PURPOSE: Urinary tract infection (UTI) in children is the most common disease during the infantile period, therefore early diagnosis and treatment are important. Pyuria is a useful clinical parameter for the initial diagnosis of a UTI. In this study we aimed to compare the clinical, laboratory, and imaging findings in relation to the duration of pyuria in infants with UTIs. METHODS: Three hundred seventy-four infants <12 months of age who were admitted between January 1995 and December 2005 for the first episode of a febrile UTI were retrospectively reviewed. Patients were divided into two groups according to the duration of pyuria as follows: group 1, pyuria resolved <3 days after initial treatment; and group 2, pyuria lasted at least 3 days after initial treatment. RESULTS: There were no significant differences between the two groups in relation to gender, age, total duration of fever, and organisms in the urine. Group 2 had a significantly higher peripheral blood leukocyte count (14,360.86+/-5,526.16 cells/mm3 vs. 11,822.55+/-5,687.26 cells/mm3, P<0.001), erythrocyte sedimentation rate (32.81+/-19.34 mm/hr vs. 23.74+/-20.43 mm/hr, P<0.001), and C-reactive protein (6.84+/-5.68 mg/dL vs. 3.78+/-3.99 mg/dL, P<0.001) than group 1. There was a significantly higher incidence of hydronephrosis and a higher grade of vesicoureteral reflux (VUR) in group 2 compared to group 1. CONCLUSION: In infants with UTI, pyuria of longer duration is related to severe UTI and higher grade VUR, therefore aggressive radiologic studies may be necessary.
Blood Sedimentation ; C-Reactive Protein ; Child ; Early Diagnosis ; Fever ; Humans ; Hydronephrosis ; Incidence ; Infant ; Leukocyte Count ; Pyuria ; Retrospective Studies ; Urinary Tract ; Urinary Tract Infections ; Vesico-Ureteral Reflux

BACKGROUND: Confluent and reticulated papillomatosis(CRP) is a rare but clinically distinct dermatosis of which the etiology is unknown. The pathomechanisms have been discussed from four different viewpoints: 1) endocrine imbalance 2) abnormal host reaction to colonization by pityrosporum orbiculare 3) disorder of keratinization 4) variant of amyloidosis cutis. However recent reports have shown that defect in the keratinization has become the predominant pathomechanism of CRP. OBJECTIVE: Our purpose was to evaluate 25 cases of CRP clinically, histopathologically and electornimcroscopically, to reviewed the literature, and to commented on the pathogenesis. MEHTODS: The 25 patients were examined clinically and pathologic specimens were obtained from lesions for routine light microdcopy and electron microscopy. RESULTS: 1. There were difference between male(68%) ad female(32%) patients. 2. Age distribution, at first visit were variable, ranging from 13 to 35, with the mean age of 20 years-old.3. Duration of symptoms were variable, ranging from 1 month to 5 years with wean duration of 1.5 years. 4. In the seasonal influence 16 cases showed aggrevation of lesions in the summer. 5. The distribution of lesions were abdomen(18 cases), chest(16 cases), back(12 cases), shoulder(7 cases), and buttock(5 were) 6. Three patients had a concomitant disease such as Graves' disease(1 case) or iron-deficiency anemia(2 cases). 7. There were no familial occurrence in any cases. 8. There were no hyphaes or sppores in KOH mount in any cases. 9. The histopathological finding of the affected tissues were characterized as follow : All cases showed laminated hyperkeratosis, epidermal atrophy, acanthosis, and papillomatosis. 23 cases showed an increase of melanin pigment in the basal layer, minimal perivascular and/or perifollicular infiltration. 20 cases showed a decrease of the granular layer. 16 cases showed mild to moderate papillary edema, and dilated or congested upper dermal vessels. 10. In an electron microscopic studies the transitional cells between the stratum corneum and stratum granulosum contained less electron-dense tonofilament-keratohyaline aggregates with electron-lucent inclusions in their cytoplasm in a thick marginal band and degraded cell organelles. These cell layers were increased to 3 or 4 layers. The sratum corneum was thichened and showed a regular keratin pattern with intracellular and extracellular vacuoles. 11. 8 of the 10 patients treated with oral etretinate for 2 months showed some improvement. 7 of the 12 patients treated with topical scalicylic acid oint and selenium sulfide solution for 2 months showed some improvement. 1 patients with oral minocyclin for 2 months showed a marked improvement. 2 patients treated with oral ketoconazole did not show any improve-showed a marked improvement. CONCLUSION: In an electron microscopic study we found that transitional cell layers between stratum corneum and stratum granulosum were increased to 3 or 4 layers. Therefore we think that CRP may be a disease of defect in the keratinization. Although this abnormal keratinization is distinctive, it is uncertain whether it is primary or secondary.
Acitretin ; Age Distribution ; Amyloidosis ; Atrophy ; Colon ; Cytoplasm ; Edema ; Estrogens, Conjugated (USP) ; Etretinate ; Humans ; Hyphae ; Ketoconazole ; Malassezia ; Melanins ; Microscopy, Electron ; Organelles ; Papilloma ; Seasons ; Selenium ; Skin Diseases ; Vacuoles

