A combination of amoxicillin and clavulanate every 12 hours vs every 8 hours for treatment of acute bacterial maxillary sinusitis.

OBJECTIVE: To compare the safety and efficacy of a combination of amoxicillin and clavulanate potassium given orally every 12 hours (amoxicillin, 875 mg; clavulanate, 125 mg) with that given every 8 hours (amoxicillin, 500 mg; clavulanate, 125 mg) for the treatment of patients with acute bacterial maxillary sinusitis. DESIGN: Multicenter double-blind randomized double-dummy controlled trial. SETTING: Physicians' offices and ambulatory care clinics. PATIENTS: One hundred seventy patients at least 18 years of age with acute bacterial maxillary sinusitis who could be treated with an oral antimicrobial agent were randomized, and data from 134 were suitable for evaluation. Four patients were withdrawn from this study because of adverse effects. INTERVENTIONS: Patients received a combination of amoxicillin and clavulanate orally every 12 hours (amoxicillin, 875 mg; clavulanate, 125 mg) or every 8 hours (amoxicillin, 500 mg; clavulanate, 125 mg) for 14 days. MAIN OUTCOME MEASURE: Clinical success at the end of therapy. RESULTS: Clinical success at the end of therapy was similar for the 2 treatment groups, 93% and 88% of patients in the every 12-hour and every 8-hour groups, respectively (P = .76; 95% confidence interval, -4.0% to 15.6%). Clinical success rates at follow-up 2 to 4 weeks after the end of therapy were also similar in the 2 groups. Adverse events related to treatment were reported with similar frequency in the 2 groups. CONCLUSION: Amoxicillin and clavulanate given every 12 hours is as effective and as safe as administration every 8 hours for the treatment of acute bacterial maxillary sinusitis.

Isotype-specific antibody responses to acute Mycoplasma pneumoniae infection.

BACKGROUND: Mycoplasma pneumoniae-induced respiratory infections affect millions of patients and have been implicated in exacerbation of bronchial asthma. IgE may be involved in such exacerbations. While specific IgG and IgM responses to Mycoplasma pneumoniae are well described, the response of other isotypes is less known. PURPOSE: To determine whether specific IgE and what subclasses of IgG are formed in response to Mycoplasma pneumoniae infection. METHODS: We studied 20 patients with acute Mycoplasma pneumoniae infection, in whom the diagnosis was confirmed by a 16-fold increase in complement fixation titer between acute and convalescent serum samples. We developed an enzyme-linked immunosorbent assay (ELISA) for the determination of IgG, IgA, and IgM antibodies specific for Mycoplasma pneumoniae protein antigens. We used Western blotting to confirm the results of the ELISA and to detect Mycoplasma-specific IgG subclasses and IgE. RESULTS: Changes in Mycoplasma pneumoniae-specific IgG, IgA, and IgM were significant. Western blots of Mycoplasma pneumoniae antigens in 13 convalescent sera showed specific IgG in all, IgM in 11, IgA in 6, and IgE in 10. The IgG response consisted mainly of IgG1 and IgG3, and to a lesser degree of IgG2 and IgG4. CONCLUSIONS: We conclude that Mycoplasma pneumoniae infection is associated with a significant specific IgA and IgE response, in addition to the well-known responses of IgG and IgM. As IgE is involved in allergic reactions, the production of Mycoplasma pneumoniae-specific IgE may have a role in exacerbation of bronchial asthma.

Comparison of serum and plasma leukotriene B4 levels in normal and asthmatic subjects.

