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Biomedical subjects

C S Koh

Publications and source records attributed to C S Koh.

At least 127 records · Page 7Linked to original sources
PubMed1989

Inhibition of thyrotropin-stimulated adenylate cyclase activation and growth of rat thyroid cells, FRTL-5, by immunoglobulin G from patients with primary myxedema: comparison with activities of thyrotropin-binding inhibitor immunoglobulins.

We studied the blocking type TSH receptor antibodies in 28 patients with primary myxedema and 21 patients with goitrous Hashimoto's thyroiditis by measuring the ability of their IgGs to inhibit TSH binding to its receptor, and to inhibit TSH-stimulated cAMP increase and [3H]thymidine incorporation in a rat thyroid cell line, FRTL-5. The incidences of TSH binding inhibitor immunoglobulin, thyroid stimulation inhibiting immunoglobulin and thyroid growth inhibiting immunoglobulin in patients with primary myxedema were 54.6, 75 and 65.2%, respectively, against 14.3, 0 and 17.7%, respectively, in goitrous Hashimoto's thyroiditis. The antibodies inhibited dose-dependently not only TSH stimulated but also Graves' IgG-stimulated cAMP increase and [3H]thymidine incorporation. The TSH binding inhibitor immunoglobulin activities in patients with primary myxedema were significantly correlated with both the thyroid stimulation inhibiting immunoglobulin (r = 0.665; P less than 0.01) and the thyroid growth inhibiting immunoglobulin (r = 0.618; P less than 0.01) activity. Thirteen patients whose TSH binding inhibitor immunoglobulin activities were more than 50% had both strong thyroid stimulation inhibiting immunoglobulin (75.1-100%) and thyroid growth inhibiting immunoglobulin (57.4-100%) activities. These data suggest that the vast majority of patients with primary myxedema have potent blocking type TSH receptor antibodies. These might play a role in primary myxedema causing hypothyroidism and thyroid atrophy through inhibiting TSH-stimulated cAMP generation.

Adenylyl Cyclases↗
PubMed1989

Graves' hyperthyroidism following primary hypothyroidism: sequential changes in various activities of thyrotropin receptor antibodies.

A 40-year-old male who developed Graves' hyperthyroidism following primary hypothyroidism is reported. He presented with clinical signs of hypothyroidism and concomitant myasthenia gravis. The thyroid was not palpable. He was treated with T4, pyridostigmine and prednisolone. One year later he developed hyperthyroidism and goitre. His initial serum IgG had no intrinsic thyroid stimulating activity, but showed almost complete inhibition of TSH-stimulated cAMP generation (99.4%, normal less than 38%) and [3H]thymidine incorporation (99.5%, normal less than 40%) into rat thyroid cells, FRTL-5 cells, with very high activity (80.2%, normal less than 15%) of TSH binding inhibitor immunoglobulin. When he developed hyperthyroidism and goitre, his IgG showed a strong thyroid stimulation, both cAMP production (27-fold increase) and [3H]thymidine incorporation (5.5-fold increase). No inhibitory activities were noted. These findings suggest that clinical states of autoimmune thyroid diseases can be changed in accordance with changes of functional properties of TSH receptor antibodies.

Adult↗
PubMed1989

RFLP analysis of HLA-DR beta and -DQ beta genes in the Korean patients with insulin-dependent diabetes mellitus.

Human genomic DNA samples from 19 Korean patients and 31 controls of known serological DR antigen specificity were studied for insulin-dependent diabetes mellitus (IDDM)-associated variation in HLA-DR beta and -DQ beta restriction fragment length polymorphisms (RFLPs). Genotyping allowed for accurate assignment of HLA-DR types. For HLA-DRw6, a 12kb/DR beta/Taq I fragment was decreased in Korean IDDM (p less than 0.05). However, we could not find an increased frequency of a 12kb/DQ beta/Bam HI fragment or decreased frequency of a 3.7kb/DQ beta/Bam HI fragment in Korean IDDM. These results suggest a possible protective role of the HLA-DRw6 specificity in IDDM, irrespective of ethnic background, the absence of a specific DQ beta RFLP pattern associated with IDDM in Koreans, and the difference of the Korean population in the genetic of IDDM, compared to the Caucasoid population.

Asian People↗
PubMed1989

Role of blocking TSH receptor antibodies on the development of hypothyroidism and thyroid atrophy in primary myxedema.

