Browsing by Author "Liao K.-M."

OBJECTIVE: To elucidate the role of ultrasound-guided fine needle aspiration cytology (FNAC) in determining whether to request an operation. STUDY DESIGN: Twenty-four consecutive patients (23 women and 1 man) with Hashimoto's thyroiditis combined with nodular lesions revealed by ultrasonography were included in the study. Ultrasound-guided FNAC was performed on their thyroid tissue compatible with Hashimoto's thyroiditis and nodular lesions. RESULTS: Two of 24 patients (8.3%) had papillary thyroid cancer, which was diagnosed from aspirates of 31 nodular lesions and confirmed by operative pathologic findings. CONCLUSION: If a patient with Hashimoto's thyroiditis has nodular lesions shown by ultrasonography, ultrasound-guided FNAC is helpful in elucidating the nature of the lesion and determining whether to request an operation.

We explored potential associations between genetic polymorphisms in genes related to DNA repair and detoxification metabolism and epidermal growth factor receptor (EGFR) mutations in a cohort of 410 never-smoking patients with lung adenocarcinoma. Multivariate-adjusted odds ratios (aORs) and corresponding 95% confidence intervals (CI) of EGFR mutation status in association with the genotypes of DNA repair and detoxification metabolism genes were evaluated using logistic regression analysis. We found an association between in-frame deletion in EGFR exon 19 and a single nucleotide polymorphism (SNP) rs1800566C/T located in NQO1 (aOR, 2.2 with 95% CI, 1.0-4.8) in female never-smokers. The SNP rs744154C/G in ERCC4 was also associated with the EGFR exon 19 in-frame deletion both in never-smokers (aOR, 1.7 with 95% CI, 1.0-3.0) and female never-smokers (aOR, 1.9 with 95% CI, 1.0-3.6). Although the association was marginally significant in multivariate logistic regression analysis, the A/A genotype of rs1047840 in EXO1 was associated with a 7.6-fold increase in the occurrence of the EGFR exon 19 in-frame deletion in female never-smokers. Moreover, risk alleles in NQO1, ERCC4 and EXO1 were associated with an increasing aOR of the EGFR exon 19 in-frame deletion both in never-smokers (p = 0.007 for trend) and female never-smokers (p = 0.002 for trend). Our findings suggest that the in-frame deletion in EGFR exon 19 is associated with polymorphisms in DNA repair and detoxification metabolism genes in never-smoking lung adenocarcinoma patients, especially in females. Copyright ? 2012 UICC.

Background: Coronary artery disease is common in patients with end-stage renal disease (ESRD). Patients with ESRD are a high-risk group for cardiac surgery and have increased morbidity and mortality. Most studies comparing ESRD patients receiving coronary artery bypass grafting (CABG) or percutaneous coronary intervention have found that the long-term survival is good in ESRD patients after CABG. The aim of our study was to compare ESRD patients who underwent CABG with the general population who underwent CABG, in terms of prognosis and hospital costs. Methods: This study analyzed data from the National Health Insurance Research Database in Taiwan for patients who were diagnosed with ESRD and received CABG (ICD-9-CM codes 585 or 586) between January 1, 2004, and December 31, 2009. The ESRD patients included in this study all received catastrophic illness cards with the major illness listed as ESRD from the Ministry of Health and Welfare in Taiwan. The control subjects were randomly selected patients without ESRD after propensity score matching with ESRD patients according to age, gender, and comorbidities at a 2:1 ratio from the same dataset. Results: A total of 48 ESRD patients received CABG, and their mean age was 62.04 ± 10.04 years. Of these patients, 29.2% were aged ?70 years, and 66.7% were male. ESRD patients had marginally higher intensive care unit (ICU) stays (11.06 vs 7.24 days) and significantly higher ICU costs (28,750 vs 17,990 New Taiwan Dollars (NTD)) than non-ESRD patients. Similarly, ESRD patients had significantly higher surgical costs (565,200 vs. 421,890 NTD), a higher perioperative mortality proportion (10.4% vs 2.1%) and a higher postoperative mortality proportion (33.3% vs 11.5%) than non-ESRD patients. Conclusions: After CABG, ESRD patients had a higher risk of mortality than non-ESRD patients, and ICU and surgery costs were also higher among the ESRD patients than among patients without ESRD. ? 2020 The Author(s).

