The incidence of fetal cardiac arrhythmia is approximately 1-3%. Sustatined fetal tachyarrhythmia may cause fetal hydrops and rnay lead to fetal death. We experienced a case of fetal atrial flutter without fetal hydrops at 34 weeks of gestation, which was diagnosed by fetal echocardiography. Transplacental fetal therapy with maternal digoxin administration resulted in restoration of normal fetal sinus rhythm. At birth, the infant showed normal electrocardiographic finding with normal Apgar scores.
Arrhythmias, Cardiac ; Atrial Flutter* ; Digoxin ; Echocardiography ; Electrocardiography ; Fetal Death ; Fetal Therapies ; Humans ; Hydrops Fetalis ; Incidence ; Infant ; Mothers* ; Parturition ; Pregnancy ; Tachycardia

No abstract available.
Jaundice

Background: The association between low-density lipoprotein (LDL-C) levels and cardiovascular disease (CVD) risk in different age groups within the diabetes mellitus (DM) population remains unclear. The cohort study was conducted to investigate this relationship. Methods: We assessed the 2009 to 2012 Korean National Health Screening and National Health Insurance Service records, with follow-up to the primary outcome (myocardial infarction [MI] or stroke) or December 2018. After excluding the participants with a history of MI or stroke, 2,227,394 participants with DM were included and categorized according to baseline LDL-C levels and age. Cox proportional hazards modeling was conducted. The CVD risk of age <40 years and LDL-C <70 mg/dL was set as the reference. In each age group, LDL-C <70 mg/dL was used as a reference for the subgroup analysis. Results: The cut-off LDL-C value for increased MI risk in each age group varied (<40 years old, LDL-C ≥160 mg/dL: hazard ratios [HR], 2.03; 95% confidence interval [CI], 1.644 to 2.506) (40–49-year-old, LDL-C <115 mg/dL: HR, 1.245; 95% CI, 1.04 to 1.489) (50–59-year-old, LDL-C <115 mg/dL: HR, 1.21; 95% CI, 1.014 to 1.445) (60-69-year-old, LDL-C <145 mg/dL: HR, 1.229; 95% CI, 1.022 to 1.479) (≥70 years old group, LDL-C <100 mg/dL: HR, 1.238; 95% CI, 1.018 to 1.504). The cut-off LDL-C values for increased stroke risk varied in each age subgroup (<40 years old, LDL-C ≥160 mg/dL: HR, 1.395; 95% CI, 1.094 to 1.779) (40–49-year-old, LDL-C <145 mg/dL: HR, 1.13; 95% CI, 1.019 to 1.253) (50–59-year-old, LDL-C <160 mg/dL: HR, 1.079; 95% CI, 1.008 to 1.154) (60–69-year-old, LDL-C <130 mg/dL: HR, 1.07; 95% CI, 1.022 to 1.119) (≥70 years old, LDL-C <115 mg/dL: HR, 1.064; 95% CI, 1.019 to 1.112). Conclusion The effect of LDL-C on the risk of CVD differs depending on the age of the population with DM.

Background: The association between low-density lipoprotein (LDL-C) levels and cardiovascular disease (CVD) risk in different age groups within the diabetes mellitus (DM) population remains unclear. The cohort study was conducted to investigate this relationship. Methods: We assessed the 2009 to 2012 Korean National Health Screening and National Health Insurance Service records, with follow-up to the primary outcome (myocardial infarction [MI] or stroke) or December 2018. After excluding the participants with a history of MI or stroke, 2,227,394 participants with DM were included and categorized according to baseline LDL-C levels and age. Cox proportional hazards modeling was conducted. The CVD risk of age <40 years and LDL-C <70 mg/dL was set as the reference. In each age group, LDL-C <70 mg/dL was used as a reference for the subgroup analysis. Results: The cut-off LDL-C value for increased MI risk in each age group varied (<40 years old, LDL-C ≥160 mg/dL: hazard ratios [HR], 2.03; 95% confidence interval [CI], 1.644 to 2.506) (40–49-year-old, LDL-C <115 mg/dL: HR, 1.245; 95% CI, 1.04 to 1.489) (50–59-year-old, LDL-C <115 mg/dL: HR, 1.21; 95% CI, 1.014 to 1.445) (60-69-year-old, LDL-C <145 mg/dL: HR, 1.229; 95% CI, 1.022 to 1.479) (≥70 years old group, LDL-C <100 mg/dL: HR, 1.238; 95% CI, 1.018 to 1.504). The cut-off LDL-C values for increased stroke risk varied in each age subgroup (<40 years old, LDL-C ≥160 mg/dL: HR, 1.395; 95% CI, 1.094 to 1.779) (40–49-year-old, LDL-C <145 mg/dL: HR, 1.13; 95% CI, 1.019 to 1.253) (50–59-year-old, LDL-C <160 mg/dL: HR, 1.079; 95% CI, 1.008 to 1.154) (60–69-year-old, LDL-C <130 mg/dL: HR, 1.07; 95% CI, 1.022 to 1.119) (≥70 years old, LDL-C <115 mg/dL: HR, 1.064; 95% CI, 1.019 to 1.112). Conclusion The effect of LDL-C on the risk of CVD differs depending on the age of the population with DM.

