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M J Dalton

Publications and source records attributed to M J Dalton.

14 recordsLinked to original sources
PubMed1996

Imaging manifestations of cat-scratch disease.

Cat-scratch disease affects an estimated 22,000 people in the United States each year, more than half of whom are children or adolescents [1]. It is caused by Bartonella henselae, a gram-negative bacillus usually introduced by the scratch of a cat [2]. In the past, diagnosis was made if three of the following four criteria were met: (1) history of cat exposure with inoculation, (2) positive skin test: (3) absent laboratory and histopathologic evidence of other diseases, and (4) biopsy findings of granulomatous inflammation [3]. Recent identification of the causative organism has led to new diagnostic tests, including serum assays for B. henselae antibodies [4]. Although response of the disease to antibiotics is poor, spontaneous recovery generally occurs within months to years [3].

Adolescent↗
PubMed1995

Oral melanoma: case reports and review of the literature.

Oral melanomas occur most often on the palate and gingiva with the maxillary arch affected 80% of the time. Melanosis may exist many years before a definitive biopsy. Long-standing lesions may ulcerate but lack rolled borders or induration, features commonly associated with squamous cell carcinoma. Melanoma that involves oral mucosa is rare with an extremely poor prognosis. Surgical management remains the preferred treatment in combination with chemotherapy. Irradiation therapy is used occasionally as a primary modality in the elderly and medically compromised patients. Lymph node dissection is not routinely practiced. The poor prognosis of oral melanomas requires that pigmented lesions of undetermined origin be routinely biopsied.

Aged↗
PubMed1995

Evaluation of the magnitude of the 1993 hantavirus outbreak in the southwestern United States.

In May 1993, an outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was caused by the previously unrecognized Sin Nombre virus (SNV). Most HPS patients had an influenza-like prodrome, followed by rapid onset of pulmonary edema (fatality rate, 52%). To define the magnitude of the outbreak, patients with milder illnesses who sought medical care in the outbreak area during the outbreak period were assessed for infection with SNV. Of 299 study subjects, 43 had illnesses similar to the HPS prodrome. One laboratory finding, thrombocytopenia, was highly discriminatory between non-HPS patients (1%) and confirmed HPS patients (71%; P < .001) during the prodrome phase. No study subject had serologic evidence (IgM antibodies) of recent SNV infection. Five had IgG titers consistent with a previous hantavirus infection: 3 of these 5 were among the 43 patients who had illnesses similar to the HPS prodrome (P < .05). These data provide evidence that mild illness is rarely caused by SNV.

Adolescent↗
PubMed1995

National surveillance for Rocky Mountain spotted fever, 1981-1992: epidemiologic summary and evaluation of risk factors for fatal outcome.

Between 1981 and 1992, the Centers for Disease Control collected and summarized 9,223 cases of Rocky Mountain spotted fever (RMSF) reported from 46 states. Four states (North Carolina, Oklahoma, Tennessee, and South Carolina) accounted for 48% of the reports. The annual incidence per million U.S. population decreased from a high in 1981 of 5.2 to a low in 1992 of 2.0, primarily due to decreased incidence in the southeast. Case report forms were filed on 7,650 patients, of whom 4,217 had laboratory-confirmed RMSF. The age group with the highest incidence was those 5-9 years of age. Most cases (90.0%) occurred between April 1 and September 30 and included a history of tick attachment (59.6%). Reported symptoms included fever (94.0%), headache (86.2%), myalgia (82.5%), and rash (80.2%). The case-fatality ratio was 4.0%. Risk factors associated with death included older age, delay in treatment or no treatment, and treatment with chloramphenicol (compared with tetracycline); however, insufficient data existed to fully assess the confounding effect of severity of illness on antibiotic choice.

Adolescent↗
PubMed1990

Kinetic effects of multiple oral doses of acetaminophen on a single oral dose of lamotrigine.