No abstract available.
Pneumothorax*

No abstract available.

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

BACKGROUND: Neonatal hypocalcemia is not an infrequent condition, especially in the premature neonate. It is effectively treated by intravenous administration of calcium gluconate. Complications of extravasation during intraveous infusion included calcification and, occasionally necrosis. But the exact mechanism of calcinosis cutis following extravasation of calcium gluconate remains unknown and there is no specific mode of treatment except cold packs and skin graft. OBJECTIVE: Our purpose was to evaluate the clinical and histological features in rabbits after subcutaneous injection of 10% calcium gluconate and a mixed solution of gluconate and triamcinolone acetonide. METHODS: Two rabbits were divided into 3 groups and were subcutaneously injected with the following materials on the back; 10% calcium gluconate, a mixed solution of calcium gluconate and triamcinolone acetonide, and 25% normal saline as controls respectively. The injection site including the skin and subcutaneous fat was excised and fixed with natural buffered formalin. The biopsied specimens were stained with Hematolxylin and Eosin. RESULTS: 1) In the 10% calcium gluconate injected group, there was some erthema and induration after three days. By the fifth to the seventh days there was more erythema and firm induration. At 15 days, nodules and large ulcreated lesions developed. Multiple, linear shaped, ulcreative surfaced and indurated masses were noted at 37days.l from 45days to 2months there was progressive healing with decrease in ulceration, and gradual disapppearance of the mass. Histologically, at the 8th day calcium was seen in the walls of the arteries and veins, after 15days, the reaction was at its peak and epidermal necrosis was seen on the injected site. From 30 to 3days, calcium deposition and granuloma formation were seen in the dermis. In addition discharge of calcium deposits began to place by means of transepidermal elimination. After 45days, although the response was subsiding, the calcium and mucin deposition was observed focally in the dermis. 2. In the 10% calcium gluconate and triamcinolone acetonide adjuvant injected group, there was development of some erythema at 8days. After 15days, some erythema and induration were seen of the injected site ad this gradually disappeared. By 37days, the injection site was normal in appearance. Histologically, at 15days calcium deposition was seen on the upper dermis and the injection site was histologically normal after one month. 3. In 25% normal saline injected group, the injection site was clinically normal. Histologically there was no reaction except for focal perivascular eosinophilia after 24horus. CONCLUSION: We conclude that the important mechanism of calcinosis cutis appears to be elevated concentration as well as the tissue damage at the site of the extravasation of calcium gluconate. The final common pathway of calcification is the formation of crystalline and insoluble calcium phosphate mineral, in the form of hydroxyapatite. The intralesional injection of triamcinolone for the treatment of calcinosis cutis in our study was effective due to its antiinflammatory effect and the reabsorption of calcium in the tissues.
Administration, Intravenous ; Arteries ; Bowen's Disease ; Calcinosis* ; Calcium Gluconate* ; Calcium* ; Carcinoma, Squamous Cell ; Crystallins ; Dermis ; Durapatite ; Eosine Yellowish-(YS) ; Eosinophilia ; Erythema ; Formaldehyde ; Granuloma ; Humans ; Hypocalcemia ; Infant, Newborn ; Injections, Intralesional ; Injections, Subcutaneous ; Keratoacanthoma ; Keratosis, Actinic ; Mucins ; Necrosis ; Proliferating Cell Nuclear Antigen ; Rabbits ; Skin ; Subcutaneous Fat ; Transplants ; Triamcinolone ; Triamcinolone Acetonide ; Ulcer ; Veins

