• Journal of the Korea Society of Computer and Information
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• v.23 no.10
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• pp.135-141
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• 2018

In this paper, we propose to evaluate the effect of resistin-like molecule alpha ($Relm{\alpha}$) on the progression of anemia of inflammation. Anemia of inflammation is a common feature of inflammatory disorders, including chronic kidney disease, infections, and rheumatoid arthritis. $Relm{\alpha}$ is highly up-regulated in various inflammatory states, especially those involving asthma, intestinal inflammation, and parasitic diseases, and regulates the pathogenesis of those diseases. However, the role of $Relm{\alpha}$ in anemia of inflammation is unknown. To explore the roles of $Relm{\alpha}$ in anemia of inflammation in vivo, we generated mouse model of the disease by injecting 0.25 mg/kg lipopolysaccharides (LPS) intraperitoneally into $Relm{\alpha}-deficient$ and wild-type (WT) mice daily for 10 days. Research data was expressed as differences between LPS-treated $Relm{\alpha}-deficient$ and WT mice by a two-tailed non-parametric Mann-Whitney U-test using GraphPad Instat program. The results of the study are as follows: LPS-treated $Relm{\alpha}-deficient$ mice had significantly (p<0.05) lower hemoglobin contents, hematocrit levels and red blood cell indices including mean corpuscular volume, mean corpuscular hemoglobin than WT controls. This decrease was accompanied by significant (p<0.05) increase in total white blood cell and monocyte counts in the blood. However, there was no significant difference in mRNA levels of hepatic hepcidin and renal erythropoietin between the two animal groups. Taken together, these results indicates that $Relm{\alpha}$ deficiency exacerbates the anemia by increasing inflammation, suggesting therapeutic value of $Relm{\alpha}$ in the treatment of anemia of inflammation.

• Clinical and Experimental Pediatrics
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• v.48 no.2
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• pp.121-125
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• 2005

Anemia can be defined as a reduction in blood hemoglobin concentration or red cell mass relative to age matched normal values. Clinical presentation may range from obviously pale and lethargy to an incidental finding during screening of an otherwise well appearing child. The differential diagnosis of anemia in each instance is broad with numerous possible etiologies. A careful history and physical examination as well as complete blood count, peripheral blood smear and additional laboratory tests are necessary in defining underlying cause of the anemia and guide in further treatment plans. In addition, Iron deficiency anemia and anemia of inflammation are common causes of mild to moderate anemia in children, but most pediatricians have some confusions to differentiate these two entities.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.23 no.2
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• pp.180-187
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• 2020

Giant cell hepatitis with autoimmune hemolytic anemia (AHA) is a rare disease of infancy characterized by the presence of both Coombs-positive hemolytic anemia and progressive liver disease with giant cell transformation of hepatocytes. Here, we report a case involving a seven-month-old male infant who presented with AHA followed by cholestatic hepatitis. The clinical features included jaundice, pallor, and red urine. Physical examination showed generalized icterus and splenomegaly. The laboratory findings suggested warm-type AHA with cholestatic hepatitis. Liver biopsy revealed giant cell transformation of hepatocytes and moderate lobular inflammation. The patient was successfully treated with four doses of rituximab. Early relapse of hemolytic anemia and hepatitis was observed, which prompted the use of an additional salvage dose of rituximab. He is currently in clinical remission.

• Journal of Periodontal and Implant Science
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• v.28 no.1
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• pp.187-191
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• 1998

Aplastic anemia is a disease characterized by general lack of bone marrow activity; It may affect not only the red blood cells but also the white blood cells and platelets, resulting in pancytopenia. Spontaneous gingival hemorrhage is present in some cases and it is related to the blood platelet deficiency. This case report presents the periodontal treatment of a patient with aplastic anemia. A 43-year-old female was referred for continuous gingival bleeding after periodontal treatment. Periodontal findings revealed generalized gingival imflammation, oozing of blood from gingival crevice, and it was diagnosed as adult periodontitis. Root planing and extraction of the upper left third molar with poor prognosis were put into operation after elevation of the platelet count with platelet transfusion. The extraction socket was sutured with 3-0 silk. Bleeding continued even after digital compression at the upper right second premolar, second molar, and left canine areas, which presented severe inflammation. Although platelets were transfused repeatedly, platelet count did not stay elevated since survival rate of the transfused platelets were low due to alloimmunization. Thrombin gauze packing was not effective. Bleeding ceased 3 days after treatment with transfusion of donor platelets. 20 days after the treatment, the gingiva was generally healthy except upper right second premolar and lateral incisor areas. The result of periodontal treatment was good, but bleeding control after treatment was troublesome. In the periodontal treatment of patient with aplastic anemia, elevation of the platelet count with platelet transfusion seems to be the best method for hemorrhage control.

