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Biomedical subjects

M Suga

Publications and source records attributed to M Suga.

At least 181 records · Page 10Linked to original sources

A case of HBs antigen negative fulminant hepatitis with IgM antibody to hepatitis B core antigen persisting more than seven years.

A 33-year old dentist developed fulminant hepatitis. At admission, a test for IgM antibody to hepatitis B core antigen (IgM anti-HBc) was positive, while tests for HBsAg and HBeAg were negative. He was cured of the disease, but in follow-up examinations from 1983 to 1990 IgM anti-HBc was continuously detected with radioimmunoassay while HBsAg and HBV-DNA were absent in the serum. However, HBcAg was found in a biopsied liver specimen and a small quantity of HBV-DNA was detectable by polymerase chain reaction assay. These observation suggest that the continuous detection of IgM anti-HBc without HBsAg in serum is due to persistent HBV infection and HBV replication in the liver.

Adult↗

Cerebral angio- and neuro-Behçet's syndrome: neuroradiological and pathological study of one case.

Cerebral angio-Behçet's syndrome is extremely rare and pathological studies are scarce. We describe a 63-year-old man who developed left homonymous hemianopsia and hemiparesis 16 years after the onset of cardinal symptoms of Behçet's syndrome. CT, MRI and PET studies disclosed cerebral lesion with reduced neuronal metabolism in the right hemisphere, which was resolved by glucocorticoid therapy. Cerebral angiography showed no filling of the right Rolandic, anterior and posterior parietal and angular arteries. The postmortem study revealed: (a) occlusive panarteritis of some medium-sized pial branches of the right middle cerebral artery, considered as angio-Behçet's pathology, and small infarctions due to the vascular occlusion; (b) patchy or confluent demyelinated foci with perivascular lymphocytic infiltration in the bilateral brain basis, predominantly in the right retro- and sublenticular structures, being equivalent to neuro-Behçet's pathology. Cerebral angio- and neuro-Behçet's syndromes could have occurred and progressed concomitantly, which suggests a close relationship between the two subclassified processes.

Arterial Occlusive Diseases↗

Detection of IgM, IgA, and IgG antibodies to preS2 antigen in hepatitis B virus infection.

Antibodies to the preS2 antigen (anti-preS2) of the hepatitis B virus (HBV), including IgA, IgM and IgG classes, were observed in patients with acute and persistent HBV infection. In acute HBV infection, rapid and marked serum IgM and IgA anti-preS2 responses were observed. Antibodies reached a peak of serum activity at about 1-2 months after the onset of clinical symptoms, and both antibodies disappeared from serum at 4 months after. IgG anti-preS2 was detected in the early phase of the illness, then the level of IgG anti-preS2 gradually rose during the recovery phase. In persistent HBV infection, IgG and IgM anti-preS2 were detected in sera where the preS2 antigen was present, and IgM anti-preS2 was significantly higher (p less than 0.05) in HBeAg-positive than in HBeAg-negative patients. These results indicate that an adequate humoral immune response to the preS2 antigen is induced during acute and persistent HBV infection.

Acute Disease↗

[Diffuse cerebrospinal gliomatosis. Case report].

A 65-year-old male was admitted with memory and gait disturbance. A computed tomography (CT) scan showed bilateral, diffuse, low-density areas with two round, slightly enhanced masses. T1-weighted magnetic resonance image revealed a low-intensity area in the left paraventricular region, which converted to increased signal intensity, extending to the right paraventricular region through the splenium, on T2-weighted images. The tumor was diagnosed as glioblastoma multiforme after needle biopsy and treated by irradiation and chemotherapy. Seven months after admission, a CT scan revealed subependymal infiltration of the tumor with spotty calcification. He died of respiratory complications 11 months after the onset of symptoms. The autopsy showed brain swelling with flattened gyri. Horizontal sections of the brain showed diffuse enlargement of the white matter and basal ganglia with scattered hemorrhage and necrosis. Microscopically, the lesion was far more extensive and diffuse than was suspected from gross examination. Wide glial tumor cell infiltration was observed in the cerebral hemispheres, basal ganglia, brainstem, cerebellum, and even the cervical spinal cord with minimum destruction of the pre-existing architecture. Calcification was found around the thrombosed vessels and necrotic lesions. The clinical diagnosis and histological features of gliomatosis cerebri are discussed with reference to reported cases.