We studied blocking type TSH receptor antibodies in 28 patients with primary myxedema and 21 patients with goitrous Hashimoto's thyroiditis by measuring the ability of their IgG to inhibit TSH binding to its receptor, and to inhibit TSH-stimulated cAMP increases and 3H-thymidine incorporation in a rat thyroid cell line, FRTL-5. The incidences of TSH binding inhibitor immunoglobulin (TBII), thyroid stimulation blocking antibody (TSBAb) and thyroid growth blocking antibody (TGBAb) in patients with primary myxedema were 53.6%, 75% and 65.2%, respectively. However, in goitrous Hashimoto's thyroiditis, these were 14.3%, 0% and 17.7%, respectively. These antibodies inhibited the receptor binding of 125I-bTSH dose-dependently, and also inhibited dose-dependently not only TSH-stimulated but also Graves' IgG-stimulated cAMP increase and 3H-thymidine incorporation. TBII activities of patients with primary myxedema were significantly correlated with both their TSBAb (r = 0.665; p less than 0.01) and TGBAb (r = 0.618; p less than 0.01) activities. Thirteen patients whose TBII activities were more than 50% had both strong TSBAb (75.1-100%) and TGBAb (57.4-100%) activities. Transient neonatal hypothyroidism was found in an infant born to a mother having potent TBII activities. Serum of the baby also had potent TBII activities and the baby's IgG inhibited TSH-stimulated cAMP increase and 3H-thymidine incorporation. These data suggest that a significant proportion of patients with primary myxedema have potent blocking type TSH receptor antibodies. These might play a role in primary myxedema causing hypothyroidism and thyroid atrophy through inhibition of TSH-stimulated cAMP generation.

Adolescent↗
PubMed1989

Pathogenetic role of thyrotropin receptor antibody in the development of hyperthyroidism following primary hypothyroidism.

The authors measured thyrotropin binding inhibitory immunoglobulin (TBII), thyroid stimulating antibody (TSAb), and thyroid stimulation blocking antibody (TSBAb) sequentially in patients who developed hyperthyroidism following primary hypothyroidism, and compared changes in these various functional parameters of thyrotropin receptor antibody (TRAb) with clinical manifestations, in order to investigate the role of TRAb in the development of hyperthyroidism following primary hypothyroidism. In a patient with goitrous chronic thyroiditis, TBII, TSAb and TSBAb were not detected at the initial hypothyroid phase. But with appearance of TBII and TSAb, the patient developed hyperthyroidism. In a patient with primary nongoitrous myxedema, initially high TBII and TSBAb were detected without TSAb activity. His TSBAb disappeared and TSAb appeared with development of goiter growth and hyperthyroidism. These two mechanisms, that is, appearance of previously absent TSAb and conversion of TSBAb to TSAb, might play a causative role in the development of hyperthyroidism following primary hypothyroidism. These phenomena might be evidence that Graves' disease, chronic thyroiditis, and primary nongoitrous myxedema are on a continuing spectrum of a common syndrome sharing similar pathophysiology, at least with respect to TRAb.

Adult↗
PubMed1989

Changes in the properties of the thyrotropin receptor antibody in patients with Graves' disease after radioiodine treatment.

We investigated the effect of a single dose of 131I upon thyrotropin receptor antibodies (TRAb) in 21 patients with Graves' disease. The thyrotropin receptor antibodies were assessed by parallel measurements of thyrotropin binding inhibitor immunoglobulin (TBII), thyroid stimulating antibody (TSAb), and thyroid stimulation blocking antibody (TSBAb) in serum by radioreceptor assay, stimulation of adenylate cyclase and inhibition of TSH-stimulated adenylate cyclase activation in FRTL-5 cells, respectively. Prior to radioiodine treatment TBII was detected in all 21 patients and TSAB in 19 patients. After radioiodine treatment TBII activities did not change during 12 months observation period, but in eight patients TSAb activities gradually decreased and were undetectable at the end of a 12 month observation period. Persistence of TSAb was not associated with clinical outcome. Eight patients developed hypothyroidism within 1 year after radioiodine treatment. Three of the hypothyroid patients developed TSBAb, and the appearance of TSBAb coincided with the development of hypothyroidism. These results suggest that TSBAb might develop after radioiodine treatment in a minority of patients with Graves' disease, and that the appearance of TSBAb, in addition to radiation induced thyroid destruction, might be involved in the development of hypothyroidism following radioiodine treatment.

Adolescent↗
PubMed1989

Anti-bovine TSH antibodies in patients with Graves' disease and primary myxedema.