• Parasites, Hosts and Diseases
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• v.60 no.2
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• pp.127-131
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• 2022

Feline hemotropic mycoplasmosis (hemoplasmosis) is an infection of the red blood cells caused by the Mycoplasma haemofelis (Mhf), Candidatus Mycoplasma haemominutum (CMhm), and Candidatus Mycoplasma turicensis (CMt). The existence of Mhf, CMhm, and CMt has been demonstrated in feral cats in Korea using molecular methods, but no clinical cases have yet been reported. This study reports 2 clinical cases of hemotropic mycoplasmosis caused by CMhm and CMt in 2 anemic cats. The first case was a client-owned intact female domestic shorthair cat that presented with fever, pale mucous membranes, and normocytic normochromic non-regenerative anemia. Prior to referral, an immunosuppressive prednisolone dose was administered at the local veterinary clinic for 1 month. The cat was diagnosed with high-grade alimentary lymphoma. Organisms were found on the surface of the red blood cells on blood smear examination. The second case was of a rescued cat that presented with dehydration and fever. The cat had normocytic normochromic non-regenerative anemia. Necropsy revealed concurrent feline infectious peritonitis. Polymerase chain reaction assay targeting 16S rRNA revealed CMhm infection in case 1 and dual infection of CMhm and CMt in case 2. Normocytic normochromic non-regenerative anemia was observed in both cats before and during the management of the systemic inflammation. This is the first clinical case report in Korea to demonstrate CMhm and CMt infections in symptomatic cats.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.22 no.1
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• pp.98-104
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• 2019

We report a rare case of Meckel's diverticulum in a boy who initially presented with chronic iron deficiency anemia (IDA) without any history of gastrointestinal (GI) bleeding at 8 years-old. Isolated small bowel Crohn's disease was suspected based on findings of small bowel ulcers on capsule endoscopy. At four years from initial presentation, he developed massive GI bleeding. Abdominal computed tomographic angiography and small bowel series revealed findings suggestive of Meckel's diverticulum. Meckel's diverticulum should be suspected in children with unexplained chronic IDA even in the absence of prominent GI bleeding and negative findings on repetitive Meckel's scans. Moreover, Meckel's diverticulum should be included in the differential diagnosis of isolated small bowel Crohn's disease when the disease is limited to a short segment of the distal small bowel, as ulcers and inflammation may result as a consequence of acid secreted from adjacent heterotopic gastric mucosa constituting the Meckel's diverticulum.

• Journal of Chest Surgery
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• v.22 no.5
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• pp.823-828
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• 1989

Aortoenteric fistula is an uncommon important complication of aortic reconstruction with a prosthetic graft. The complication often is difficult to diagnose and is associated with poor prognosis. Aortoenteric fistula could be divided into true aortoenteric fistula and paraprosthetic-enteric fistula. In case of true aortoenteric fistula, an actual communication between the gastrointestinal tract and the aortic lumen is present. So, massive gastrointestinal hemorrhage is the presenting manifestation. In paraprosthetic-enteric fistula, characterized by communication between the gastrointestinal tract and the external surface of synthetic vascular prosthesis without actual fistularization into the vascular lumen, the predominant clinical manifestation were sepsis, fever and anemia. We experienced one case of paraprosthetic-enteric fistula in a 16 years old male after abdominal aortic reconstruction with a prosthetic graft. The interval from the operation to onset of symptoms was 40 months. The initial clinical manifestation was sepsis, fever and anemia without massive gastrointestinal hemorrhage. Surgical treatment consists of complete excision of infected graft, two layers closure of jejunal wall defect and pledgets suture of aortic stump with surrounding health tissue. Anatomic revascularization was not able to be done: because of extensive retroperitoneal inflammation and extraanatomic revascularization did not performed due to adequate distal blood supply through rich collateral circulation. After operation, he complained numbness on left foot on moderate exertion and felt coldness on left leg compared with right leg but not showed skin color change. 43 days after operation, he discharged without gait disturbance except numbness on left foot on moderate exertion.

