• Tuberculosis and Respiratory Diseases
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• v.42 no.2
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• pp.156-164
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• 1995

Background: We had undergone this study to investigate clinical progress of this disease and to decide the role of aggressive diagnostic approaches, the efficacy of treatments and prognoses. Methods: A retrospective study was done on 113 patients who had been diagnosed to metastatic adenocarcinoma of pleura by pleural fluid cytology(106 cases) or pleural needle biopsy(22 cases), at Presbyterian Medical Center, from Jan. 1990 to Dec. 1994. Results: 1) The patients were composed of 59 males(52.2%) and 54 females(47.8%), and the mean age distribution was $57.4{\pm}12.1$ years. 2) The site of origin was lung cancer 46.9%(53/113), stomach cancer 20.4%(23/113), breast cancer 11.5%(13/113), and unknown primary site 6.2%(7/113 cases), as a whole. In male, lung cancer was 55.9%(33/59), stomach cancer was 28.8%(17/59), and in female, lung cancer was 37%(20/54), breast cancer was 24.1%(13/54) of cases. 3) The cardinal symptoms were dyspnea(69%), cough(61%), chest pain(50%), weight loss(50%), anorexia(49%), sputum(43%), malaise(30%). 4) The pleural fluid findings were exudative in 94.4%(102/108), serosanguinous or bloody in 36~53%, unilateral involvement in 74.3%(84/113) of cases, and lymphocyte predominance($71{\pm}27%$) in differential count of WBC. 5) CEA levels in pleural fluid or plasma were over 10ng/ml in 60.6%(40/66), and ADA levels in pleural fluid were under 40U/L in 95%(57/60) of cases. 6) The patients were managed by various methods, but the efficacy of treatment was uncertain. 7) The mean survival time was $12.7{\pm}13.5$ weeks. Conclusion: It seems to be no effective treatment methods yet and the prognosis was very poor in this disease, so the objectives of diagnostic approaches and treatment methods should be directed to early diagnosis, treatment and prevention of curable disease. And we must make our best endeavors to lengthen the survival time and improve the quality of patients' life.

• Journal of Genetic Medicine
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• v.6 no.1
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• pp.74-80
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• 2009

Purpose: To assess the value of first-trimester pregnancy-associated plasma protein-A (PAPP-A), nuchal translucency (NT) and second-trimester alpha-fetoprotein (AFP), human chorionic gonadotropin (hCG), unconjugated estriol (uE3), and inhibin-A in predicting pregnancy complications other than fetal aneuploidy. Materials and Methods: A retrospective study in 3,121 singleton pregnancies with integrated testing was performed at Kangnam CHA hospital between January 2005 and December 2006. Baseline characteristics, pregnancy outcomes, and serum marker levels were obtained by review of the medical records. We analyzed the data to identify associations between the integrated screening markers and adverse pregnancy outcomes. Statistical analyses were performed with the SPSS program. Results: In preterm labor and preeclampsia, high AFP, hCG, and inhibin-A levels and low PAPP-A and NT levels were found to be significantly correlated (P<0.05). Elevated second-trimester inhibin-A levels were associated with preeclampsia (odds ratio 2.843), low birth weight (odds ratio 1.446), and preterm labor (odds ratio 1.287), and while decreased first-trimester PAPP-A levels were associated with preeclampsia (odds ratio 0.51) and preterm labor (odds ratio 0.75). Conclusion: First- and second-trimester maternal serum markers screening can be used for predicting high-risk pregnancies.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6721-6726
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• 2013

Background: Changes in DNA methylation patterns are believed to be early events in hepatocarcinogenesis. A better understanding of methylation states and how they correlate with disease progression will aid in finding potential strategies for early detection of HCC. The aim of our study was to analyze the methylation frequency of tumor suppressor genes, P14, P15, and P73, and a mismatch repair gene (O6MGMT) in HCV related chronic liver disease and HCC to identify candidate epigenetic biomarkers for HCC prediction. Materials and Methods: 516 Egyptian patients with HCV-related liver disease were recruited from Kasr Alaini multidisciplinary HCC clinic from April 2010 to January 2012. Subjects were divided into 4 different clinically defined groups - HCC group (n=208), liver cirrhosis group (n=108), chronic hepatitis C group (n=100), and control group (n=100) - to analyze the methylation status of the target genes in patient plasma using EpiTect Methyl qPCR Array technology. Methylation was considered to be hypermethylated if >10% and/or intermediately methylated if >60%. Results: In our series, a significant difference in the hypermethylation status of all studied genes was noted within the different stages of chronic liver disease and ultimately HCC. Hypermethylation of the P14 gene was detected in 100/208 (48.1%), 52/108 (48.1%), 16/100 (16%) and 8/100 (8%) among HCC, liver cirrhosis, chronic hepatitis and control groups, respectively, with a statistically significant difference between the studied groups (p-value 0.008). We also detected P15 hypermethylation in 92/208 (44.2%), 36/108 (33.3%), 20/100 (20%) and 4/100 (4%), respectively (p-value 0.006). In addition, hypermethylation of P73 was detected in 136/208 (65.4%), 72/108 (66.7%), 32/100 (32%) and 4/100 (4%) (p-value <0.001). Also, we detected O6MGMT hypermethylation in 84/208 (40.4%), 60/108 (55.3%), 20/100 (20%) and 4/100 (4%), respectively (p value <0.001. Conclusions: The epigenetic changes observed in this study indicate that HCC tumors exhibit specific DNA methylation signatures with potential clinical applications in diagnosis and prognosis. In addition, methylation frequency could be used to monitor whether a patient with chronic hepatitis C is likely to progress to liver cirrhosis or even HCC. We can conclude that methylation processes are not just early events in hepatocarcinogenesis but accumulate with progression to cancer.