BACKGROUND: Leukotriene B4 (LTB4) serum and plasma concentrations were reported to be higher in some asthmatic patients than in normal subjects; however, reported LTB4 concentrations in normal subjects vary widely. One study suggested that blood clotting causes the increased LTB4 concentration. OBJECTIVE: To determine whether LTB4 concentration is increased in asthmatic patients, and whether it is affected by clotting. METHODS: We studied seven normal subjects and nine clinically stable asthmatic patients. Venous blood was drawn into test tubes without additives; containing heparin; or containing heparin and cyclo- and lipoxygenase inhibitors. Cells were separated after 30 minutes. Leukotriene B4 was measured by radioimmunoassay following its extraction from serum or plasma. In three subjects, plasma was separated also at times 0 through 30 minutes. RESULTS: Serum and plasma concentrations of LTB4 in normal volunteers and asthmatic patients were similar, but the variance of LTB4 concentrations among the asthmatic patients was significantly higher than in the normal subjects. Leukotriene B4 concentrations, measured in plasma only, were significantly reduced in both asthmatic and nonasthmatic subjects in the presence of inhibitors. There was no significant difference in LTB4 concentrations between time 0 and 30 minutes, but there was considerable variability. CONCLUSIONS: We conclude that clotting is unlikely to affect serum LTB4 concentrations. Leukotriene B4 serum and plasma concentrations are not consistently increased in asthmatic patients; however, LTB4 is synthesized during and possibly after blood has been drawn. Proper handling of the specimens and probably the addition of cyclo-oxygenase and lipoxygenase inhibitors is of the utmost importance for accurate LTB4 determination.

Dramatic responses to intravenous immunoglobulin in vasculitis.

Intravenous immunoglobulin (IVIG) has been successfully used to treat autoimmune diseases. We report dramatic, rapid and sustained responses to its use in two cases of vasculitis: a patient with primary angitis of the central nervous system: and a patient with hepatitis-B-antigen-related polyarteritis nodosa, who failed treatment with corticosteroids. Improvement in gait and a marked decrease in serum creatinine, respectively, were observed within 24 h of the first dose of IVIG. Both patients remained stable for several months. We conclude that IVIG should be considered in patients with vasculitis who fail corticosteroids, or when a rapid response is required.

Pulmonary perivascular and interstitial inflammation in MRL/MpJ-lpr/lpr mice. III. Modulation by cyclophosphamide and sex hormones in 4- and 6-month-old animals.

Estradiol (E) abolished clearing of pulmonary inflammation in 2-month-old male MRL/MpJ-lpr/lpr (MRL/l) mice treated with cyclophosphamide (CY). To determine if this effect persisted in animals with advanced disease, we studied male and female MRL/l mice, aged 4 and 6 months (4M, 6M, 4F, and 6F, respectively). Mice were treated, beginning at 1 month of age, with saline, CY (12 mg/kg/day), CY + castration, CY + castration + testosterone (T) in females, and CY + castration + E in males. CY had no effect on pulmonary inflammation in 4M, possibly because of the development of relatively mild lesions. However, CY was highly effective in 6M. CY + castration + T significantly reduced overall inflammation in 6F and showed a trend in 4F. CY alone had a variable effect on bronchoalveolar lavage fluid (BALF) cells and BALF IgG in both males and females. However, concurrent treatment with T was required for histologic changes of pulmonary inflammation to fully respond to a high dose of CY in female mice. E-treated males had reduced responsiveness to CY.

Serum leukotriene B4 levels in patients with obstructive pulmonary disease.

Leukotriene B4 has been found to be increased in the serum of cigarette smokers and some patients with bronchial asthma, as well as in the sputum of patients with cystic fibrosis and COPD. Corticosteroids supposedly may block the formation of LTB4. To determine if the effect of CS on airway disease is by reduction in LTB4, we studied serum LTB4 levels in clinically stable patients with asthma or COPD who were treated with or without CS. The LTB4 was extracted from serum and assayed by radioimmunoassay. Serum LTB4 concentrations, expressed as the mean +/- SD, were 0.36 +/- 0.15 ng/ml in ten normal controls, 0.56 +/- 0.18 ng/ml in nine asthmatic subjects, 0.67 +/- 0.2 ng/ml in eight asthmatic subjects receiving CS, 0.81 +/- 0.19 ng/ml in seven patients with COPD, and 0.97 +/- 0.29 ng/ml in eight patients with COPD receiving CS. Serum LTB4 levels in normal controls differed significantly from all groups with COPD or asthma (p less than 0.01). Levels of LTB4 in asthmatic subjects differed from levels in patients with COPD (p less than 0.03), and levels in asthmatic subjects receiving CS differed from subjects with COPD receiving CS (p less than 0.03). Concentrations of LTB4 within either the COPD or the asthmatic groups were not lower in the patients treated with CS. We conclude that serum LTB4 concentrations are higher in COPD than in asthma or normal controls and that administration of CS is not associated with low LTB4 levels. The beneficial effects of CS in obstructive airway disease appear to be mediated by mechanisms other than reduction of LTB4.