Background: The association between low-density lipoprotein (LDL-C) levels and cardiovascular disease (CVD) risk in different age groups within the diabetes mellitus (DM) population remains unclear. The cohort study was conducted to investigate this relationship. Methods: We assessed the 2009 to 2012 Korean National Health Screening and National Health Insurance Service records, with follow-up to the primary outcome (myocardial infarction [MI] or stroke) or December 2018. After excluding the participants with a history of MI or stroke, 2,227,394 participants with DM were included and categorized according to baseline LDL-C levels and age. Cox proportional hazards modeling was conducted. The CVD risk of age <40 years and LDL-C <70 mg/dL was set as the reference. In each age group, LDL-C <70 mg/dL was used as a reference for the subgroup analysis. Results: The cut-off LDL-C value for increased MI risk in each age group varied (<40 years old, LDL-C ≥160 mg/dL: hazard ratios [HR], 2.03; 95% confidence interval [CI], 1.644 to 2.506) (40–49-year-old, LDL-C <115 mg/dL: HR, 1.245; 95% CI, 1.04 to 1.489) (50–59-year-old, LDL-C <115 mg/dL: HR, 1.21; 95% CI, 1.014 to 1.445) (60-69-year-old, LDL-C <145 mg/dL: HR, 1.229; 95% CI, 1.022 to 1.479) (≥70 years old group, LDL-C <100 mg/dL: HR, 1.238; 95% CI, 1.018 to 1.504). The cut-off LDL-C values for increased stroke risk varied in each age subgroup (<40 years old, LDL-C ≥160 mg/dL: HR, 1.395; 95% CI, 1.094 to 1.779) (40–49-year-old, LDL-C <145 mg/dL: HR, 1.13; 95% CI, 1.019 to 1.253) (50–59-year-old, LDL-C <160 mg/dL: HR, 1.079; 95% CI, 1.008 to 1.154) (60–69-year-old, LDL-C <130 mg/dL: HR, 1.07; 95% CI, 1.022 to 1.119) (≥70 years old, LDL-C <115 mg/dL: HR, 1.064; 95% CI, 1.019 to 1.112). Conclusion The effect of LDL-C on the risk of CVD differs depending on the age of the population with DM.

BACKGROUND: Frailty is considered to be a clinical syndrome characterized by decreased physiological reserves associated with a greater risk of health-related problems, hospitalization, and death. The current study examined hospitalization, falls, cognitive decline and disability between robust, prefrail and frail elderly in one year. METHODS: 110 participants aged 65 or more who visited two senior welfare centers in Seoul from February 2008 to June 2008 were surveyed again from March 2009 to June 2009 with demographic characteristics, number of chronic diseases and medication, study of osteoporotic fractures (SOF) frailty index, instrumental activity of daily living (IADL), depression, mini-mental state examination-Korean version (MMSE-K), falling history and admission history within one year. These results were compared with participants' previous survey done one year ago. RESULTS: Among total 110 subjects, 48 (44%) robust, 30 (27%) prefrail, and 32 (29%) frail subjects changed to 26 (24%), 54 (49%), and 30 (27%) respectively over the year. There were statistical significances in age, number of chronic disease, depressive mood, MMSE, falls, hospitalization, IADL disability contributing to frailty (P < 0.05). Frailty defined by SOF frailty index was associated with greater risk of adverse outcomes. Frail subjects had a higher age-adjusted risk of cognitive function decline (odds ratio [OR], 3.57), disability (OR, 9.64), fall (OR, 5.42), and hospitalization (OR, 4.45; P < 0.005). CONCLUSION: The frailty index like SOF frailty index might predict risk of falls, disability, hospitalization, and cognitive decline in the elderly, emphasizing special attention to the individuals showing frailty in outpatient examination.
Aged ; Chronic Disease ; Depression ; Frail Elderly ; Hospitalization ; Humans ; Osteoporotic Fractures ; Outpatients ; Retrospective Studies

