Transient Hepatic Dysfunction in an Infant of an Epileptic Mother Treated with Carbamazepine during Pregnancy and Breastfeeding

1992 ◽  
Vol 26 (12) ◽  
pp. 1563-1565 ◽  
Author(s):  
Paul Merlob ◽  
Naomi Mor ◽  
Aviva Litwin
Keyword(s):  
Hepatic Dysfunction ◽  
Liver Enzymes ◽  
Case Reports ◽  
Data Extraction ◽  
Normal Liver ◽  
Complete Disappearance ◽  
Data Synthesis ◽  
Epileptic Mother ◽  
Enzymatic Induction ◽  
High Concentrations

OBJECTIVE: A case is reported of a carbamazepine (CBZ)-treated epileptic mother whose newborn presented with transient hepatic dysfunction characterized by direct hyperbilirubinemia and high concentrations of gamma-glutamyltransferase (GGT). DATA SOURCES: Information was obtained from case reports, clinical trials, and relevant bibliographic laboratory studies. DATA EXTRACTION: Data from case reports were evaluated and compared with those from our patient. The hepatotoxic reactions together with the microsomal enzymatic induction of CBZ were reviewed. DATA SYNTHESIS: A female infant bom to an epileptic mother treated with CBZ throughout pregnancy and breastfeeding presented with transient direct hyperbilirubinemia and high concentrations of GGT. The characteristics of her transient hepatic dysfunction were: early appearance (during the first day of life); discrepancy between the normal liver enzymes and high GGT concentrations; slow decrease of GGT, which nevertheless remained at above-normal concentrations even after the complete disappearance of direct hyperbilirubinemia; and spontaneous resolution in spite of only occasional breastfeeding. The possible explanations of this transient hepatic dysfunction (like enzymatic induction) are discussed. CONCLUSIONS: CBZ-induced hepatic dysfunction in neonates appears to have different clinical expressions. Infants of epileptic mothers treated with CBZ throughout pregnancy and breastfeeding should be carefully monitored for possible adverse effects.

Nonthrombocytopenic Purpura Associated Sequentially with Nifedipine and Diltiazem

1992 ◽  
Vol 26 (9) ◽  
pp. 1089-1090 ◽  
Author(s):  
Margaret Kuo ◽  
Nancy Winiarski ◽  
Serafino Garella
Keyword(s):  
Adverse Effect ◽  
Channel Blocker ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Cutaneous Vasculitis ◽  
Laboratory Studies ◽  
Pertinent Literature ◽  
Data Synthesis ◽  
Purpuric Rash

OBJECTIVE: To report the case of a patient who developed nonthrombocytopenic purpura sequentially following the administration of nifedipine and diltiazem. DATA SOURCES: Case reports, MEDLINE review of pertinent literature, and review of relevant studies. DATA EXTRACTION: Data were extracted from direct patient observation and review of laboratory studies and published reports. DATA SYNTHESIS: Nonthrombocytopenic purpura secondary to cutaneous vasculitis is a known, although rare, adverse effect of nifedipine. It has not been reported in association with diltiazem. We report the case of a 75-year-old woman in whom a purpuric rash demonstrated by biopsy to be attributable to cutaneous vasculitis developed in the course of nifedipine therapy. The rash disappeared after discontinuation of the drug; however, it recurred when diltiazem therapy was initiated. CONCLUSIONS: Nonthrombocytopenic purpura may be associated with diltiazem as well as with nifedipine. When this adverse effect occurs following administration of a calcium-channel blocker, caution is advised in using other agents of the same class.

Isoniazid-Associated Psychosis: Case Report and Review of the Literature

1993 ◽  
Vol 27 (2) ◽  
pp. 167-170 ◽  
Author(s):  
Karen A. Pallone ◽  
Morton P. Goldman ◽  
Matthew A. Fuller
Keyword(s):  
Case Report ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Review Of The Literature ◽  
Data Synthesis ◽  
Medline Search ◽  
Study Selection ◽  
Language Literature

Objective To describe a case of isoniazid-associated psychosis and review the incidence of this adverse effect. Data Sources Information about the patient was obtained from the medical chart. A MEDLINE search of the English-language literature published from 1950 to 1992 was conducted and Index Medicus was manually searched for current information. Study Selection All case reports describing isoniazid-associated psychosis were reviewed. Data Extraction Studies were evaluated for the use of isoniazid, symptoms of psychosis, onset of symptoms, and dosage of isoniazid. Data Synthesis The case report is compared with others reported in the literature. The incidence of isoniazid-associated psychosis is rare. Conclusions The mechanism of isoniazid-associated psychosis is uncertain. It appears that isoniazid was associated with the psychosis evident in our patient and in the cases reviewed.