Background/Purpose: Central diabetes insipidus (DI) is an established phenomenon after hypoxic encephalopathy or brain death, but hypopituitarism is seldom described. This study investigated the characteristics of 11 patients with DI and hypopituitarism which developed after severe hypoxic encephalopathy. Methods: The medical records of patients with DI and hypopituitarism after severe hypoxic encephalopathy from 1997 to 2002 were retrospectively reviewed. Eleven patients with DI and hypopituitarism after severe hypoxic episodes were included. Demographic data, primary diagnosis, the time of onset of DI, the time of diagnosis of hypopituitarism, the presence of symptoms of hypopituitarism, and outcome of these patients were analyzed. Results: Eleven patients comprising nine females and two males aged 47.4 ± 19.3 years (range, 24-74 years) were included. The mean interval from the precipitating event to the onset of DI was 60 ± 46 hours (range, 11-131 hours). The mean interval from the precipitating event to the diagnosis of hypopituitarism was 423 ± 182 hours (range, 132-672 hours). The average duration of hospitalization was 63 ± 35 days (range, 9-113 days). The overall mortality rate during hospitalization was 45%. Four patients died of sepsis and one died of heart failure due to acute myocardial infarction. Conclusion: The development of DI after severe hypoxic encephalopathy is a sign of severe brain damage. It usually ensues immediately or days after loss of brain stem reflexes. Hypopituitarism developed several weeks later than DI in these patients. Recognition and treatment of these deficiencies may prevent organ dysfunction. ? 2006 Elsevier & Formosan Medical Association.

Objectives: This case-control study was carried out to investigate the association of female lung adenocarcinoma with environmental risk factors and genetic polymorphisms of DNA repair enzymes, and to assess the effect of gene-environment interaction on the disease. Methods: A total of 107 female patients affected with lung adenocarcinoma and 263 healthy controls were recruited serially from National Taiwan University Hospital. History of exposures to environmental risk factors was obtained through personal interview using on a structured questionnaire. Genetic polymorphisms of DNA repair enzymes were determined by polymerase chain reaction with restriction fragment length polymorphism. Results: After adjustment for age and schooling years, the odds ratio of developing adenocarcinoma was 1.73 for exposures to tobacco smoking, 2.42 for exposures to cooking fume in unventilated kitchen, 2.70 for using coal and charcoal as cooking fuel, and 2.88 for using lard as cooking oil. The multivariate-adjusted odds ratio of developing lung adenocarcinoma was 2.31 (95% CI: 1.12-4.76) for XRCC1 Gln/Gln genotype compared with Arg/Arg or Arg/Gln genotypes, 2.08 (95%CI: 0.99-7.81) for XRCC3 Thr/Met genotype compared with Thr/Thr genotype, 2.70 (95%CI: 1.51-4.82) for XPD Lys/Gln or Gln/Gln genotypes compared with Lys/Lys genotype, and 3.69 (95%CI: 1.42-9.62) for hMLH1 GA or AA genotypes compared with GG genotype. Conclusions: Exposures to tobacco smoking, and cooking fumes were important environmental risk factors for female lung adenocarcinoma. The genetic polymorphisms of DNA repair enzymes including XRCC1, XRCC3, XPD and hMLH1 were associated with an increased risk of the disease.

To cure acromegalic patients, transsphenoidal surgery is considered first, especially for microadenoma. However, less than 50% of patients with macroadenoma achieve satisfactory biochemical control. Moreover, surgery may cause hypopituitarism. Medical therapy may offer the prospect of near normalization of growth hormone (GH)/insulin-like growth factor-1 levels with substantial tumor shrinkage in a significant number of patients. Here, we report two cases of acromegaly under treatment with somatostatin analogs alone for more than 10 years. Case 1 was a 54-year-old man with a pituitary macroadenoma. He received 4 years of octreotide treatment followed by 6 years of prolonged-release (PR) lanreotide resulting in normal GH level. Case 2 was a 60-year-old woman with a 1.3 cm pituitary tumor. She received 8 years of octreotide treatment followed by 6 years of PR lanreotide resulting in subnormal GH level and gallbladder sludge. She had received bilateral total hip replacement for hip osteoarthritis at the age of 59 years. These cases illustrate that long-term treatment with somatostatin analogs offers an alternative choice in selected acromegalic patients, such as those with pituitary tumor who cannot be cured by surgery, those who have unacceptable anesthetic risk and those who refuse surgery. ? 2006 Elsevier & Formosan Medical Association.Indications:2 patients with acromegaly secondary to pituitary tumor (microadenoma in 1 patient). Concomitant disease: hypertension (2).Patients:2 patients (inpatient and outpatient). Case 1: 54-year-old male patient. Case 2: 60-year-old female patient.TypeofStudy:This study described the outcome of long-term somatostatin analogs (Sandostatin and lanreotide) treatment in patients with acromegaly. 2 case reports.DosageDuration:Case 1: initially 50 mcg tid (=150 mcg daily) sc for the first 2 days and then 100 mcg tid (=300 mg daily) sc thereafter. Duration: 3 years and 4 months. Case 2: 100 mcg tid (=300 mcg daily) sc. Duration: at least 8 years.FreeText:Case 1 presented with enlarged nose, forehead, and jaw in 1993 (at age 42 years). By October 1993, acromegaly was suspected. In August 1995, he developed blurred vision in the left eye and elevated serum growth hormone (GH, 25 mcg/L) and prolactin (76.5 mcg/L) levels were noted. Magnetic resonance imaging (MRI) of the pituitary showed a tumor at the right side of the sella. Sandostatin treatment was initiated. Concomitant drugs were valsartan and indapamide. Case 2 presented with enlarged fingers in 1985 (at age 42 years). Three years later, elevated serum GH level (36 mcg/L) was noted. Computer tomography (CT) scan of the head revealed a pituitary tumor (1.3 cm in diameter) at the right side. On admission in April 1990, she showed prognathism, frontal bossing, enlarged thyroid gland, oily skin, and widely spaced teeth with malocclusion. Her hand volume was 300 ml for both hands. Tests showed elevated GH levels (56 mcg/L) and oral glucose tolerance tests revealed nonsuppressible GH levels (all more that 49 mcg/L). Skull x-ray disclosed a double contoured sella turcica. Sandostatin treatment was initiated. Concomitant drugs were antihypertensive agents.Results:In case 1, no significant side effect was observed following Sandostatin sc injection. Sandostatin treatment was begun on October 1995 and by April 1996, his serum GH levels was 4.8 mcg/L and MRI revealed a smaller pituitary tumor. His blurred vision also improved. By January 1999, his serum GH level was 2 mcg/L. In the beginning of February 1999, Sandostatin treatment was substituted by lanreotide. In case 2, no significant adverse effect was observed following Sandostatin sc injection (April 1990). In July 1990, her serum GH level decreased to 8 mcg/L. Cranial CT scan revealed a reduction in the pituitary tumor size. At the time of Sandostatin withdrawal, her serum GH level was >75 mcg/L. She continued to receive Sandostatin treatment from another hospital for 4 years and at her most recent visit, her serum GH level was 24.5 mcg/L. In March 1995, MRI showed a pituitary tumor 1.2 cm. In February 1999, prior to the start of lanreotide treatment, her serum GH level was 6-8 mcg/L.AdverseEffects:Unspecified side effects occurred.AuthorsConclusions:These cases illustrate that long-term treatment with somatostatin analogs offers an alternative choice in selected acromegalic patients, such as those with pituitary tumor who cannot be cured by surgery, those who have unacceptable anesthetic risk and those who refuse surgery.

