokine profiles within the
host which may allow the organism to survive the immune response. This immunomodulation follows a pattern of T-
helper 1 (TH1) suppression in favor of T-helper 2 (TH2) processes. In contrast, it has been shown that the optimal
immune response to Bb infection involves an early, robust TH1 response and a later conversion to TH2 dominance
once the infection is controlled or cleared. It has been proposed that a reconstitution of proper immune-competency in
the infected host may improve clinical outcomes in Lyme disease. Cimetidine (CIM) is an over-the-counter histamine-2
(H2) antagonist that is primarily used to lower acid secretions in the stomach. T-regulatory (Treg) cells also possess
the H2 receptor, which has spurred interest in CIM as a potential immunomodulator. CIM therapy has been shown to
increase levels of the TH1 associated cytokines IL-12, TNF-α, and IFN-γ while decreasing levels of the TH2
associated cytokine IL-10. The author proposes a novel theory that CIM therapy during early Bb infection may
promote a more appropriate immune response and increase the utility of antibiotic therapy during early stage Lyme
disease, thus improving clinical outcomes of the disease.

Cimetidine in the treatment of symptomatic gastroesophageal reflux: a double blind controlled trial.

The effectiveness of cimetidine for symptomatic relief in patients with chronic gastroesophageal reflux was studied in a
multicenter, double blind clinical trial. Patients were entered into the study for a total of 8 weeks, receiving either
cimetidine, 300 mg four times daily, or identical placebo tablets. Throughout the trial, frequent assessments were
made of symptom severity and frequency, combined with careful measurement of antacid use. Esophagoscopy,
esophageal acid sensitivity, and lower esophageal pressures were performed before and at the completion of the
treatment period. Significant (P less than 0.05) decreases in symptom frequency and severity were noted throughout
the study in the cimetidine-treated patients, as compared with the placebo group. This subjective improvement was
corroborated by a concomitant decrease in antacid use, which was significantly (P less than 0.05) reduced in the
cimetidine-treated group. In addition, significant improvement in esophageal acid sensitivity resulted from cimetidine
therapy. No objective improvement in esophageal endoscopic appearance or sphincter pressures was noted. The
results of this double blind trial indicate that cimetidine is more effective than the placebo for the relief of symptoms of
gastroesophageal reflux.

Cimetidine in the treatment of active duodenal and prepyloric ulcers

44 patients with endoscopically confirmed duodenal (36) or prepyloric (8) ulcers have received in a double-blind trial
either the histamine H2-receptor antagonist cimetidine (30 patients) or placebo (14 patients) for six weeks. At three
weeks 67% of patients treated with cimetidine and 17% of those receiving placebo had endoscopically healed ulcers
(χ2=8.49; P<0.005). At six weeks all except 3 patients receiving cimetidine (90%) had healed ulcers compared with
36% receiving placebo (χ2=11.11; P<0.001). Those receiving cimetidine had less daytime and nocturnal pain than
patients on placebo. The differences were statistically significant for daytime pain during four of six weeks. The
cimetidine-treated patients consumed significantly less antacids than placebo-treated patients and these patients'
overall assessments of their wellbeing were significantly better. All patients on cimetidine had a significant reduction
(P<0.0005) of their basal and pentagastrin-stimulated acid secretion, but no reduction in acid secretion was measured
in the group who received placebo.
REFERÊNCIAS

SHEMENSKI J. Cimetidine as a novel adjunctive treatment for early stage Lyme disease. Med Hypotheses. 2016 Apr. Disponível em:<
http://www.ncbi.nlm.nih.gov/pubmed/27107653>. Acesso em: 12 de Maio de 2016, às 08:44.

BEHAR J.; BRAND D.L,.; BROWN F.C.; CASTELL D.O.; COHEN S.; CROSSLEY R.J.; POPE C.E.; WINANS C.S. Cimetidine in the treatment of
symptomatic gastroesophageal reflux: a double blind controlled trial. Gastroenterology. V.74, p.441-8. Feb. 1987. Disponível em:<
http://www.ncbi.nlm.nih.gov/pubmed/340333>. Acesso em: 23 de fevereiro de 2016, às 14:22.

BODEMAR G.; WALAN A. Cimetidine in the treatment of active duodenal and prepyloric ulcers. The Lancet. V.308, nº 7978, p.161–164. July
1976. Disponível em:< http://www.sciencedirect.com/science/article/pii/S0140673676923424>. Acesso em: 23 de Fevereiro de 2016 às 14:35.