Drug-Induced Yawning—A Review

2011 ◽  
Vol 45 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
Edna Patatanian ◽  
Nancy Toedter Williams
Keyword(s):  
Case Reports ◽  
Data Extraction ◽  
Background Information ◽  
Drug Induced ◽  
Data Synthesis ◽  
Search Terms ◽  
Dopaminergic Agents ◽  
Study Selection ◽  
Physiologic Function ◽  
Induction Agents

Objective: To review the current literature on drug-induced yawning. Data Sources: Literature was accessed through MEDLINE/PubMed (1996-July 2011), International Pharmaceutical Abstracts (1997-July 2011), and EMBASE, using the search terms yawning, drug-induced yawning, and adverse drug reactions. Study Selection and Data Extraction: Relevant clinical trials and case reports were selected and included to present background information. Bibliographies of all relevant articles were reviewed for additional citations. Data Synthesis: Yawning is a common stereotype behavior with unknown physiologic function that occurs in most vertebrates and humans as early as 15 weeks of intrauterine life. Yawning Is under the control of several neurotransmitters and neuropeptides, Including dopamine, serotonin, oxytocin, and acetylcholine. Among drugs, antidepressants, opioids, dopaminergic agents, benzodiazepines, and induction agents are the main pharmacologic classes associated with yawning. Conclusions: Yawning is rarely a serious adverse reaction and is not frequently listed in the drug summary. Most available data are based on case reports, small studies, and older literature. Clinicians should be aware of the agents commonly triggering this behavior.

Weight Gain Associated with Cinnarizine

1992 ◽  
Vol 26 (7-8) ◽  
pp. 928-930 ◽  
Author(s):  
Joaquin Navarro-Badenes ◽  
Inocencia Martínez-Mir ◽  
Vicente Palop ◽  
Elena Rubio ◽  
Francisco J. Morales-Olivas
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Randomized Trials ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Initial Weight ◽  
Data Synthesis ◽  
Previous Level ◽  
The Mean

OBJECTIVE: To report four cases of cinnarizine-induced weight gain. DATA SOURCES: Case reports from a local obesity center and review articles. DATA EXTRACTION: Data were abstracted from spontaneous comments made by patients to one of the authors, who was a doctor at the clinic, and reviewed by the remaining authors. DATA SYNTHESIS: We reviewed the cases of four women, aged 50–57 years without endocrine or metabolic pathologies, that showed weight gain associated with the intake of cinnarizine for one to two years. No other drugs usually were administered during the period in which the women gained weight, although in two cases cinnarizine was associated with dihydroergocristine in the same medicine (Clinadil). The mean weight increase was 6.25 kg (range 4–10). The increases do not appear to be related to whether the patients' initial weight was ideal or excessive. The weight gain was always associated with increased appetite and food intake. One patient discontinued cinnarizine treatment and her weight returned to its previous level. CONCLUSIONS: Cinnarizine is a piperazine derivative used in the treatment of vertigo and in the prophylaxis of migraine. In contrast to related drugs, data about cinnarizine are scarce because randomized trials of cinnarizine have been inconclusive. Our observations indicate that cinnarizine may cause weight gain, as observed with other drugs in the same class.

Pediatrics: Treatment of Tinea Capitis

1997 ◽  
Vol 31 (3) ◽  
pp. 338-348 ◽  
Author(s):  
Susan M Abdel-Rahman ◽  
Milap C Nahata
Keyword(s):  
Comparative Studies ◽  
Tinea Capitis ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Oral Formulation ◽  
Open Label ◽  
Medline Search ◽  
The Us ◽  
High Concentrations

Objective To review the epidemiology, pathogenesis, mycology, clinical presentation, and pharmacotherapy of tinea capitis, and describe the role of newer antimycotic agents. Data Sources A MEDLINE search restricted to English-language articles published from 1966 through 1996 and journal references were used in preparing this review. Data Extraction The data on mycology, pharmacokinetics, adverse effects, and drug interactions were obtained from controlled studies and case reports appearing in the literature. Both open-label and comparative studies were evaluated to assess the efficacy of antimycotics in the treatment of this infection. Data Synthesis Griseofulvin is the drug of choice in the treatment of tinea capitis. Newer agents with greater efficacy or shorter treatment durations continue to be explored. Ketoconazole, the first azole studied for efficacy in tinea capitis, has not demonstrated any clinical advantage over griseofulvin in several controlled clinical trials. Itraconazole is effective, but the available data are limited to case reports and a single uncontrolled study. Terbinafine similarly has shown promise in the treatment of tinea capitis, but the oral formulation was only recently approved in the US. Existing studies reflect the results in infection with pathogens not seen in the US. Both itraconazole and terbinafine achieve high concentrations in the hair and stratum corneum that persist for several weeks following drug administration. This may enable shorter courses of therapy; however, comparative studies need to be conducted in the US. Conclusions Tinea capitis remains the most common dermatophyte infection in young urban children. Oral antifungal therapy is required for effective treatment, often for several months. The combination of griseofulvin with a selenium sulfide shampoo continues to be the mainstay of therapy until more experience is gained with the newer antimycotics.

