We measured the platelet activation and the rate of erythrocyte aggregation simultaneously employing venous blood from 31 patients with cerebral infarction during the acute phase (less than 7 days after onset) and 73 patients with cerebral infarction
We retrospectively evaluated the clinical findings of 10 cases of tuberculous meningitis who had been admitted to our department from 1987 to 1994. Four patients were male and six were female. All of them were Japanese, and their age ranged from 17 to 74 years old. Regarding the patient's delay, nine patients visited a doctor in 1 to 20 days after the onset of headache, and one patient visited a doctor in 14 days after the onset of general malaise. It is suggested that the patient's delay could not be longer than 3 weeks because of progressively worsening symptoms of tuberculous meningitis such as severe headache and fever. The time interval between the first contact of the patient to a doctor and the commencement of antituberculous therapy (doctor's delay), ranged from 14 to 66 days. When the diagnosis of meningitis was obtained based on the findings of the cerebrospinal fluid (CSF), focal neurological signs including psychological symptoms, cranial nerve palsies and seizure were noted besides meningeal signs or the disturbance of consciousness in 4 patients. The CSF revealed an increase in cell counts with mononuclear cell dominance in 9 patients, but the findings typical for tuberculous meningitis such as increase in total protein content and a decrease in glucose concentration were obtained in only 5 patients. Mycobacterium tuberculosis had not been detected in all cases when the antituberculous chemotherapy was started. Later, it was found to be positive in the CSF sample from only three patients by culture or polymerase chain reaction (PCR) method. When the antituberculous therapy was completed, meningitis was cured without remaining any symptom or sign in all patients. All patients had no active pulmonary tuberculosis when the meningitis was diagnosed, and only one of them had sequels of lung tuberculosis. Four patients had the past history of tuberculosis, and 1 had the familial history of pulmonary tuberculosis. At the first contact to a doctor, seven patients were diagnosed as having common cold or headache related with fever because of the lack of typical signs of meningitis. Similarly three other patients were initially diagnosed as having meningitis due to viral infection or unknown etiology. In summary, it was difficult to obtain the solid diagnosis of tuberculous meningitis at the initial stage of this disease, since the symptoms and signs at its onset often similar to those of common cold or non-specific headache. Therefore, when we see the patients with subacute onset of headache and fever followed by the meningeal signs, tuberculous meningitis should always be included in the list of diseases requiring differential diagnosis. In addition, when tuberculous meningitis is suspected, the antituberculous therapy should be started without any delay.
Using video-enhanced contrast (VEC)-differential interference contrast (DIC) microscopy, ultrastructural observations were made of the activation of polymorphonuclear leukocytes (PMNLs), the interaction between activated PMNLs and endothelial cells (ECs), and the effects of pentoxifylline (PTX). The ECs were obtained from a commercial source as human umbilical cord vein endothelial cells (HUVECs) or were obtained from pig or rat brains. They were cultured on a coverglass with DMEM for about 1 week. The human PMNLs were obtained from the authors' venous blood. The control appearance of the PMNLs resembled an elastic ball covered with fine villi. The PMNL was activated spontaneously and became flattened on the glass surface within 10 min in the observation chamber. The activation of the PMNLs was estimated arbitrarily from the polymorphous changes in cell shape, agitation of the intracellular granules, and apparent increase in adhesiveness. Preadministered PTX prevented such PMNL activation, and the PMNLs remained round for more than 15 min. PMNL activation was accelerated by chemoattractants (PAF, fMLP, and PMA). In one case, a PMNL that had been activated by PMA tended to recover its round shape with PTX, but finally ended by swelling and bursting. When PMNLs were introduced into the EC-containing chamber, they became entrapped by the ECs and activated, with degranulation followed by release of a smoke-like material. After about 3 h, the EC with an attached PMNL shrank and fell into a state of coagulation necrosis. When PTX was introduced at the time of adhesion of the flattened PMNL, the PMNL appeared to be deactivated, becoming smaller and assuming its previous round shape, and detached from the EC. PTX prevented the spontaneous activation of PMNLs, and of deactivated PMNLs even after their adherence to the endothelium.
A 22-year old male was admitted to Ashikaga Red Cross Hospital because of the progressing abdominal distension in May 1988. The physical examinations disclosed marked hepato-splenomegaly, lymphadenopathy and cachexic state. In the laboratory examinations, anemia, leukocytosis with left shift of nuclei and severe inflammatory reactions were found. Bone marrow aspirations were dry taps, and the biopsy showed myelofibrotic changes. Abdominal computed tomography and ultrasonography revealed a marked hepatomegaly and a giant splenomegaly with subcapsular hematoma. Philadelphia chromosome was negative and neutrophilic alkaline phosphatase score was slightly high. A little amount of peritoneal effusions was obtained and yielded S. aureus. A diagnosis of myelofibrosis with subcapsular hematoma due to spontaneous rupture of spleen and peritonitis of unknown cause was made. Operative indication was considered, but his family did not agree with it. Then conservative therapies for general conditions, those are, administrations of antibiotics and diuretics, and blood transfusions were taken. On the enlarged spleen, total irradiation was done. After the therapies, his spleen got smaller and hematoma was going to be absorbed. A rare case of myelofibrosis with splenic hematoma is reported and the conservative therapies were effective to this case.