Aged↗

Chronic progressive spinobulbar spasticity with disturbance of voluntary eyelid closure. Report of a case with special reference to MRI and electrophysiological findings.

We describe a 56-year-old man who had a progressive pseudobulbar palsy, spastic tetraparesis, forced laughing and disturbance of voluntary eyelid closure, and was clinically compatible with chronic progressive spinobulbar spasticity. Magnetic resonance images (MRI) revealed atrophy of the bilateral motor cortices and single photon emission tomography after intravenous injection of N-isopropyl-p-iodoamphetamine iodine-123 (IMP-SPECT) showed hyporadioactivity in the same regions. Electrophysiological studies on supranuclear paralysis of eyelid closure demonstrated that so-called apraxia and motor impersistence coexisted and that in attempts to keep the eyelid closed the inhibition of basal activity of the levator palpebrae superioris muscle and activation of the orbicularis oculi muscle were insufficient, indicating the impaired reciprocity of these ocular muscles. The corresponding lesion of these eyelid symptoms was considered to be the bilateral motor cortices.

Blinking↗

Stimulus- and cumulative dose-dependent inhibition of O2- production by polymorphonuclear leukocytes of patients receiving corticosteroids.

Since early in vivo studies in man have remained controversial as to the suppressive effects of glucocorticosteroids on the function of polymorphonuclear leukocytes (PMN), we tried to clarify those effects. The study population involved 19 inpatients on daily and prolonged corticosteroid therapy. Superoxide (O2-) production and chemotaxis were determined as a function of peripheral blood PMN, using various stimuli: concanavalin A (ConA) + cytochalasin D (CD), N-formyl-methionyl-leucyl-phenylalanine (FMLP) and phorbol myristate acetate (PMA), and the chemoattractants FMLP and zymosan activated serum (ZAS). In addition, the relationship between PMN function and corticosteroid dose was also evaluated. There was significant inhibition of PMN O2- production in the patients receiving corticosteroids depending on the stimulus (FMLP or PMA, 51% or 56% of controls; ConA + CD, not inhibited) but no significant inhibition of PMN chemotactic activity. Stimulation with FMLP showed an inverse relationship between O2- production and cumulative prednisolone dose (r = -0.41) in serial determination of O2- production in patients with a negative C-reactive protein (CRP) test. In the serial study of each patient with negative CRP we confirmed the suppression. These results suggest that O2- production by PMN could be inhibited, depending on the cumulative dose of corticosteroids in steroid-treated patients. This may be one possible mechanism of impaired host defences caused by corticosteroid therapy in man.

Adult↗

Triggering effects of opsonized-IgG antibody on the superoxide release in the phagosome and phagosome-lysosome fusion by pulmonary alveolar macrophages in rabbits.

We studied the triggering effects of opsonized-IgG antibody on the superoxide (O2-) release and phagosome-lysosome fusion in the phagosome of pulmonary alveolar macrophages (PAM). Both were histochemically assayed in the same cell to enable simultaneous observation, using the qualitative superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction test and the acridine orange (AO) method. When PAM from normal rabbit lungs were made to phagocytize the IgG-treated yeasts, the cells showed the enhanced release of O2- which acted directly on the antibody-coated yeasts as an oxidant, and the enhanced phagosome-lysosome fusion that was inhibited by SOD and was closely related to the enhanced release of O2- in the phagosomes. In contrast, neither enhanced O2- release nor phagosome-lysosome fusion was observed in the PAM which phagocytized saline-treated yeasts. These results may suggest that the opsonized-IgG antibody enhances the O2- release in the phagosome, resulting in the enhanced phagosome-lysosome fusion.

Animals↗

[An autopsy case of Neuro-Behçet's disease with the right middle cerebral artery occlusion on cerebral angiogram].