Three patients with Graves' disease and one patients with primary myxedema had serum TSH-binding immunoglobulins of high affinity detected by the TSH binding inhibition immunoglobulin (TBII) assay. These IgGs bound 61%, 33%, 60% and 53% of radiolabeled TSH, respectively, higher than the maximal specific binding (25%) in the TBII assay. Such binding was detected even in the absence of TSH receptor with only small differences in the precipitable radioactivity (61%, 28%, 61%, 54%, respectively, in comparison with the assay non-specific binding 11.3%). The 125I-bTSH binding of IgGs was competitively inhibited by the addition of bTSH, but not inhibited by hTSH. Moreover IgG binding to bTSH was not inhibited by the addition of serial dilutions of TBII positive pooled Graves' IgG (0.1-10 mg/ml) from different untreated patients. The titers of these TSH binding antibodies were not changed during the treatment of Graves' disease. Following guinea pig fat cell membrane receptor purification, the IgG of one patient with Graves' disease revealed TBII activity of 43.7% inhibition of 125I-bTSH binding to the TSH receptor without binding activity of 125I-bTSH in the absence of the TSH receptor. These studies suggest that anti-TSH antibodies and TSH receptor antibodies are present independent of one another in sera of some patients with autoimmune thyroid diseases and anti-TSH antibodies result in false TBII assay results.

Adult↗
PubMed1989

[Detection of immune complexes in the sera and around the muscle fibers in a case of myasthenia gravis and polymyositis].

A case of myasthenia gravis accompanied with polymyositis and malignant thymoma, detected immune complexes in the sera and around the muscle fibers, was described. A 37-year-old woman was admitted to Shinshu University Hospital in September, 1987 because of dyspnea, dysphagia and muscle weakness. She first noticed her right blepharoptosis 3 weeks before admission. Weakness of all four limbs and myalgia of lower extremities were noticed one week later. These symptoms got worse and nocturnal dyspnea, dysphagia and easy fatigability at mastication appeared. On admission, she looked ill and neurological examination revealed left blepharoptosis, bilateral facial weakness, weakness of all four limbs, more prominent in proximal muscles and tenderness of lower extremities. Edrophonium test was positive, improving her muscle weakness. Laboratory examination revealed the elevated serum levels of CK, the increased titre of circulating immune complexes and high titres of acetylcholine receptor antibodies and anti-skeletal muscle antibodies. Electromyographic study showed myogenic pattern and Harvey-Masland test revealed waning at low frequency stimulation. Muscle biopsy showed marked perivascular infiltration of lymphocytes, accompanied by phagocytosis and interstitial fibrosis. IgG deposits were shown around the muscle fibers exclusively around the infiltrates of mononuclear cells. Granular deposits of C3 were also shown specifically around the muscle fibers exclusively around the infiltrates of mononuclear cells. Thymectomy was performed on September 21, 1987. Invasion of thymoma, predominantly lymphocytic type, to right lung and pericardium was observed histologically. After thymectomy, she got better. Immunological data and immunohistochemical examination of the present case suggest that in the case of myasthenia gravis accompanied with polymyositis and malignant thymoma, immune complexes may play a primary role on the pathogenesis of myositis.

Adult↗
PubMed1989

[A case of rhabdomyolysis following long time immobile posture caused by schizophrenia].

A 39-year-old female with several past psychiatric hospitalization for schizophrenia was admitted to our hospital because of severe pain and swelling of her legs. A few days before onset, she had often sat down upon her heels in water closet, agitated and talking to herself for many hours. Two days before the admission, she had suffered from severe pain and swelling of her bilateral calf-muscles, and her urine became brownish. On admission, neurological findings revealed delirious state, moderate rigidity of limbs, hyporeflexia of legs, marked swelling and severe spontaneous pain in bilateral legs. She was afebrile with body temperature of 36.4 degrees C. Laboratory data showed marked increase of levels of serum CK to 163,000 U/1, myoglobin to 9,860 ng/ml and aldolase to 42.8 IU/1, and the diagnosis of rhabdomyolysis was made. Although she fell into acute renal failure, the renal function recovered after repeated hemodialysis. Several days after admission, swelling and pain of calf-muscles began to improve, and serum CK, myoglobin and aldolase decreased rapidly. One month later, she was able to walk on her own legs. In the literature, rhabdomyolysis associated with immobile posture caused by schizophrenia is extremely rare, and this is the first case reported in Japan. The relationship between rhabdomyolysis and schizophrenia was discussed.

Adult↗
PubMed1989

[A case of Sjögren's syndrome with mononeuritis associated with high levels of circulating immune complexes].