The occurrence of an abdominal wall hematoma caused by abdominal paracentesis in patients with liver cirrhosis is rare. This paper presents a case of an abdominal wall hematoma caused by abdominal paracentesis in a 67-year-old woman with liver cirrhosis with a review of the relevant literature. Two days prior, the patient underwent abdominal paracentesis for symptom relief for refractory ascites at a local clinic. Upon admission, a physical examination revealed purpuric patches with swelling and mild tenderness in the left lower quadrant of the abdominal wall. Abdominal computed tomography revealed advanced liver cirrhosis with splenomegaly, tortuous dilatation of the para-umbilical vein, a large volume of ascites, and a large acute hematoma at the left lower quadrant of the abdominal wall. An external iliac artery angiogram showed the extravasation of contrast media from the left deep circumflex iliac artery. Embolization of the target arterial branches using N-butyl-2-cyanoacrylate was then performed, and the bleeding was stopped. The final diagnosis was an abdominal wall hematoma from the left deep circumflex iliac artery after abdominal paracentesis in a patient with liver cirrhosis.

Parkinson’s disease is a neurodegenerative disease compromising progressive motor and non-motor features for a long disease course. Although many drugs controlling parkinsonian symptoms were discovered, treatment with disease-modifying or halting effect was not developed to date. The exploration of reliable biomarkers would be helpful for better predicting disease progression and thereby successful development of disease-modifying therapy. In this review, we will review the clinical biomarkers in the prodromal stage and biomarkers using biological tissue in Parkinson’s disease.

Primary mucosa-associated with a lymphoid tissue (MALT) lymphoma is a rare distinct subtype of non-Hodgkin’s lymphoma that occurs in approximately 8% of all non-Hodgkin lymphomas. Primary gastrointestinal MALT lymphoma usually occurs in the stomach, but duodenal involvement is extremely rare. Therefore, the clinical manifestations, treatment, and prognosis of primary duodenal MALT lymphoma have not yet been validated because of its rarity. This paper reports a case of a 40-year-old male with primary duodenal MALT lymphoma who was treated successfully with radiation therapy alone. A 40-year-old male visited for a medical check-up.Esophagogastroduodenoscopy revealed whitish multi-nodular mucosal lesions in the second and third portions of the duodenum. Biopsy specimens from mucosal lesions in the duodenum were reported to be suspicious for MALT lymphoma of the duodenum. He received a total dose of 3,000 cGy in 15 fractions with external beam radiation therapy for three weeks. Three months after radiation therapy, an endoscopic examination revealed complete resolution of the duodenal lesions. The follow-up 12 months after radiation therapy showed no evidence of tumor recurrence.

The role of the kidney in combating metabolic acidosis has been a subject of considerable interest for many years. The present study was aimed to determine whether there is an altered regulation of renal acid base transporters in acute and chronic acid loading. Male Sprague-Dawley rats were used. Metabolic acidosis was induced by administration of NH4Cl for 2 days (acute) and for 7days (chronic). The serum and urinary pH and bicarbonate were measured. The protein expression of renal acid base transporters [type 3 Na+/H+ exchanger (NHE3), type 1 Na+/HCO3- cotransporter (NBC1), Na-K+ ATPase, H(+)-ATPase, anion exchanger-1 (AE-1)] was measured by semiquantitative immunoblotting. Serum bicarbonate and pH were decreased in acute acid loading rats compared with controls. Accordingly, urinary pH decreased. The protein expression of NHE3, H(+)-ATPase, AE-1 and NBC1 was not changed. In chronic acid loading rats, serum bicarbonate and pH were not changed, while urinary pH was decreased compared with controls. The protein expression of NHE3, H(+)-ATPase was increased in the renal cortex of chronic acid loading rats. These results suggest that unaltered expression of acid transporters combined with acute acid loading may contribute to the development of acidosis. The subsequent increased expression of NHE3, H(+)-ATPase in the kidney may play a role in promoting acid excretion in the later stage of acid loading, which counteract the development of metabolic acidosis.
Acidosis ; Adenosine Triphosphatases ; Ammonium Chloride ; Animals ; Humans ; Hydrogen-Ion Concentration ; Immunoblotting ; Kidney ; Male ; Proton-Translocating ATPases ; Quaternary Ammonium Compounds ; Rats ; Rats, Sprague-Dawley ; Sodium-Hydrogen Antiporter