Anaphylaxis due to cornstarch surgical glove powder.

Two nurses suffered anaphylaxis to cornstarch glove powder. Both exhibited (1) positive prick skin tests to cornstarch powder in water, with resultant anaphylaxis in one and (2) negative prick skin tests and RAST to corn. Analysis of the powder revealed only glucose and inorganic salts. We were unable to detect in vitro histamine release or cornstarch powder specific IgE. Because of the positive skin tests and the resultant anaphylaxis, we suspect that cornstarch is the responsible allergen.

Multiple malignancies in immunocompetent patients.

We have reported two patients with multiple primary cancers in the presence of normal tests of cellular immune function, including normal natural killer cell activity. Immunodeficiency has been associated with an increased incidence of neoplastic disorders, but the resulting malignancies are unique, consisting of non-Hodgkin's lymphomas and a limited number of carcinomas. Immunosuppressive therapy and AIDS have been associated with aggressive sarcomas. Immunocompetence is of major importance against certain tumors. On the other hand, in spite of the limitations of the clinical evaluation of immunologic function, immunocompetence is insufficient to protect against neoplasia.

Psychopathology masquerading as food allergy.

Three patients who presented with vague symptoms previously diagnosed as food allergy are reviewed. No evidence for allergy to foods was found in any of the patients. Two were depressed with psychotic thinking and the third had moderately severe anxiety with depression. All three improved following psychiatric diagnosis and intervention. One was treated with antidepressant and one with antidepressant-antipsychotic medication. All three maintained improvement two years later. The diagnosis of food allergy must be based on showing a direct relationship between the inciting food and the immunologically mediated reaction. Anxiety and depression may masquerade as food allergy. Evidence of psychopathology should be present to make such a diagnosis.

Pathogenesis of trehalose dimycolate-induced interstitial pneumonitis. IV. Evidence against roles for immunoglobulins and the complement system.

We showed previously that trehalose dimycolate (TDM) in oil administered intraperitoneally into susceptible mice produced interstitial and hemorrhagic pneumonitis by the seventh day after injection and that mature T cells are necessary for the production of these lesions. TDM has been reported to activate complement and to be chemotactic for macrophages in vitro. Accordingly, we looked for involvement of humoral mechanisms in the pathogenesis of TDM-induced pneumonitis. Genetically C5-deficient B10D2/oSn mice developed pulmonary lesions just as well as C5-sufficient mice. No activation of C3 occurred in the plasma of TDM-treated mice as determined by crossed immunoelectrophoresis. Some splitting of C3 occurred in bronchoalveolar lavage fluids, but this was similar in control and experimental mice. By immunofluorescence microscopy, there was no deposition of C3 or immunoglobulins (Ig) along the alveolar membranes. These findings and our published data provide additional evidence that TDM-induced interstitial inflammation in mice is exclusively a T-lymphocyte-dependent process.

Mycoplasma pneumoniae is a frequent cause of exacerbation of bronchial asthma in adults.

The possible role of infection with Mycoplasma pneumoniae (MP) in exacerbation of bronchial asthma in adults was studied in 95 patients hospitalized due to acute asthma. Twenty (21%) of these patients had evidence of a recent MP infection as determined by the presence of high levels of MP-specific IgM antibodies. In addition, high levels of both IgM and IgG but not IgA serum immunoglobulins were observed in the MP-infected group as compared to a control group of 20 non-MP-infected asthmatics. Five out of 20 MP-infected asthmatics exhibited rheumatoid factor (RF) in their sera while patients in the control group were all negative for RF. It is concluded that MP infection may be significant in exacerbation of asthma in adults.