• Journal of Yeungnam Medical Science
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• v.8 no.2
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• pp.106-113
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• 1991

A clinical review of 31 cases of multiple myeloma which were diagnosed by criteria of the SWOG between May 1983 and February 1990 at Yeungnam University Hospital was done. The results were as followings : 1. The peak incidence was in 7th decade and male to female ratio was 1.8 : 1. 2. The most common presenting symptom at first diagnosis was bone pain (58%), but fever, dyspnea, dizziness and palpable mass were also noted. 3. The distribution of laboratory findings as following diagnostic criteria of Southwest oncology group(SWOG) : plasmacytoma on tissue biopsy was noted 6 cases, bone marrow plasmacytosis with more than 10% plasma cells was 22 cases, monoclonal globulin spike on serum electrophoresis was 24 cases, lytic bone lesions was observed 22 cases. 4. Initial clinical stages were classified as 2 cases in stage I, 3 cases in stage II, 26 cases in stage III(84%) 5. Immunoelectrophoresis revealed the distribution of IgG 64%, light chain 22%, IgA 10%. Kappa to Lambda ratio of 1.1 : 1. 6. Hematologic & biochemical fingins revealed anemia with <8.5% of hemoglobulin in 42%, hypercalcemia with < 10.6mg% of serum calcium in 22%, azotemia >2.0mg% of serum creatinine in 19%. 7. The multiple punched out lesion of bone x-ray examination were noticed skull(65%), rib(42%), L-spine(35%), pelvis(23%), T-spine(19%). The initial skeletal roentgenographic findings showed osteoporosis, osteolytic lesion and fracture in 55%, only osteolytic lesion in 23%, only osteoporosis in 10%. 8. Complications of multiple myeoloma, such as 10 cases of renal impairment, 8 cases of infection, 16 cases of compression fracture of spine were observed.

• Clinical and Experimental Pediatrics
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• v.53 no.2
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• pp.152-157
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• 2010

Purpose : Vitamin D deficiency rickets is a significant public health problem that results from insufficient exposure to sunlight and inadequate vitamin D supplementation. The purpose of this study is to identify the clinical characteristics of vitamin D deficiency rickets in infants. Methods : Data of 35 infants diagnosed as vitamin D deficiency rickets at Sanggye-Paik Hospital, Seoul, Korea, from March 2007 to May 2009 were reviewed. Children with plasma 25-hydroxyvitamin D levels <15 ng/mL and 15-30 ng/mL were considered to have vitamin D deficiency and vitamin D insufficiency, respectively. Results : Thirty-five infants (22 boys, 13 girls) were diagnosed with rickets. Mean age at diagnosis was $7.4{\pm}7.1$ months (range: 0.1-29.8 months). Eighteen infants (51%) were vitamin D deficient and seventeen infants (49%) were insufficient. Twenty-eight of all (80%) diagnosed as subclinical rickets. Twenty-nine infants (83%) were below the age of 12months. Twenty infants (57%) had breastfed and ten infants (29%) had iron deficiency anemia. Nine of breastfed infants (45%) were vitamin D deficient and ten of their mothers were vitamin D insufficient. Overall, radiographic evidence of rickets was present in 93% of the cases. Radiographic sign of rickets was evident even in vitamin D insufficient state. Conclusion : It is important for the clinician to screen for subclinical vitamin D deficiency rickets in inadequately supplemented infants by pairing 25-hydroxyvitamin D levels with wrist radiographs. A nationwide epidemiological study of vitamin D deficiency rickets must be conducted and evidence-based national guidelines must be defined to prevent rickets.

