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We had cases in which peripheral neuropathy was augmented after changing from mFOLFOX6, a chemotherapy for colorectal cancer, to FOLFIRI and comparatively examined disease status and trends. There were no shared points with respect to patient characteristics, timing of peripheral neuropathy augmentation, drug dosage, etc. It appeared that the change in chemotherapy itself had an effect on neuropathic symptoms. Regarding the change in chemotherapy, the therapeutic agent was switched from oxaliplatin to irinotecan; the cause was unknown, but some effects of these two drugs were suggested. Future investigation, including the examination of genetic mutations, is necessary.

Febrile neutropenia(FN)is one of the serious treatment-related toxicities after FEC100(5-fluorouracil 500mg/m2, epiru- bicin 100mg/m2, cyclophosphamide 500 mg/m2)chemotherapy for breast cancer. Granulocyte-colony stimulating factor(GCSF) is used as a support therapy for FN. Thus, we evaluated retrospectively the safety of administering pegfilgrastim the day after FEC100 chemotherapy in Japanese patients with breast cancer as compared with lenograstim. Grade 3 or 4 neutropenia was observed in 91.7% patients after pegfilgrastim administration and in 63.2% after lenograstim. The incidence rate of FN was 7.0%after pegfilgrastim administration and 9.7%after lenograstim, a difference that was not significantly different(p= 0.741). The mean relative dose intensity was good at 0.98 for pegfilgrastim and 0.97 for lenograstim. In conclusion, pegfilgrastim is not inferior to lenograstim in the incidence of FN. However, we do not recommend administering pegfilgrastim on the day after FEC100 therapy because it causes more severe neutropenia and has a high risk of FN. The timing of administration of pegfilgrastim in FEC100 therapy requires further study.

Purpose: To investigate the effects of botulinum toxin type A(botulinum A toxin) on the autonomic and other non-adrenergic, non-cholinergic nerve terminals., Methods: The effects of neurotoxin on twitch contractions evoked by electrical field stimulation (EFS) were studied in isolated rabbit iris sphincter and dilator muscles using isometric tension recording., Results: Botulinum A toxin(150 nM) inhibited the fast cholinergic and slow substance P-ergic component of contraction evoked by EFS in the rabbit iris sphincter muscle without affecting the response to carbachol and substance P. Botulinum A toxin(150 nM) did not affect the twitch contraction evoked by EFS in the rabbit iris dilator muscle., Conclusion: These data indicated that botulinum A toxin may inhibit not only the acetylcholine release in the cholinergic nerve terminals, but also substance P release from the trigeminal nerve terminals of the rabbit iris sphincter muscle. However, neurotoxin has little effect on the adrenergic nerve terminals of the rabbit iris dilator muscle.

We examined 24 pediatric patients to evaluate the usefulness of sudden near maximal exercise test (dash method), where the subjects began to run at Bruce protocol of the last stage. 1) No considerable differences between two protocols were found in maximal oxygen consumption (V O2max), maximal heart rate (HRmax), maximal systolic blood pressure, and findings of electrocardiography. 2) The sudden maximal exercise test could be completed during a shorter period compared to Bruce protocol. 3) The sudden maximal exercise protocol reached 84% of HRmax and 47% of V O2max at one minute after the onset of the protocol, and produced 96% of HRmax and 89% of V O2max at two minutes after the onset. We considered that sudden maximal exercise protocol was useful to obtain a response similar to Bruce protocol at maximal exercise within a short period. We have to pay attention to the safety of the patients because their cardiopulmonary response to sudden maximal exercise protocol is dramatic.

The absorption and excretion of a new doxycycline solution for intravenous use (DOTC iv) were studied with the following results. 1. Serum levels following one shot intravenous injection of DOTC iv in glucose solution showed a good dose-response comparable with that of the same dose injection of pyrrolidinomethyltetracycline (PRM-TC). The urinary excretion was also examined. In 200 mg injection, nausea, general warm feeling, odor in mouth and tongue numbness were complained. 2. When DOTC iv was injected intramuscularly, the serum level did not reach the peak value and low level continued for a long time. Moderate local pain was complained at the site of injection. 3. The serum level following drip infection of DOTC dry fill showed a dose-response as well. The local vein tolerated well. 4. No abnormalities were found in clinical and laboratory examinations in all volunteers.

The antibacterial spectrum of cefroxadine was as wide as that of CEX, and its antibacterial effect was as strong as that of CEX or even 2-fold stronger against E. coli and Klebsiella. Cefroxadine was also proved to have stronger bactericidal or bacteriolytic effect than CEX and have better affinity with penicillin binding proteins. In clinical trials, an efficacy rate of 82.7% was achieved in a total of 2,009 cases of various infections analyzed. Cefroxadine displayed particularly good clinical and bacteriological effects for the infections of skin, soft tissues, respiratory tract and urinary tract. The rate of bacteria eradication in a total of 1,410 cases was 81.6%, showing good results against the bacteria such as S. aureus (83.9%, 167/199), E. coli (89.0%, 528/593), Klebsiella (78.0%, 78/100) and P. mirabilis (80.0%, 36/45). As for side effects, their incidence was a low of only 2.3%, the main ones being eruption and gastrointestinal symptoms just as recognized in conventional cephalosporins, and none of them was serious. Abnormal laboratory test values were only increases in eosinophil, S-GOT, S-GPT and Al-P values, and their incidence was low. From these findings, we may say that the drug is an effective, safe, and useful antibiotic among all other orally administered cephalosporins.

The serum and urinary levels and urinary recovery of cephaloridine during and after two-hour drip infusion of 1 or 2 grams of cephaloridine dissolved in 500 ml of physiological saline solution were determined in four healthy volunteers in cross-over fashion. Using the values of serum levels obtained from this experiment, pharmacokinetic parameters were calculated and simulation curves of serum levels for various doses and durations of cephaloridine drip infusion were drawn.

A sixty-three years old female patient with subacute bacterial endocarditis was treated with clindamycin-2-phosphate parenterally, because she had a history of hypersensitive reaction to penicillins. She had received erythromycin, cephaloridine and cephalexin previously, but had no bacteriological response. When clindamycin-2-phosphate was given intramuscularly, the bacteremia disappeared for the first time. However, after the cessation of this treatment Streptococcus viridans grew in her blood again. It was suggested that this drug was bacteriostatic rather than bactericidal. During this therapy, local tenderness was noticed at the injected sites and a transient maculopapular rash developed which resolved in a few days.

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.