Several ultra-sensitive methods for T790M in plasma cell-free DNA (cfDNA) have been developed for lung cancer. The correlation between mutation-allele frequency (MAF) cutoff, drug responsiveness, and outcome prediction is an unmet needs and not fully addressed. An innovative combination of peptide nucleic acid (PNA) and Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS) was used to proof of concept for monitoring cfDNA T790M in EGFR-mutant patients. Mutant enrichment by PNA was optimized and the detection limit was evaluated through serial dilutions. The cut-off value was identified by receiver-operating-characteristic (ROC) curve analysis utilizing serial sampled plasmas of patients from EGFR-tyrosine kinase inhibitor (TKI) pretreatment to progressive-disease (PD). Results, comparisons, and objective response rate (ORR) were analyzed in 103 patients’ tumor and cfDNA T790M, with 20 of them receiving an additional COBAS test. The detection limit was 0.1% MAF. The cut-off for PD and imminent PD was 15% and 5% with an ROC area under the curve (AUC) of 0.96 and 0.82 in 2 ml plasma. Detection sensitivity of cfDNA T790M was 67.4% and overall concordance was 78.6%. ORR was similar in T790M-positive cfDNA (69.6%) and tumor samples (70.6%) treated with osimertinib. Among 65 T790M-positive tumors, 15 were negative in cfDNA (23.1%). Seven of 38 T790M-positive cfDNA samples were negative in the tumors (18.4%). PNA-MALDI-TOF MS had a higher detection rate than COBAS. In conclusion, identification of T790M cut-off value in cfDNA improves cancer managements. We provide a strategy for optimizing testing utility, flexibility, quality, and cost in the clinical practice. ? 2018 Su et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Non-alcoholic fatty liver disease (NAFLD) is a problem in obese people caused by increasing intake of high-calorie food such as fructose implicated in the elevated prevalence. It is necessary to identify novel drugs to develop effective therapies. In this study, we combined LOPAC? (The Library of Pharmacologically Active Compounds) and High-Content screening to identify compounds that significantly reduced intracellular lipid droplets (LD) after high fat medium (HFM) treatment. Among 1280 compounds, we identified 239 compounds that reduced LD by >50%. Of these, 17 maintained cell viability. Nine of them were selected for validation using normal primary hepatocytes, of which five compounds showed dose-dependent efficacy. Whole genome transcriptomic network analysis was performed to construct the underlying regulatory network. There were 831 (711 up-regulated and 120 down-regulated genes) and 3480 (2009 up-regulated and 1471 down-regulated genes) genes that showed a significant change (>2-fold; p < 0.05) after 12 and 24 h HFM treatment, respectively. Gene enrichment and pathway analysis showed several immune responses mediated by MIF, IL-17, TLR, and IL-6. These compounds modulate lipogenesis via GSK3β and CREB1, which is followed by an alteration in the expression of several downstream genes related to hepatocellular carcinoma and hepatitis. CREB1 is a core transcription factor and may be a potential therapeutic target for liver disease. In conclusion, this proof of concept provides a strategy for identifying novel drugs for treatment of fatty liver disease as well as elucidates their underlying mechanisms. This research provides opportunity for developing future pharmaceutical therapeutics. ? 2018 Elsevier B.V.