Kawasaki disease is a form of vasculitis, mainly in small and medium arteries of unknown origin, occurring frequently in childhood. It is the leading form of childhood-onset acquired heart disease in developed countries and leads to complications of coronary artery aneurysms in approximately 25% of cases if left untreated. Although more than half a century has passed since Professor Tomisaku Kawasaki's first report in 1957, the cause is not yet clear. Currently, intravenous immunoglobulin therapy has been established as the standard treatment for Kawasaki disease. Various treatment strategies are still being studied under the slogan, “Ending powerful inflammation in the acute phase as early as possible and minimizing the incidence of coronary artery lesions,” as the goal of acute phase treatments for Kawasaki disease. Currently, in addition to immunoglobulin therapy, steroid therapy, therapy using infliximab, biological products, suppression of elastase secretion inside and outside the neutrophils, inactivated ulinastatin therapy and cyclosporine therapy, plasma exchange, etc. are performed. This chapter outlines the history and transition of the acute phase treatment for Kawasaki disease.
Aneurysm ; Arteries ; Biological Products ; Coronary Vessels ; Cyclosporine ; Developed Countries ; Heart Diseases ; Immunization, Passive ; Incidence ; Inflammation ; Infliximab ; Mucocutaneous Lymph Node Syndrome ; Neutrophils ; Pancreatic Elastase ; Plasma Exchange ; Prednisolone ; Vasculitis

Kawasaki disease is a form of vasculitis, mainly in small and medium arteries of unknown origin, occurring frequently in childhood. It is the leading form of childhood-onset acquired heart disease in developed countries and leads to complications of coronary artery aneurysms in approximately 25% of cases if left untreated. Although more than half a century has passed since Professor Tomisaku Kawasaki's first report in 1957, the cause is not yet clear. Currently, intravenous immunoglobulin therapy has been established as the standard treatment for Kawasaki disease. Various treatment strategies are still being studied under the slogan, “Ending powerful inflammation in the acute phase as early as possible and minimizing the incidence of coronary artery lesions,” as the goal of acute phase treatments for Kawasaki disease. Currently, in addition to immunoglobulin therapy, steroid therapy, therapy using infliximab, biological products, suppression of elastase secretion inside and outside the neutrophils, inactivated ulinastatin therapy and cyclosporine therapy, plasma exchange, etc. are performed. This chapter outlines the history and transition of the acute phase treatment for Kawasaki disease.

To clarify changes in body temperature during endurance exercise in patients with spinal cord injury (SCI), we measured tympanic temperature (Tty) and skin temperature in the head, arm, chest, thigh, shin and calf in 5 patients with SCI (T6-T 12) and 7 normal controls during 30 minutes arm cranking exercise (20 watts) from 10 minutes before the initiation of exercise until 10 minutes after the termination of exercise in an artificial climate room at a temperature of about 25°C with a relative humidity of about 50%. The Tty in the SCI group was lower than that in the control group from 10 minutes before the initiation of exercise to 10 minutes after the termination of exercise with a significant difference only at the initiation of exercise. The difference in Tty slightly decreased with continuation of exercise. The Tty in the SCI group at rest was 36.05-37.15°C. Four patients in this group showed a decrease of 0.04-0.12°C in the early stage and an increase of 0.66°C±0.19 (mean±SD) at the end of exercise over the value at the initiation of exercise.
The skin temperature was lower in the SCI group than in the control group in all sites excluding the arm. Significant differences were observed in the head in the early stage of exercise and after exercise, in the chest from 10 minutes before the initiation of exercise to 5 minutes after the termination of exercise, in the thigh from 10 minutes before the initiation of exercise to 10 minutes after the termination of exercise, in the shin 10 minutes and 5 minutes before the initiation of exercise, and in the calf from before to 15 minutes after the initiation of exercise. In the SCI group, marked individual differences were observed in the skin temperatures in the thigh, shin, and calf, suggesting specificity of the skin temperature response in and near the paralysis area.
Results in Tty in this study suggested no heat retention in the SCI patients. Therefore, the risk for heat disorders seems to be low during moderate or mild exercise under moderate temperature environment at a temperature of about 25°C with a relative humidity of about 50% even when the skin temperature is low, and thermolysis is not marked.

It has been experienced that Kampo, with its philosophy that every disease is psychosomatic in origin and that herbs affect both the psyche and the soma, sometimes has a dramatic effect on somatoform disorders, though there has been no study examining the effects of Kampo on somatoform disorders. In this preliminary study, the morbidity of somatoform disorders among patients who visited the Keio Kampo Clinic and the patients' psychological well-being were examined.
One hundred patients (17 males and 83 females; mean age [±SD], 39±16) who sought Kampo treatment for the first time at Keio University Hospital participated in this study. A Japanese checklist derived from the somatoform disorders schedule (version 1.1) was used to check the somatoform symptoms. To assess psychological well-being, the subjective well-being inventory (SUBI) was performed. The subjects' clinical records were examined afterwards to rule out symptoms which could be medically explained.
Somatoform patients and medically ill (non-somatoform) patients were 65% and 26% of the total respectively. The somatoform patients showed significantly lower SUBI positive scores than the non-somatoform patients (p=0.042), while SUBI negative scores were significantly higher (p=0.001). Among the somatoform patients, there was a negative correlation between numbers of somatoform symptoms and SUBI positive scores (r=0.267; p=0.032), and a positive correlation between numbers of somatoform symptoms and SUBI negative scores (r=0.337; p=0.006).
Following the SUBI scores through treatment courses may lead to a better understanding of the pathology of somatoform disorders and to more effective use of Kampo.

As a screening tool for detecting latent pre-locomotive syndrome (latent pre-LS) in women over the age of 40, measuring handgrip strength with a cut-off value of 26 kg was proposed in a previous report. However, this screening method missed 22% of latent pre-LS. It would be beneficial to screen almost persons with latent pre-LS in community pharmacies. In this study, it was investigated whether screening using the combination of measuring handgrip strength and the questionnaire, “Loco-check,” which was proposed by the Japanese Orthopaedic Association, improved the detection of latent pre-LS in the same group mentioned above. Combining only one of the “Loco-check” questions, “I cannot put on a pair of socks while standing on one leg,” with the measurement of handgrip strength with the cut-off value of 26 kg, the detection of latent pre-LS was increased to 90.2%. The odds ratio was 9.72 in logistic regression analysis. Using the combination of the measurement of handgrip strength and the response to one question is both rapid and convenient. Therefore, in this study, this screening combination is proposed to be a useful tool in community pharmacies for detecting early latent pre-LS.