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The Cochrane Database of Systematic... Sep 2010Women with hyperthyroidism in pregnancy have increased risks of miscarriage, stillbirth, preterm birth, and intrauterine growth restriction; and they can develop severe... (Review)
Review
BACKGROUND
Women with hyperthyroidism in pregnancy have increased risks of miscarriage, stillbirth, preterm birth, and intrauterine growth restriction; and they can develop severe pre-eclampsia or placental abruption.
OBJECTIVES
To assess the effects of interventions for preventing or treating hyperthyroidism in pregnant women.
SEARCH STRATEGY
We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (28 July 2010).
SELECTION CRITERIA
We intended to include randomised controlled trials comparing antithyroid treatments in pregnant women with hyperthyroidism.
DATA COLLECTION AND ANALYSIS
Two review authors would have assessed trial eligibility and risk of bias, and extracted data.
MAIN RESULTS
No trials were located.
AUTHORS' CONCLUSIONS
As we did not identify any eligible trials, we are unable to comment on implications for practice, although early identification of hyperthyroidism before pregnancy may allow a woman to choose radioactive iodine therapy or surgery before planning to have a child. Designing and conducting a trial of antithyroid drugs for pregnant women with hyperthyroidism presents formidable challenges. Not only is hyperthyroidism a relatively rare condition, both of the two main drugs used have potential for harm, one for the mother and the other for the child. More observational research is required about the potential harms of methimazole in early pregnancy and about the potential liver damage from propylthiouracil.
Topics: Female; Humans; Hyperthyroidism; Pregnancy; Pregnancy Complications; Randomized Controlled Trials as Topic
PubMed: 20824882
DOI: 10.1002/14651858.CD008633.pub2 -
BMJ Clinical Evidence Jul 2010Hyperthyroidism is characterised by high levels of serum thyroxine and triiodothyronine, and low levels of thyroid-stimulating hormone. The main causes of... (Review)
Review
INTRODUCTION
Hyperthyroidism is characterised by high levels of serum thyroxine and triiodothyronine, and low levels of thyroid-stimulating hormone. The main causes of hyperthyroidism are Graves' disease, toxic multinodular goitre, and toxic adenoma. About 20 times more women than men have hyperthyroidism.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of drug treatments for primary hyperthyroidism? What are the effects of surgical treatments for primary hyperthyroidism? What are the effects of treatments for subclinical hyperthyroidism? We searched: Medline, Embase, The Cochrane Library, and other important databases up to February 2010 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 15 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: adding thyroxine to antithyroid drugs (carbimazole, propylthiouracil, and thiamazole), antithyroid drugs (carbimazole, propylthiouracil, and thiamazole), radioactive iodine, and thyroidectomy.
Topics: Antithyroid Agents; Graves Disease; Humans; Hyperthyroidism; Incidence; Methimazole; Thyrotropin
PubMed: 21418670
DOI: No ID Found -
BMJ Clinical Evidence Mar 2008Hyperthyroidism is characterised by high levels of serum thyroxine and triiodothyronine, and low levels of thyroid-stimulating hormone. The main causes of... (Review)
Review
INTRODUCTION
Hyperthyroidism is characterised by high levels of serum thyroxine and triiodothyronine, and low levels of thyroid-stimulating hormone. The main causes of hyperthyroidism are Graves' disease, toxic multinodular goitre, and toxic adenoma. About 20 times more women than men have hyperthyroidism.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of drug treatments for primary hyperthyroidism? What are the effects of surgical treatments for primary hyperthyroidism? What are the effects of treatments for subclinical hyperthyroidism? We searched: Medline, Embase, The Cochrane Library and other important databases up to June 2007 (Clinical Evidence reviews are updated periodically, please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 14 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: adding thyroxine to antithyroid drugs (carbimazole, propylthiouracil, and thiamazole), antithyroid drugs (carbimazole, propylthiouracil, and thiamazole), radioactive iodine, and thyroidectomy.
Topics: Antithyroid Agents; Graves Disease; Humans; Hyperthyroidism; Incidence; Methimazole; Thyrotropin
PubMed: 19450325
DOI: No ID Found -
Annals of Internal Medicine May 2007Nonchemotherapy drug-induced agranulocytosis is a rare adverse reaction that is characterized by a decrease in peripheral neutrophil count to less than 0.5 x 10(9)... (Review)
Review
BACKGROUND
Nonchemotherapy drug-induced agranulocytosis is a rare adverse reaction that is characterized by a decrease in peripheral neutrophil count to less than 0.5 x 10(9) cells/L due to immunologic or cytotoxic mechanisms.
PURPOSE
To systematically review case reports of drugs that are definitely or probably related to agranulocytosis.