In this double-blind, randomized, crossover, placebo-controlled study, the effect of multiple oral doses of acetaminophen on lamotrigine disposition was examined in healthy volunteers. Eight volunteers received two single 300 mg oral doses of lamotrigine, administered 20 days apart. Acetaminophen (2.7 gm/day) or placebo was taken for 24 hours before and continued for 10 days after each lamotrigine dose. Area under the plasma concentration-time curve for lamotrigine [AUC(O-infinity)] and lamotrigine half-life were statistically decreased by 20% (229.0 +/- 62.5 micrograms.hr/ml versus 191.2 +/- 42.1 micrograms.hr/ml, p less than 0.01) and 15% (35.7 +/- 9.3 hours versus 30.2 +/- 7.3 hours, p less than 0.01), respectively, when concurrently administered with acetaminophen. There was no significant difference in the peak plasma concentration or the time to reach peak plasma concentration. The percentage of the dose of lamotrigine recovered in the urine (total) was significantly higher during the acetaminophen treatment (65.9% +/- 12.3% versus 72.5% +/- 5.7%, p = 0.048). Acetaminophen seems to facilitate lamotrigine removal through a yet to be determined mechanism(s).

Acetaminophen↗
PubMed1987

Characteristics of pyridoxine overdose neuropathy syndrome.

A newly recognised neurotoxic syndrome due to pyridoxine (B6) overdose is described. It is the largest series of B6 intoxication hitherto reported. A raised serum B6 level was present in 172 women of whom 60% had neurological symptoms, which disappeared when B6 was withdrawn and reappeared in 4 cases when B6 was restarted. The mean dose of B6 in the 103 women with neurological symptoms was 117 +/- 92 mgs, compared with 116.2 +/- 66 mgs in the control group. There was a significant difference (P less than 0.01) in the average duration of ingestion of B6 in the neurotoxic group of 2.9 +/- 1.9 years compared with 1.6 +/- 2.1 years in controls. The symptoms were paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb. These women were taking a lower dose of B6 than previously described (1,2), which may account for the complete recovery within 6 months of stopping B6.

Dose-Response Relationship, Drug↗
PubMed1985

Ranitidine does not alter single-dose carbamazepine pharmacokinetics in healthy adults.

In our recent study, oral cimetidine increased carbamazepine plasma levels after a single oral dose by 26 percent and prolonged the elimination half-life by 18 percent. This effect of cimetidine on carbamazepine could have resulted from enhanced carbamazepine absorption and/or inhibited metabolism. To gain an insight into which mechanism was responsible, we repeated the study with ranitidine, which has nearly identical gastrointestinal effects as cimetidine, but does not inhibit oxidative metabolism. Eight healthy subjects received a single dose of carbamazepine 600 mg po on two occasions separated by one month. In a randomized sequence, they also received ranitidine 300 mg/d or matching placebo starting two days before and continuing until seven days after the carbamazepine dose. Ranitidine did not change the carbamazepine area under the plasma concentration-time curve (324.2 +/- 71.1 micrograms h/ml, placebo vs. 326.3 +/- 65.0 micrograms h/ml, ranitidine; p = 0.84) or the elimination half-life (32.2 +/- 6.4 h, placebo vs. 31.7 +/- 6.1 h, ranitidine; p = 0.62). Since ranitidine does not alter the pharmacokinetic profile of oral carbamazepine, it is unlikely that the changes observed with cimetidine were due to increased carbamazepine absorption. Therefore, the mechanism of the single-dose carbamazepine-cimetidine interaction is probably metabolic inhibition, although the exact pathway (or pathways) affected has not been identified.

Adult↗
PubMedDate not supplied

The influence of cimetidine on single-dose carbamazepine pharmacokinetics.

The purpose of this study was to evaluate the influence of cimetidine on carbamazepine pharmacokinetics in healthy adults, since carbamazepine toxicity in a patient has been attributed to an interaction with cimetidine and in vitro and in vivo studies in rats have shown that cimetidine inhibits carbamazepine metabolism. Eight healthy volunteers received a single 600-mg oral dose of carbamazepine on two occasions, separated by 1 month. In a randomized crossover sequence, cimetidine 1,200 mg/day or placebo was taken for 48 h before and continuing for 7 days after each carbamazepine dose. Plasma concentrations of carbamazepine and carbamazepine-10,11-epoxide and urine concentrations of carbamazepine, the 10,11-epoxide, and the transdiol metabolite were measured in samples collected for 154 h following each carbamazepine dose. Cimetidine treatment was associated with increases of 26 and 18% in carbamazepine area under the concentration-time curve (AUC) and elimination half-life, respectively. There was also an increase in carbamazepine-10,11-epoxide AUC (27%) and t 1/2 (12%) during cimetidine treatment. There was no difference in the ratio of the 10,11-epoxide to the carbamazepine AUC between treatments. The urinary excretion (expressed as molar percentage of the administered dose) of carbamazepine, 10,11-epoxide, and transdiol metabolite all increased with cimetidine. Although cimetidine appears to inhibit carbamazepine elimination based on the increased elimination half-life, the effect must be on carbamazepine metabolic pathways that we could not measure and that account for greater than 80% of the administered dose. The clinical significance of this interaction should be verified under steady-state conditions when carbamazepine autoinduction is present.