A case of Neuro-Behçet's disease with the right cerebral artery occlusion on cerebral angiogram was reported. A 63 years old man complained of headache and slight fever without exacerbations of ocular and mucocutaneous lesions, 16 years after he had suffered from recurrent oral aphthous ulcers, genital ulcers, uveitis and erythema nodosum. Laboratory examination demonstrated pleocytosis in the cerebrospinal fluid, a low density area with contrast enhancement in right temporal and parietal lobes in brain CT, a high signal intensity in the same area in T2-weighted image in brain MRI and the occlusion of the right middle cerebral artery on cerebral angiogram. After admission, left homonymous hemianopsia and hemiparesis appeared. With steroid therapy, these symptoms diminished and abnormal findings in brain CT and MRI disappeared, but psychiatric symptoms were exacerbated gradually. Finally he died of agranulocytosis and pneumonia. Neuropathologic findings showed panarteritis of branches of the right middle cerebral artery and infarction of its territories in addition to perivascular infiltrations and foci of demyelination which were prominent in the cerebral basal regions.

Arterial Occlusive Diseases↗

[A case of chronic inflammatory demyelinating polyradiculoneuropathy with nocturnal myoclonus].

A 43-year-old man began to notice progressive tingling sensation in his legs and unsteadiness in walking in 1983. His symptoms diminished with prednisolone treatment. In 1986, the same symptoms developed again and abated with prednisolone and plasmapheresis. In 1988 he was admitted because of progression of the symptoms in the legs. Neurological examinations showed mild muscle atrophy and weakness in the legs, loss of the deep reflexes, and impairment of cutaneous and deep sensation of the extremities. Heel-knee test was unsteady, and his gait was wide-based. In addition, Babinski and Chaddock signs were positive bilaterally. He had spontaneous myoclonic jerks of his legs, so-called "tonic triple flexion". These jerks were particularly evident during sleep, and were considered to be "nocturnal myoclonus". The same jerks were provoked by painful stimuli or Babinski's, Marie-Foix's maneuver. These jerks were considered to be so-called "spinal automatism" of spinal or brainstem origin. The latencies of VEP on both sides were prolonged and ABR showed abnormalities indicative of brainstem lesion. There were no abnormalities in cranial and spinal MRI. Our case was proven to have central nervus system lesions in addition to findings of chronic inflammatory demyelinating polyradiculoneuropathy.

Adult↗

[Transient monocytic skin infiltrate during preleukemic phase of acute myelomonocytic leukemia].

An acute myelomonocytic leukemia presenting transient skin rash during preleukemic phase was described. Following four years of unexplained leukopenia, a generalized exanthema developed and subsequently regressed spontaneously. The skin biopsy and immunohistochemistry revealed monocytic infiltration into the dermis. Twenty-eight months later, the patient became leukemic and died. The skin lesions, however, did not occur after leukemic transformation. Probably transient monocytic skin infiltrate was a symptom of preleukemia, a stem cell neoplasm manifested by functionally abnormal maturation.

Aged↗

Cooperative study on arterial regional chemotherapy for primary liver cancer in Hokkaido.

The Liver Study Group of Hokkaido analyzed a total of 57 patients with non-resectable primary liver cancers, which were treated by intra-arterial adriamycin infusion chemotherapy combined with lipiodol and/or the Gelform embolization of the hepatic arteries. Of the ten patients considered clinical responders, three complete response patients and seven partial response cases were obtained. The overall response rate was 17.5%. The median survival period at each clinical stage was as follows: stage I: 13.0 months, stage II: 16.0 months, stage III: 11.5 months and stage IV: 4.7 months. The common side-effects of this treatment were nausea, vomiting and anorexia. Hematological toxicities were also found, but there was no patient who suffered from severe complications.

Adult↗

[Primitive neuroectodermal tumor with peritoneal metastasis through a ventriculoperitoneal shunt. Case report].

A 13-month-old boy admitted with lethargy and hydrocephalus was found to have a right thalamic mass. Ventricular drainage was instituted, and the tumor mass was reduced by partial resection and local irradiation. A ventriculoperitoneal shunt was then placed. However, the tumor recurred 16 months later, with extensive ventricular seeding and peritoneal metastasis through the shunt tube. The child died 22 months after onset. Histological study of surgical specimens of the primary tumor and autopsy specimens of the brain and peritoneal metastatic tumors revealed poorly differentiated, small, round cells with numerous mitotic figures. In addition, autopsy specimens of the brain tumor contained areas of ependymal, oligodendroblastic, and spongioblastic differentiation. On immunohistochemical study, the tumor cells of each specimen were positive for anti-neuron specific enolase and anti-neurofilament antibodies, but negative for anti-glial fibrillary acidic protein antibodies. Electron microscopy revealed some zonulae adherens. These findings strongly suggest that the tumor originated from primitive multipotential cells capable of differentiating into ependymal, glial, and neuronal lines.