A 32-year-old woman with Sjögren's syndrome accompanied by mononeuritis of right lower extremity was described. She admitted Shinshu University Hospital with the chief complaints of Raynaud's phenomenon and generalized lymphadenopathy. One year before admission Raynaud's phenomenon of right hand was first noticed. One month later she complained of a gritty sensation in the eyes and severe dryness of the mouth. On admission, she had systemic lymphadenopathy. Neurological examination revealed decreased light touch and pinprick sensations and decreased deep tendon reflexes in right lower extremity. Lip biopsy revealed marked mononuclear cell infiltrates around the salivary glands. Laboratory data included IgG 3,007 mg/dl, circulating immune complexes 1,200 micrograms AHGeq/ml (Raji-cell ELISA), anti-nuclear antibody 2,560X (speckled pattern) and anti-SSA antibody 256X. The levels of total protein, IgG and immune complexes were increased in the CSF of this patient. Sural nerve biopsy revealed a decreased number of large myelinated fibers and perivascular lymphocyte infiltration of vasa nervorum. Direct immunofluorescent staining showed deposition of IgG and C3 in the endoneural vessel walls. The increased level of immune complexes were decreased in the sera of the patient, accompanied by remission. These results suggest that immune complexes may be involved in the pathogenesis of a mononeuritis associated with Sjögren's syndrome.

Adult↗
PubMed1989

[A case of aseptic meningoencephalitis with recurrent abnormal behavior, status epilepticus and aphthous stomatitis, improved by acyclovir].

A case of aseptic meningoencephalitis with recurrent abnormal behavior, status epilepticus and aphthous stomatitis was described. A 39-year-old man, who had a history of low grade fever and abnormal behavior over 2 years without mucocutaneo-ocular symptoms, was admitted to Shinshu University Hospital because of status epilepticus. On admission, neurological examination revealed comatose state with neck stiffness, anisocoria (right greater than left), conjugate deviation to right and bilateral pyramidal tract signs. His cerebrospinal fluid examination revealed a total protein content of 206 mg/dl with 22 lymphocytes and 134 polymorphonuclear leukocytes/mm3. EEG recorded on the 3rd hospital day showed periodic sharp waves and polyspikes, occurring every 1 seconds, predominantly arise from the right hemisphere, which corresponds to periodic lateralized epileptiform discharges (PLEDs). Herpes simplex encephalitis was suspected and acyclovir was administered. Neck stiffness and cerebrospinal fluid findings were improved and PLEDs disappeared. But aphthous stomatitis appeared and meningoencephalitis was relapsed. Laboratory examination revealed erythrocyte sedimentation rate 40 mm/hr, positive C-reactive protein, elevated CH50 and sialic acid, enhanced migration of neutrophils and HLA-B 51. Neuro-Behçet's syndrome was strongly suspected with laboratory data but the clinical course was atypical. His clinical signs were markedly improved after administration of prednisolone. The present case suggests that neuro-Behçet's syndrome with only a part of major symptoms could be diagnosed as viral encephalitis and acyclovir may be effective for the treatment of neuro-Behçet's syndrome.

Acyclovir↗
PubMed1988

Artificial induction of intravascular lipolysis by lipid-heparin infusion leads to insulin resistance in man.

Although extensive evidence indicates that free fatty acids can decrease glucose utilization in vitro, it is still controversial how an increase in lipolysis affects glucose metabolism in man. To test the hypothesis that an increase in lipolysis is related to insulin resistance, we examined the effect of lipid-heparin infusion on glucose metabolism in ten normal subjects by the euglycaemic glucose clamp technique and isotopic determination of glucose turnover. In the control euglycaemic clamp studies with insulin infusion at 0.2 and 1.0 mU.kg-1.min-1, endogenous glucose production was suppressed from the basal rate of 2.0 +/- 0.3 mg.kg-1min-1 to 1.1 +/- 0.7 mg.kg-1.min-1 and -0.4 +/- 0.7 mg.kg-1min-1 respectively. Glucose utilization increased from the basal rate of 2.0 +/- 0.3 mg.kg-1min-1 to 2.3 +/- 0.5 mg.kg-1min-1 and 5.9 +/- 1.8 mg.kg-1min-1 respectively. When the euglycaemic clamp studies were coupled with lipid-heparin infusion at comparable low and high rates of insulin infusion, endogenous glucose production increased (1.8 +/- 0.7 mg.kg-1.min-1, p less than 0.001, and 0.3 +/- 0.6 mg.kg-1.min-1, p less than 0.05, respectively), and glucose utilization decreased (2.1 +/- 0.3 mg.kg-1.min-1, not significant, and 3.2 +/- 0.7 mg.kg-1.min-1, p less than 0.001 respectively). These data suggest that the artificial induction of intravascular lipolysis by lipid-heparin infusion leads to a state of insulin resistance in man.

