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Abstract Background Non-HIV Pneumocystis pneumonia (PCP) can occur in immunosuppressed patients having malignancy or on immunosuppressive agents. To classify severity, the A-DROP scale proposed by the Japanese Respiratory Society (JRS), the CURB-65 score of the British Respiratory Society (BTS) and the Pneumonia Severity Index (PSI) of the Infectious Diseases Society of America (IDSA) are widely used in patients with community-acquired pneumonia (CAP) in Japan. To evaluate how correctly these conventional prognostic guidelines for CAP reflect the severity of non-HIV PCP, we retrospectively analyzed 21 patients with non-HIV PCP. Methods A total of 21 patients were diagnosed by conventional staining and polymerase chain reaction (PCR) for respiratory samples with chest x-ray and computed tomography (CT) findings. We compared the severity of 21 patients with PCP classified by A-DROP, CURB-65, and PSI. Also, patients’ characteristics, clinical pictures, laboratory results at first visit or admission and intervals from diagnosis to start of specific-PCP therapy were evaluated in both survivor and non-survivor groups. Results Based on A-DROP, 18 patients were classified as mild or moderate; respiratory failure developed in 15 of these 18 (83.3%), and 7/15 (46.7%) died. Based on CURB-65, 19 patients were classified as mild or moderate; respiratory failure developed in 16/19 (84.2%), and 8 of the 16 (50%) died. In contrast, PSI classified 14 as severe or extremely severe; all of the 14 (100%) developed respiratory failure and 8/14 (57.1%) died. There were no significant differences in laboratory results in these groups. The time between the initial visit and diagnosis, and the time between the initial visit and starting of specific-PCP therapy were statistically shorter in the survivor group than in the non-survivor group. Conclusions Conventional prognostic guidelines for CAP could underestimate the severity of non-HIV PCP, resulting in a therapeutic delay resulting in high mortality. The most important factor to improve the mortality of non-HIV PCP is early diagnosis and starting of specific-PCP therapy as soon as possible.

Anaphylaxis is a common condition observed in emergency departments and is sometimes associated with a fatal outcome. This may be a good way to prevent I Anisakis i allergy.[[4]] Although previous studies conducted in Spain reported I Anisakis i allergy incidences of 10.8%-11.1%,[[6]] I Anisakis i -related anaphylaxis has rarely been reported in other areas.[[1], [8]] The consumption of a raw fish diet in Japan may have contributed to this epidemiological difference. [Extracted from the article]

The numbers of β-adrenergic receptors on lymphocytes in normal subjects and asthmatic patients were measured by the use of [125I]hydroxybenzylpindolol. The numbers of β-adrenergic receptors per lymphocyte in normal subjects, drug-free asthmatics and patients taking β-stimulants were 1146±98, 845±114 and 582±47 sites/cell (mean ± SE), respectively. The differences were statistically significant (P < 0.05) among these groups, while no statistically significant differences were found in dissociation constants. A 42% decrease in the number of β-adrenergic receptors per lymphocyte after administration of 6 mg/day of terbutaline for 7 days was noted in four volunteers. There was significant correlation (r = 0.68, P < 0.01) between the number of β-adrenergic receptors per lymphocyte and the percentage increase in blood sugar 20 min after subcutaneous injection of 4 μg/kg epinephrine. There was also significant correlation (r = 0.78, P < 0.005) between the number of β-adrenergic receptors per lymphocyte and the respiratory threshold for acetylcholine. These results suggest that β-blockade and bronchial hypersensitivity in asthmatic patients may in part be due to a decreased number of β-adrenergic receptors. [ABSTRACT FROM AUTHOR]

Decreased response of beta-adrenergic receptor has been considered to be one of the causes of increased responsiveness of the bronchi in asthma. Since beta-adrenergic receptor has two subtypes, beta1 and beta2, and the bronchodilating effect of beta stimulants is mediated by beta2-receptor, responsiveness of the bronchi is expected to correlate to the cyclic AMP response of lymphocytes to a beta2-stimulant. Responsiveness of the bronchi was expressed as respiratory threshold to acetylcholine (RT-Ach), which was the minimal concentration of acetylcholine solution to cause an initial decrease of FEV1 of more than 20% of the baseline value. Beta1- and beta2-responses were expressed as the increments of cyclic AMP content of 106 lymphocytes incubated with norepinephrine (beta1-stimulant) and salbutamol (beta2-stimulant). RT-Ach showed a significant correlation with the beta2-cyclic AMP response of lymphocytes, but not with the beta1-response among patients with asthma. Sixteen symptomatic patients on continuous beta-stimulants showed lower RT-Ach value and diminished beta2-receptor activity of lymphocytes compared with 14 patients in remission. These results suggest that selective beta2-adrenergic blockade may he one of the causes of bronchial hypersensinvity in asthma, though it should be noted that in this study beta-adrenergic responses were examined in lymphocytes and were compared with the responsiveness oldie bronchi. Possible beta-receptor subsensitivity induced by administration of beta-stimulants is discussed. [ABSTRACT FROM AUTHOR]