DATA SOURCES
English-language and German-language reports in MEDLINE (1966 to 2006) or EMBASE (1989 to 2006) and in bibliographies of retrieved articles.
STUDY SELECTION
Published case reports of patients with nonchemotherapy drug-induced agranulocytosis.
DATA EXTRACTION
One reviewer abstracted details about cases and assessed causality between drug intake and agranulocytosis by using World Health Organization assessment criteria.
DATA SYNTHESIS
Causality assessments of 980 reported cases of agranulocytosis were definite in 56 (6%), probable in 436 (44%), possible in 481 (49%), and unlikely in 7 (1%). A total of 125 drugs were definitely or probably related to agranulocytosis. Drugs for which more than 10 reports were available (carbimazole, clozapine, dapsone, dipyrone, methimazole, penicillin G, procainamide, propylthiouracil, rituximab, sulfasalazine, and ticlopidine) accounted for more than 50% of definite or probable reports. Proportions of fatal cases decreased between 1966 and 2006. More patients with a neutrophil count nadir less than 0.1 x 10(9) cells/L had fatal complications than did those with a neutrophil count nadir of 0.1 x 10(9) cells/L or greater (10% vs. 3%; P < 0.001). Patients treated with hematopoietic growth factors had a shorter median duration of neutropenia (8 days vs. 9 days; P = 0.015) and, among asymptomatic patients at diagnosis, had a lower proportion of infectious or fatal complications (14% vs. 29%; P = 0.030) than patients without such treatment.
LIMITATIONS
Case reports cannot provide rates of drug-induced complications, sometimes incompletely assess or describe important details, and sometimes emphasize atypical features and outcomes.
CONCLUSIONS
Many drugs can cause nonchemotherapy drug-induced agranulocytosis. Case fatality may be decreasing over time with the availability of better treatment.
Topics: Agranulocytosis; Drug-Related Side Effects and Adverse Reactions; Granulocyte Colony-Stimulating Factor; Granulocyte-Macrophage Colony-Stimulating Factor; Humans; Risk Factors
PubMed: 17470834
DOI: 10.7326/0003-4819-146-9-200705010-00009 -
The Cochrane Database of Systematic... Oct 2005Randomised clinical trials have addressed the question whether propylthiouracil has any beneficial effects in patients with alcoholic liver disease. (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Randomised clinical trials have addressed the question whether propylthiouracil has any beneficial effects in patients with alcoholic liver disease.
OBJECTIVES
To assess the beneficial and harmful of propylthiouracil for patients with alcoholic liver disease.
SEARCH STRATEGY
The Cochrane Hepato-Biliary Group Controlled Trials Register (May 2005), The Cochrane Central Register of Controlled Trials in The Cochrane Library (Issue 2, 2005), MEDLINE (1950 to May 2005), EMBASE (1980 to May 2005), and The Web of Science (May 2005) were searched. These electronic searches were combined with full text searches. Manufacturers and researchers in the field were also contacted.
SELECTION CRITERIA
Randomised clinical trials studying patients with alcoholic steatosis, alcoholic fibrosis, alcoholic hepatitis, and/or alcoholic cirrhosis were included irrespective of blinding, publication status, or language. Interventions encompassed propylthiouracil at any dose versus placebo or no intervention.
DATA COLLECTION AND ANALYSIS
All analyses were performed according to the intention-to-treat method in RevMan Analyses. The methodological quality of the randomised clinical trials was evaluated by components (generation of the allocation sequence; allocation concealment; double blinding; follow-up).
MAIN RESULTS
Combining the results of six randomised clinical trials including 710 patients demonstrated no significant effects of propylthiouracil versus placebo on all-cause mortality (relative risks (RR) 0.93, 95% confidence interval (CI) 0.66 to 1.30), liver-related mortality (RR 0.80, 95% CI 0.50 to 1.29), complications of the liver disease, or liver histology. Propylthiouracil was associated with a non-significant increased risk of non-serious adverse events and with the seldom occurrence of serious adverse events (leukopenia).
AUTHORS' CONCLUSIONS
We could not demonstrate any significant beneficial effect of propylthiouracil on all-cause mortality, liver-related mortality, liver complications, and liver histology of patients with alcoholic liver disease. Propylthiouracil was associated with adverse events. Confidence intervals were wide. Accordingly, there is no evidence for using propylthiouracil for alcoholic liver disease outside randomised clinical trials.
Topics: Antimetabolites; Humans; Liver Diseases, Alcoholic; Propylthiouracil; Randomized Controlled Trials as Topic; Treatment Outcome
PubMed: 16235302
DOI: 10.1002/14651858.CD002800.pub2 -
The Cochrane Database of Systematic... 2002Alcohol is the most common cause of liver disease in the Western world today. Randomised clinical trials have addressed the question whether propylthiouracil has any... (Review)
Review
BACKGROUND
Alcohol is the most common cause of liver disease in the Western world today. Randomised clinical trials have addressed the question whether propylthiouracil has any efficacy in patients with alcoholic liver disease.