Brain Neoplasms↗

[Clinical evaluation of PIVKA-II as a marker of hepatocellular carcinoma].

PIVKA-II (protein induced vitamin K absence or antagonist-II) levels in plasma were measured using ELISA in patients with hepatocellular carcinoma (HCC). PIVKA-II was detected in 53 of 97 patients (54.6%) of HCC, and the combination assay of PIVKA-II and AFP identified 69 of 97 patients (71.1%) with HCC. However, the positive rate of PIVKA-II (6.1%) was lower than that of AFP (37.5%) in patients with HCC less than 2 cm in diameter. The concentration of PIVKA-II was markedly reduced within 2 weeks after treatment in patients with HCC showing a favorable response to Lp-TAE or Lp-TAI. Although PIVKA-II is a valuable marker for the diagnosis and follow-up of patients with HCC, it must be noted that the change to negative concentration of PIVKA-II after treatment does not mean complete necrosis of the tumor.

Aged↗

[A case of pulmonary alveolar proteinosis accompanied with the elevation of CEA (carcinoembryonic antigen) in bronchoalveolar lavage fluid].

A 44-year-old man was admitted with increasing dyspnea and butterfly shadow on his chest roentgenogram. Both the bronchoalveolar lavage and transbronchial lung biopsy (TBLB) led to a diagnosis of pulmonary alveolar proteinosis. CEA level in his bronchoalveolar lavage fluid (BALF) (216.8 ng/ml) was markedly elevated more than that in his serum (50.6 ng/ml). The localization of CEA on TBLB specimen stained by peroxidase-antiperoxidase technique using anti-CEA antibody was investigated and it was found that some alveolar epithelial cells and the material filling the alveoli were positively stained. Functions of alveolar macrophages in BALF were also studied, that is, adherence to glass, cell spreading, the nitroblue tetrazolium reduction, phagocytosis of immunobeads, and the activity of lysosomal enzymes, and found that all of those functions were lower than that of normal smokers. It was suggested that type II alveolar epithelial cells were those which produced and secreted CEA into the alveoli, as they do surfactant-like material in pulmonary alveolar proteinosis, and that the dysfunction of alveolar macrophages was secondary to the overingestion of the proteinaceous material in the alveoli.

Bronchoalveolar Lavage Fluid↗

[Usefulness of serum adenosine deaminase activity in the early diagnosis of Mycoplasma pneumonia].

It is sometimes difficult to clinically diagnose mycoplasma pneumonia at an early stage before the rise of titer of antibody to Mycoplasma pneumoniae. Mycoplasma pneumonia may be related with T-lymphocyte activity, and its inflammatory process is different from that of bacterial pneumonia. Adenosine deaminase (ADA) activity is a predominant T-lymphocyte enzyme, and its plasma activity is high in diseases in which cellular immunity is stimulated. In this study, we have investigated 31 cases with pneumonia (11 cases of mycoplasma pneumonia and 20 cases of bacterial pneumonia) within 10 days after onset to evaluate the usefulness of ADA measurement in the diagnosis of mycoplasma pneumonia. Serum ADA activity in the group of mycoplasma pneumonia was 32.1 +/- 12.0 U/l (63.9-18.8 U/l), that of non-mycoplasma pneumonia 12.5 +/- 3.3 (4.6-18.6) U/l, and that of normal control 14.0 +/- 3.4 (6.3-19.3) U/l. ADA activity of the group of mycoplasma pneumonia was significantly higher than those of non-mycoplasma pneumonia and normal control (p less than 0.001). This results suggest that serum ADA activity in patients with acute pneumonia may be useful for the early diagnosis of mycoplasma pneumonia.

Adenosine Deaminase↗