Ciprofloxacin-Induced Psychosis

1992 ◽  
Vol 26 (7-8) ◽  
pp. 930-931 ◽  
Author(s):  
Roy R. Reeves
Keyword(s):  
Preventive Measures ◽  
Case Reports ◽  
Data Extraction ◽  
Data Sources ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Data Synthesis ◽  
Receptor Sites ◽  
The Brain ◽  
Mild Headache

OBJECTIVE: To report a case of ciprofloxacin-induced psychosis and to discuss occurrence rates, risk factors, possible etiologies, preventive measures, and treatment courses for this adverse reaction. DATA SOURCES: Case reports and review articles identified by MEDLINE. DATA EXTRACTION: Data from pertinent published sources were reviewed and abstracted. DATA SYNTHESIS: A 49-year-old man developed symptoms of severe psychosis concomitant with ciprofloxacin (250 mg bid) treatment. Central nervous system effects secondary to ciprofloxacin treatment are uncommon and usually consist only of minor dizziness or mild headache, although rare occurrences of seizures and hallucinations have been reported. The mechanism by which ciprofloxacin causes these adverse effects is not fully understood. It has been suggested that quinolones may produce an epileptogenic effect by inhibiting the binding of gamma-aminobutyric acid to its receptor sites in the brain. There is yet no explanation for the occurrence of hallucinations or psychosis. CONCLUSIONS: Caution should be exercised when using ciprofloxacin in the treatment of patients with personality abnormalities or symptoms of psychosis.

Examination of the Relationship Between Antimicrobials and Thrombocytosis

2012 ◽  
Vol 46 (10) ◽  
pp. 1425-1429 ◽  
Author(s):  
Christy C Forehand ◽  
Jennifer Cribb ◽  
J Russell May
Keyword(s):  
Antimicrobial Therapy ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Acute Phase Reactant ◽  
Drug Event ◽  
Probability Scale ◽  
Data Synthesis ◽  
Study Selection ◽  
The Relationship

Objective: To evaluate whether there is a relationship between antimicrobial therapy and the development of thrombocytosis. Data Sources: Literature was accessed through EMBASE (1977-June 2012) and MEDLINE (1977-June 2012) using the terms thrombocytosis and antimicrobial. In addition, reference citations from publications identified were reviewed. Study Selection and Data Extraction: All English-language publications identified were evaluated. For case reports, the Naranjo probability scale was used to calculate the likelihood of the drug causing the reaction. Data Synthesis: Thrombocytosis occurring during antimicrobial therapy is well documented, with several case reports and clinical trial observations. However, a direct causal relationship is not yet supported by the available literature. Platelets are welt known to be an acute phase reactant, with an elevated count occurring after acute conditions such as blood loss, inflammation, or infection. Thrombocytosis during antimicrobial therapy may be the result of an infectious process and not an adverse drug event. Conclusions: Based on the current available literature, a definitive link cannot be established between antimicrobial therapy and occurrence of thrombocytosis.

Prolonged Recurrence of Pentamidine-Induced Torsades de Pointes

1992 ◽  
Vol 26 (11) ◽  
pp. 1365-1369 ◽  
Author(s):  
Linda M. Cortese ◽  
Robert A. Gasser ◽  
Darrel C. Bjornson ◽  
Michael J. Dacey ◽  
Charles N. Oster
Keyword(s):  
Cardiac Arrhythmias ◽  
Medical Records ◽  
Binding Capacity ◽  
Case Reports ◽  
Data Extraction ◽  
Serum Magnesium ◽  
Torsades De Pointes ◽  
Patient Case ◽  
Data Synthesis ◽  
The Subject