OBJECTIVES
The objectives were to assess the efficacy of propylthiouracil on mortality, clinical symptoms and complications, liver biochemistry, and liver histology in patients with alcoholic liver disease. Adverse events were also analysed.
SEARCH STRATEGY
The Cochrane Hepato-Biliary Group Controlled Trials Register (searched July 2001), The Cochrane Controlled Trials Register (Cochrane Library Issue 3, 2001), MEDLINE (January 1966 to July 2001), EMBASE (January 1985 to July 2001) were searched. These electronic searches were combined with full text searches. Manufacturers and researchers in the field were also contacted.
SELECTION CRITERIA
Randomised clinical trials studying patients with alcoholic steatosis, alcoholic fibrosis, alcoholic hepatitis, and/or alcoholic cirrhosis were included. Interventions encompassed propylthiouracil at any dose versus placebo or no intervention. The trials could be double-blind, single-blind, or unblinded. The trials could be unpublished or published as an article, an abstract, or a letter and no language limitations were applied.
DATA COLLECTION AND ANALYSIS
All analyses were performed according to the intention-to-treat method. The statistical package (RevMan and MetaView) provided by the Cochrane Collaboration was used. The methodological quality of the randomised clinical trials was evaluated by components of quality and the Jadad-scale.
MAIN RESULTS
Combining the results of six randomised clinical trials including 710 patients demonstrated no significant effects of propylthiouracil versus placebo on mortality (Peto odds ratio (OR) 0.91, 95% confidence interval (CI) 0.59 to 1.40), liver related mortality (OR 0.78, 95% CI 0.45 to 1.33), complications of the liver disease (OR 1.14, 95% CI 0.58 to 2.24), or liver histology. Propylthiouracil was associated with a non significant trend towards an increased risk of non-serious adverse events (OR 1.49, 95% CI 0.74 to 2.99) and with the seldom occurrence of serious adverse events (leukopenia).
REVIEWER'S CONCLUSIONS
This systematic review could not demonstrate any significant efficacy of propylthiouracil on any clinically important outcomes (mortality, liver related mortality, liver complications, and liver histology) of patients with alcoholic liver disease and propylthiouracil was associated with adverse events. Accordingly, there is no evidence for using propylthiouracil for alcoholic liver disease outside randomised clinical trials.
Topics: Antimetabolites; Humans; Liver Diseases, Alcoholic; Propylthiouracil; Randomized Controlled Trials as Topic
PubMed: 12076451
DOI: 10.1002/14651858.CD002800 -
Liver Dec 2001The aim of this review was to determine the benefits and adverse effects of propylthiouracil for patients with alcoholic liver disease. (Meta-Analysis)
Meta-Analysis Review
AIMS/BACKGROUND
The aim of this review was to determine the benefits and adverse effects of propylthiouracil for patients with alcoholic liver disease.
METHODS
Systematic Cochrane Review of randomised clinical trials. The Cochrane Hepato-Biliary Controlled Clinical Trials Register, The Cochrane Library, MEDLINE, and full text searches were combined. All analyses were performed according to the intention-to-treat method. Only randomised clinical trials studying patients with alcoholic steatosis, alcoholic fibrosis, alcoholic hepatitis and/or alcoholic cirrhosis were included. Interventions encompassed propylthiouracil at any dose versus placebo or no intervention. The trials could be double-blind, single-blind or unblinded.
RESULTS
Six randomised clinical trials randomising 710 patients demonstrated no significant effects of propylthiouracil versus placebo on mortality (Peto odds ratio (OR) 0.91, 95% confidence interval (CI) 0.59 to 1.40), liver-related mortality (OR 0.78, CI 0.45 to 1.33), complications to the liver disease (OR 1.14, CI 0.58 to 2.24), and liver histology. Propylthiouracil was associated with a nonsignificant trend toward an increased risk of nonserious adverse events (OR 1.49, CI 0.74 to 2.99) and with the rare occurrence of serious adverse events (leukopenia).
CONCLUSIONS
This systematic review could not demonstrate any significant effect of propylthiouracil on any clinically important outcomes (mortality, liver-related mortality, liver complications and liver histology) of patients with alcoholic liver disease.
Topics: Antithyroid Agents; Hepatic Encephalopathy; Humans; Liver Cirrhosis, Alcoholic; Propylthiouracil; Randomized Controlled Trials as Topic; Sensitivity and Specificity; Survival Rate; Treatment Outcome
PubMed: 11903884
DOI: 10.1034/j.1600-0676.2001.210606.x