Adult↗
PubMedDate not supplied

Cimetidine and carbamazepine: a complex drug interaction.

Cimetidine has been shown to inhibit the elimination of carbamazepine after a single oral dose. The mechanism of this interaction is thought to be inhibition of carbamazepine metabolism by the hepatic microsomal enzyme system. Because carbamazepine metabolism undergoes autoinduction with chronic administration, it is not known whether or not the clinical significance of this interaction can be predicted from the results of a single-dose study. The purpose of this study was to evaluate the presence of an interaction under steady-state enzyme-induced conditions. Using an open treatment design, carbamazepine, 300 mg b.i.d., was taken by eight healthy volunteers for 42 days (days 1-42). Cimetidine, 400 mg t.i.d., was taken for 7 days (days 29-35). Steady-state carbamazepine increased 17% after 2 days of cimetidine treatment (from 4.7 +/- 0.8 to 5.5 +/- 1.4 micrograms/ml; p less than 0.05). Six of the eight subjects noted side effects shortly after starting cimetidine treatment. Carbamazepine returned to the pre-cimetidine level and the side effects diminished by the 7th day of cimetidine administration. Therefore, the clinical significance of this interaction appears to be time dependent, and could not be predicted from the results of single-dose studies.

Adult↗
PubMedDate not supplied

Consultative total parenteral nutrition teams: the effect on the incidence of total parenteral nutrition-related complications.

A two part, prospective study was undertaken to establish the existing frequency of total parenteral nutrition-(TPN) related mechanical, metabolic, and septic complications in an institution with a consultative TPN team (group A) and to determine if increasing the involvement of the TPN team in patient monitoring and verifying adherence to TPN infection control guidelines would reduce the incidence of these complications (group B). The initial 28 consecutive patients were managed entirely by their primary physicians with the role of the TPN team limited to consultative activities while the next 29 patients receiving TPN were managed jointly by their primary physicians and the TPN team. Analysis of the results show group B to have a significant reduction in metabolic complications, decreased incidence of mechanical abnormalities, and approximately equal incidences of documented sepsis. However, when compared to the results of an institution in which the TPN team has complete control of TPN therapy, even the group B patients had a relatively excessive number of TPN-related complications especially in the categories of mechanical and metabolic abnormalities. Thus, consultative TPN teams do not necessarily ensure optimum TPN therapy and institutions using this approach to provide nutrition parenterally must be prepared to establish the incidence of TPN-related complications and to expand the involvement of the TPN team as required to control the frequency of these anomalies.

Aged↗
PubMedDate not supplied

Use of Bartonella antigens for serologic diagnosis of cat-scratch disease at a national referral center.

BACKGROUND: Bartonella henselae (formerly the genus Rochalimaea) has recently been isolated from patients with cat-scratch disease and their cats, and since September 1992 the Centers for Disease Control and Prevention has offered an indirect fluorescent antibody assay for Bartonella-specific antibody. METHODS: Physicians submitted serum samples from patients suspected of having cat-scratch disease or other Bartonella-associated illness and completed a questionnaire that recorded clinical information. Indirect fluorescent antibody assay was performed with the use of antigen derived from three Bartonella species: B henselae, Bartonella quintana, and Bartonella elizabethae. RESULTS: During 16 months, 3088 serum samples were received. The largest numbers of specimens and the highest percentages positive (titer, > or = 64) were observed in the fall and winter. Clinical histories of the first 600 patients for whom serum samples and completed information forms were received were examined in detail; seropositivity was significantly associated with cat contact, cat age of less than 1 year, cat scratch, presence of an inoculation papule, and regional adenopathy. Of 91 patients whose illness met a strict clinical definition of cat-scratch disease, 86 (95%) had titers of 64 or greater to either B henselae or B quintana. A fourfold rise or fall in titer was observed in 87 of 132 patients with paired serum samples. CONCLUSIONS: The indirect fluorescent antibody assay for Bartonella-specific antibody is sensitive for the diagnosis of cat-scratch disease. Redefinition of cat-scratch disease on the basis of cause and use of this assay as a diagnostic criterion is recommended.

Adolescent↗