OBJECTIVE: To report a case of recurrent pentamidine-induced torsades de pointes (TdP) and to review previously reported cases in the literature. DATA SOURCES: Medical records of the subject patient, case reports, and relevant studies identified by MEDLINE. DATA EXTRACTION: Data were abstracted from pertinent published sources by one author and reviewed by the remaining authors. DATA SYNTHESIS: A 43-year-old woman with AIDS experienced pentamidine-induced TdP. TdP and other cardiac arrhythmias recurred repeatedly for 13 days after pentamidine therapy was discontinued and in the presence of normal magnesium and potassium serum concentrations. Infusions of magnesium, lidocaine, and isoproterenol were used to treat the arrhythmias. The exact mechanism of pentamidine-induced TdP has not been clearly established. It is postulated, however, that the similarity of pentamidine's structure to procainamide may contribute to its proarrhythmic effects. The tissue-binding capacity of pentamidine may result in a prolongation of its effects. No distinctive characteristic appears to predispose people to the development of cardiac arrhythmias. Laboratory values that should be monitored include serum magnesium, potassium, and creatinine. The corrected QT interval also should be monitored. CONCLUSIONS: Recurrent arrhythmias may be seen for many days after intravenous administration of pentamidine has been discontinued. Clinicians should consider this phenomenon as they decide how to monitor patients who have received this drug.

Mitomycin-Induced Pulmonary Toxicity: Case Report and Review of the Literature

1992 ◽  
Vol 26 (4) ◽  
pp. 481-484 ◽  
Author(s):  
Donna C. Linette ◽  
Karen H. McGee ◽  
James A. McFarland
Keyword(s):  
Pulmonary Toxicity ◽  
English Language ◽  
Case Reports ◽  
Data Extraction ◽  
Vinca Alkaloid ◽  
Corticosteroid Treatment ◽  
Data Synthesis ◽  
Medline Search ◽  
Pulmonary Response ◽  
Study Selection

OBJECTIVE: This report describes a case of mitomycin-induced pulmonary toxicity and reviews the incidence of this adverse effect, reported patterns of toxicity and associated dosages of the drug, and the use of corticosteroids in the management of pulmonary toxicity. DATA SOURCES: Information about our patient was obtained in part from the medical chart; we had also treated him personally in the past. We conducted a MEDLINE search of the English language literature (restricted to human studies) from 1966 to 1991 and manually searched Index Medicus for current information. STUDY SELECTION: All case reports that described pulmonary toxicity possibly associated with mitomycin were reviewed. DATA EXTRACTION: Studies were evaluated for the dosages of mitomycin given to patients, the nature and onset of symptoms, management course, and corticosteroid use. DATA SYNTHESIS: Our case is similar to others described in the literature. The incidence of mitomycin-induced pulmonary toxicity has been reported to range from 2 to 38 percent. Concurrent vinca alkaloid administration may potentiate the risk of an acute pulmonary insult secondary to mitomycin use. The toxicity is usually of slow onset and the average total dosage of drug implicated is 78 mg. A formal evaluation of corticosteroid treatment has not been performed, but various authors have reported success with different regimens. CONCLUSIONS: The incidence of pulmonary toxicity associated with mitomycin is unpredictable, but more likely to occur at higher dosages. Treatment with corticosteroids is encouraged to improve pulmonary response.

Fulminant Hepatic Failure Possibly Related to Ciprofloxacin

1992 ◽  
Vol 26 (5) ◽  
pp. 636-639 ◽  
Author(s):  
Bradford K. Grassmick ◽  
Victoria Tutag Lehr ◽  
Alistair S. Sundareson
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Case Reports ◽  
Data Extraction ◽  
Hepatic Function ◽  
Data Synthesis ◽  
The Past ◽  
Serum Aspartate Aminotransferase ◽  
History Of ◽  
Oral Ciprofloxacin

OBJECTIVE: To report a case of hepatic failure in a patient who was receiving oral ciprofloxacin. DATA SOURCES: Case reports, review articles, and relevant laboratory studies identified by MEDLINE. DATA EXTRACTION: Data were abstracted from pertinent published sources by one author and reviewed by the remaining authors. DATA SYNTHESIS: A 66-year-old man was admitted for hip arthroplasty and developed fulminant hepatic failure during oral ciprofloxacin therapy. Ciprofloxacin was started on postoperative day 13 for treatment of a urinary tract infection. Over the next three days he became confused and hypoglycemic. His prothrombin time increased to >90 s. Serum aspartate aminotransferase and alanine aminotransferase concentrations were markedly elevated. The patient died on postoperative day 20. Postmortem examination of the liver revealed extensive centrilobular necrosis. A skin biopsy was consistent with a drug reaction. It is unknown whether the patient had received a quinolone compound in the past or had a history of exposure to hepatotoxins. CONCLUSIONS: It cannot be concluded that ciprofloxacin directly caused hepatic failure in this patient. It is possible that the drug evoked a hypersensitivity reaction or exacerbated a preexisting hepatotoxicity. A detailed patient history and evaluation of hepatic function should be obtained prior to initiating ciprofloxacin therapy. A nonquinolone antimicrobial may be a safer alternative for patients with hepatic dysfunction.

Sign in / Sign up

Export Citation Format

Share Document