• Clinical and Experimental Pediatrics
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• v.51 no.8
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• pp.827-833
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• 2008

Purpose : Early identification of iron deficiency in young children is essential to prevent damaging long-term consequences. It is often difficult for the pediatrician to know which indices should be used when diagnosing these conditions especially in hospitalized young children. This study investigated the clinical significances of reticulocyte hemoglobin content in young children with acute infection. Methods : We studied 69 young children aged from 6 to 24 months admitted with acute infection in a single center. Venous blood was drawn to determine hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), hemoglobin content (CH), reticulocyte hemoglobin content (CHr), and red blood cell distribution width (RDW) using ADVIA 120 (Bayer Diagnostics, NY, USA). For evaluating iron status, iron, total iron binding capacity, ferritin and transferrin saturation (Tfsat) were determined. Iron deficiency was defined as Tfsat less than 20%, and iron deficiency anemia as Tfsat less than 20% and Hb level less than 11 g/dL. Results : In all, 47 were iron deficient; 17 of these had iron deficiency anemia. CHr was the only significant predictor of iron deficiency (likelihood ratio test=71.25; odds ratio=0.67; P<0.05). Plasma ferritin level had no predictive value (P=0.519). Subjects with CHr less than 27.4 pg had lower Hb level, MCH, CH, Tfsat, and iron levels than those with CHr 27.4 pg or more (P<0.05 for all). Conclusion : CHr level was a sensitive screening tool and the strongest predictor of iron deficiency in hospitalized infants with acute infection; it was cost saving and avoiding additional sampling. However its reference range should be established.

• Journal of Veterinary Clinics
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• v.10 no.1
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• pp.111-130
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• 1993

Lead toxicity was evaluated in forty-five cats on a balanced diet, Treated with 0(control), 10, 100(low), 1, 000, 2, 000, and 4, 000(high) ppm of lead acetate orally on a body weight basis. The objectives were to establish toxic dosage level of leaf in cats, to characterize changes in behavior and clinical pathology, and to demonstrate what blood lead concentrations correlate with the known dosages of lead. Some high dose cats showed projectile vomiting, hyperactivity, and seizures. The growth rates did not appear to be altered in any of the dosed groups. Normal blood lead concentration in cats were lower than that of humans, dogs, and cattle. Blood lead concentrations of 3 to 20$\mu\textrm{g}$/100$m\ell$ could be termed a 'subclinical' range in the cat. Clinical lead toxicity in cats may have blood lead concentrations ranging 20 to 120$\mu\textrm{g}$/100$m\ell$. Zinc protoporphyrin concentrations were proportional to lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverss dose response relationship for all lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverse dose response relationship for all lead dosages and appears to be a good indicator of lead exposure in cats. Urinary aminolevuliruc acid concentrations generally increased with lead dosage, but individual values varied. Hair lead concentrations rose proportionately to lead dosages. Lead at least in high doses appears to inhibit chemotactic activity of polymorphonuclear cells and monocytes. No consistent dose response relationships were observed in hemoglobin, RBC, WBC, neutrophil, lymphocyte, monocyte, and eosinophil counts. There were no consistent dose related changes in total protein, plasma protein, BUN, and ALT values. Reticulocyte counts did not increase significantly in most lead dosage levels, and are probably of little value in diagnosing lead toxicity in cats. The fact that no significant changes were found in nerve conduction velocities may support that there was no segmental demyelination resulting from lead ingestion. The lethal dose in cats appear to range from 60 to 150mg/kg body weight. A reliable diagnosis of lead poisoning can be made utilizing blood lead, ZPP, and ALAD, and hair lead.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.21 no.1
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• pp.15-21
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• 2021

Purpose: Urea cycle disorder (UCD) is an inherited inborn error of metabolism, acting on each step of urea cycle that cause various phenotypes. The purpose of the study was to investigate the long-term clinical consequences in different groups of UCD to characterize it. Methods: Twenty-two patients with UCD genetically confirmed were enrolled at Pusan National University Children's hospital and reviewed clinical features, biochemical and genetic features retrospectively. Results: UCD diagnosed in the present study included ornithine transcarbamylase deficiency (OTCD) (n=10, 45.5%), argininosuccinate synthase 1 deficiency (ASSD) (n=6, 27.3%), carbamoyl-phosphate synthetase 1 deficiency (CPS1D) (n=3, 13.6%), hyperornithinemia-hyperammonemia-homocitrullinuria syndrome (HHHS) (n=2, 9.1%), and arginase-1 deficiency (ARG1D) (n=1, 4.5%). The age at the diagnosis was 32.7±66.2 months old (range 0.1 to 228.0 months). Eight (36.4%) patients with UCD displayed short stature. Neurologic sequelae were observed in eleven (50%) patients with UCD. Molecular analysis identified 37 different mutation types (14 missense, 6 nonsense, 6 deletion, 6 splicing, 3 delins, 1 insertion, and 1 duplication) including 14 novel variants. Progressive growth impairment and poor neurological outcomes were associated with plasma isoleucine and leucine concentrations, respectively. Conclusion: Although combinations of treatments such as nutritional restriction of proteins and use of alternative pathways for discarding excessive nitrogen are extensively employed, the prognosis of UCD remains unsatisfactory. Prospective clinical trials are necessary to evaluate whether supplementation with BCAAs might improve growth or neurological outcomes and decrease metabolic crisis episodes in patients with UCD.