• Journal of Nutrition and Health
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• v.32 no.8
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• pp.887-896
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• 1999

The purpose of this research is to assess hematological and biochemical status and the prevalence of iron deficiency of pregnant women by gestational age to provide the primary data about iron nutritional status of pregnant women. Pregnant women visiting public health centers in Ulsan participated in study and were divided into 3 trimester by last menstrual period(LMP). Hemoglobin (Hgb), hematocrit(Hct)and mean corpuscular volume(MCV) among iron status indices were not statistically different from normal distribution, however total iron binding capacity(TIBC) and serum ferritin were skewed to left and serum iron and transferrin saturation(TS) were skewed to right. Hgb was positively correlated with Hct(r=0.93, p<0.001) but TIBC was negatively correlated with all indices. Serum ferritin was also correlated with all indices, especially in 3rd trimester but not reached to 1st trimester level. Mean corpuscular hemoglobin(MCH), mean corpuscular hemoglobin concentration(MCHC), Red cell distribution width(RDW), serum iron and TS were not significantly different by trimester, however when serum serum iron was adjusted with hematocrit to correct the hemodilution, it significantly decreased in 2nd trimester. MCV increased in 2nd trimester and was maintained until late pregnancy, TIBC continued to increase throughout the trimester. The prevalence of anemic by CDC(Centers for Disease Control) Hgb criteria(Hgb <11.0g/dl in 1st and 3nd trimester, Hgb<10.5g/dl in 2nd trimester) was 2.8% in 1st trimester, 22.5% in 2nd trimester, 27.1% in 3rd trimester and was similar with prevalence by CDC Hct criteria(Hct < 33% in 1st and 3rd, Hct < 32% in 2nd). The prevalence of anemic of total subjects was 32.7% by WHO criteria(Hgb < 11.0g/dl). Although almost iron status indices increased in 3rd trimester, the prevalence of anemia by different criteria of all indices increased throughout the trimester, so iron nutritional status was considered as serious during late pregnancy. However, since factors other than iron deficiency, such as infection, infection, inflammation, other nutrient deficiency may also play a significant role, to differentiate the anemia due to mainly iron deficiency from the anemia due to other factors, serum ferritin is among the more useful indices in distinguishing the two conditions because it is depressed only in iron deficiency. Hgb<11.0g/dl and serum ferritin<12.0ug/L as the criteria of iron deficiency was suggested by CDC. 17.8% of all subjects were classified as iron deficient anemia, 14.9% as anemic from other reasons, 21.2% as iron deficiency any only 46.2% were in normal iron status.

• Clinical and Experimental Pediatrics
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• v.52 no.4
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• pp.435-440
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• 2009

Purpose : The concentration of soluble transferrin receptor (sTfR) is estimated as an iron parameter to evaluate erythropoiesis and iron status. The aim of our study is to evaluate the correlation between sTfR concentration and inflammatory parameters and to distinguish iron deficiency anemia from anemia of inflammation. Methods : One hundred and forty-four infants younger than two years of age who visited Gyeongsang University Hospital for 7 years from 2000 to 2006 were enrolled. Patients who had hemoglobin (Hb) <11 g/dL and ferritin <12 mg/L were excluded. Routine hematologic lab, serum ferritin, sTfR, and inflammatory markers [C-reactive protein(CRP), interleukin-6(IL-6), and absolute neutrophil count (ANC)] were investigated. Results : In all patients, the sTfR concentration showed a correlation with Hb, ferritin, MCV, and ANC, but not with CRP and IL-6. In multiple regression models, positive correlations were found between sTfR concentration and IL-6 (r=0.078, P=0.043), and negative correlations were found between sTfR concentration and ANC (r=-0.117, P=0.033) and MCV (r=-0.027, P=0.009). Conclusion : sTfR concentration was influenced by inflammatory parameters. Therefore, sTfR does not appear to be a useful parameter for discriminating between iron deficiency anemia and anemia of inflammation in infants.

• Clinical and Experimental Pediatrics
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• v.65 no.4
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• pp.182-187
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• 2022

We frequently encounter newborn infants with thrombocytosis in the neonatal intensive care unit. However, neonatal thrombocytosis is not yet fully understood. Thrombocytosis is more frequently identified in newborns and young infants, notably more often in those younger than 2 years than in older children or adults. The production of megakaryocytes (megakaryopoiesis) and platelets (thrombopoiesis) is mainly regulated by thrombopoietin (TPO). Increased TPO levels during infection or inflammation can stimulate megakaryopoiesis, resulting in thrombopoiesis. TPO concentrations are higher in newborn infants than in adults. Levels increase after birth, peak on the second day after birth, and start decreasing at 1 month of age. Initial platelet counts at birth increase with gestational age. Thus, preterm infants have lower initial platelet counts at birth than late-preterm or term infants. Postnatal thrombocytosis is more frequently observed in preterm infants than in term infants. A high TPO concentration and low TPO receptor expression on platelets leading to elevated plasma-free TPO, increased sensitivity of megakaryocyte precursor cells to TPO, a decreased red blood cell count, and immaturity of platelet regulation are speculated to induce thrombocytosis in preterm infants. Thrombocytosis in newborn infants is considered a reactive process (secondary thrombocytosis) following infection, acute/chronic inflammation, or anemia. Thrombocytosis in newborn infants is benign, resolves spontaneously, and, unlike in adults, is rarely associated with hemorrhagic and thromboembolic complications.