Adult↗
PubMed1988

Autoimmune encephalomyelitis in rhesus monkeys induced by immunization with cerebral endothelial cell membrane.

It is postulated that multiple sclerosis might be an autoimmune demyelinating disease of the central nervous system (CNS). The mechanisms involved are unknown but, since the blood-brain barrier (BBB) is damaged, injury to endothelial cells is likely to have occurred. Our previous studies have led us to investigate the autoimmune effect of injuring the blood-brain barrier by immunizing rhesus monkeys with an endothelial cell membrane from the same kind of animals. The immunized animals developed a chronic or a relapsing neurological illness. Histological and ultrastructural examinations of the brain in the acute stage showed infiltrates of mononuclear cells around the blood vessels of the white matter of cerebrum, cerebellum, pons and midbrain, while in the chronic phase, large areas of demyelination and remyelination, especially in the white matter regions, were present. The animals immunized with extraneural antigen, an endothelial cell membrane obtained from human umbilical cord, developed no neurological illness. This results indicate that the brain endothelial cell membrane has an inflammatory encephalitogenic activity which could produce widespread demyelination in animals. The animal model described here may prove to be useful in the pathogenetic investigation of human autoimmune demyelinating diseases.

Animals↗
PubMed1988

In vitro degradation of amyloid material by four proteases in tissue of a patient with familial amyloidotic polyneuropathy.

The effects of 4 proteolytic enzymes, alpha-chymotrypsin, bromeline, collagenase, and lysozyme on amyloid tissue sections from a patient with familial amyloidotic polyneuropathy (FAP) were evaluated. Degradation of amyloid fibrils was significant with alpha-chymotrypsin, moderate with bromeline and collagenase, and slight with lysozyme. All of these proteases except collagenase are used as oral mucolytics in humans. The possibility of their clinical usefulness in the treatment or prevention of the development of FAP is discussed.

Amyloid↗
PubMed1988

Transient neonatal hypothyroidism due to transplacental transfer of maternal immunoglobulins that inhibit TSH binding, TSH-induced cAMP increase and cell growth.

Transient neonatal hypothyroidism due to transplacental transfer of maternal blocking type TSH receptor antibodies (TRAb) was found in a baby born to a 27-yr-old mother, who had been receiving thyroxine medication for primary myxedema. Maternal IgG inhibited radiolabelled TSH binding to its receptor (TBII), TSH-stimulated thyroid adenylate cyclase (AC) activation (TSII) and TSH-stimulated 3H-thymidine uptake (TGII) in cultured rat thyroid cells (FRTL-5). At birth, the baby's IgG showed similar activities to maternal IgG but all these activities decreased gradually, and disappeared from her serum within 12 weeks of age. In the baby, initially nonvisualized thyroid was clearly visualized on 99 m-Tc thyroid scintigraphy when all these blocking activities disappeared, TSII and TGII being decreased more slowly than TBII, and the baby remained euthyroid after discontinuation of thyroxine. This study suggests that such IgGs induced hypothyroidism and thyroid atrophy in the mother and were responsible for transient neonatal hypothyroidism in the baby.

Adult↗
PubMed1988

Computerized quality control of radioimmunoassay in Korea.

Automated data processing and quality control of radioimmunoassays offer not only increased speed but also a more thorough and statistically rigorous analysis of results. An external quality assessment scheme for serum thyroxine, triiodothyronine and thyroid stimulating hormone (TSH) assays was performed in five nuclear medicine laboratories in Korea to compare with the assay performances of the World Health Organization Radioimmunoassay Program. The required radioimmunoassay kits were supplied through the International Atomic Energy Agency (IAEA). We have determined the weighted root mean squared error, and variance ratio as the indices of standard curve and also the average batch coefficient of variation (ABCV) as the parameters of response error relationship curve and precision profile. There was a good fit for the triiodothyronine assay, but 3 of 5 laboratories showed possible bad fit in the T4 and TSH assay systems. The ABCV was less than 5 percent for the T3 and T4 assay system, however for the TSH system, only 1 laboratory showed the ABCV value of less than 5 percent. We have also calculated the within batch variation (drift) and between laboratory variations.

Electronic Data Processing↗