Recent studies have increasingly revealed a close association of the blood coagulation system with inflammation and immune reactions. Coagulation factors can work as inflammatory mediators or immune modulators, and, vice versa, some inflammatory or immune stimuli are linked to blood coagulation. First, leukocyte expression of tissue factor, the blood coagulation initiator, and the TF expression regulatory factors associated with inflammation and immune reactions, and assembly of coagulation factors on leukocytes are discussed. Secondly, evidence of leukocyte tissue factor expression and subsequent fibrin deposition are demonstrated at the sites of infection and allergic reactions using immunohistochemical staining and in situ hybridization. Thirdly, the progress in the investigation of thrombin, factor X, and fibrinopeptides is reviewed from the viewpoint of their effects on inflammation (vascular permeability enhancement, leukocyte chemotaxis, chemical mediator release, etc) and immune reactions (T-cell proliferation, cytokine production, etc). Evidence presented here reveals a cross-talk between blood coagulation, and inflammatory and immune reactions.

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Since the citizens used to play a subsidiary role in rescuing sudden cardiac arrest victims only by their giving early 119 call and early cardiopulmonary resuscitation (CPR) until the paramedics arrive, it led to a 3% survival to discharge rate. Recently, Japanese government has declared their intention of approving automated external defibrillator (AED) use by laypeople, which will increase citizens' role in promoting public access defibrillation (PAD), an easy, safe, and most effective approach to saving one's life.

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A Dumon-type bronchial stent was placed in a lung cancer patient presenting left lung collapse due to stenosis of the left main bronchus. High frequency jet ventilation was then applied to the left lung through a channel of a bronchofiberscope introduced in the left main bronchus proximal to the stent. Immediately after re-expansion of the left lung, circulatory collapse including severe hypotension, bradycardia and hypoxia developed. Considering that abrupt ST elevation and complete A-V block on ECG monitor and cerebral infarction on later CT examination were also accompanied with the event, multiple emboli was suspected as one of the causes of circulatory collapse in addition to re-expansion pulmonary edema. It was presumable that thrombi or tumor breakdowns existed in the left pulmonary vessel might have entered in the systemic circulation following re-expansion and might have been transported to the heart and brain. We should be aware of developing not only re-expansion pulmonary edema but also multiembolism after rapid re-expansion of the lung by jet ventilation in a patient with long term collapse of the lung.

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An 81-year-old man with history of hypertension and chronic renal insufficiency was admitted to a hospital because of diarrhea and melena. The patient was diagnosed as inflammatory bowel disease (IBD) by colonoscopy and was given predonisolone and mesalazine. He was transferred to our hospital three days later following emergence of respiratory failure and anuria. The cause of these organ failures was digestive tract perforation and sequential panperitonitis. An emergency subtotal colectomy and ileostomy was done and the patient was pathologically diagnosed as amoebic colitis. Postoperative course was complicated by severe Aspergillus pneumonia. Combination therapy of antibiotics and antifungals could not improve his pneumonia and the patient passed away on the 12th ICU day. Amoebiasis sometimes develops without apparent history of chance of infection. Insufficiency of immune system of any kinds was supposed to be a determinant. Complications like Aspergillus pneumonia in this case may relate to immuno-insufficiency of the patient. Amoebiasis itself has good outcome unless digestive tract perforation occurs. Amoebiasis must be considered in differential diagnosis of idiopathic IBD and its early diagnosis and treatment should be important for better outcome.

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We reported a rare case of toxic shock-like syndrome (TSLS) caused by group A streptococci with soft tissue infection by group G streptococci, which demonstrated the necessity of early investigation of undiagnosed malignancy. A 41-year-old man without relevant clinical history was transferred to the ICU in a university hospital for shock-like signs, jaundice, bleeding tendency, and bulky and flushed swelling with tenderness on pudendal region. Blood culture taken before administration grew group A streptococci. Group G streptococci were also isolated from discharge of penis. Antibiotics (ampicillin, clindamycin), γ-globulin, steroid, artificial ventilation, and continuous hemodiafiltration (CHDF) improved his general condition. Destructively infected soft tissue was debrided about one month later following successuful infection control. Persistent agranulocytosis, however, forced us to do bone marrow study three months after admission and was found to result from acute myeloid leukemia. Intensive chemotherapy failed to induce remission and the patient passed away about 10 months after admission. An investigation for underlying malignancy was important in any patient showing marked pancytopenia, splenomegaly, severe infection of group G streptococci whose close correlation with malignancy was well known, and agranulosis after recovery from critical sepsis.

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