No abstract available.
Pulmonary Edema*

OBJECTIVES: Anticardiolipin antibody (ACA) and lupus anticoagulant (LA) are acquired antiphospholipid antibodies (APAs), which are regarded as important risk factors far vascular thrombosis and recurrent fetal loss. Although the clinical relevance of APAs in dialysis patients is uncertain, recent studies have suggested that APAs are involved in bioincompatibility and thrombogenic complications in hemadialysis (HD) patients. METHOD: We performed a cross sectional study of ACA and LA in 50 stable HD patients and their 68 vascular accesses (52 native arteriovenous fistulae and 16 synthetic arterovenous grafts), with the analysis of factors associated with the presence of APAs and the retrospective evaluation of vascular access occlusion (VAO). LA was assessed by platelet neutralization method whereas IgG-ACA was measured by a solid phase ELISA. Values higher than 23GPLU/ml (IgG phospholipid units) were considered to be positive for IgG-ACA and positive values for LA was more than 8 seconds in prolongation of the clotting time with human platelet lysate. Vascular access survival was assessed by Kaplan- Meier method, RESULTS: The mean age of the subject (M:F 21:29) was 46 years and the mean duration of hemodialysis was 49 months. The frequency of VAO in entire subjects was 0.45+/-0.98 episodes/patient year. The median value of IgG-ACA was 16.0 GPLU/ml with a distribution from 2.7 to 46.1GPLU/ ml. The median titer of I.A was 4.5 (3.1-45.6) seconds. Fourteen patients (28%) were found to have at least one episode of VAO. In spite of comparable clinical and biochemical data according to the presence of VAO, the titers of IgG-ACA (13.6+/-7.7 vs, 20.3+/-8.7GPLIJ/ml, P<0.05) and LA (4.5+/-2.9 vs. 11.7 +/-12.6sec, P<0.05) were significantly higher in VAO group. Six out of 50 patients(12%) had an increased titer of IgG-ACA and LA was found in 11 patients(22%). No patients were positive for ACA and LA simultaneously. There was no significant difference in sex, etiology of ESRD, diabetic status, the dosage of heparin during HD or the amount of erythropoietin administered according to the presence of APAs. We could not find any significant correlation between the titer of APAs and age, duration of dialysis, blood pressure, platelet count and biochemical parameters. In the patients with positive ACA, the frequency of VAO was 1.05+/-0.12 episodes/patient year, which was significantly higher than patients without ACA (0.33+/-0.17 episodes/ patient year, P<0.05). In the patients with the presence of LA(1.06+/-0.43 vs. 0.12+/-0.06 episodes/ patients year, P<0.01). The median vascular access survival time in IgG-ACA positive patients (32.7 months) was significantly decreased compared to 66.8 months in IgG-ACA negative group. CONCLUSION: Our data suggest that the presence of APAs (ACA and/or LA) affects the event-free vascular access survival in HD patients. Therefore the evaluation of APAs status have to be included in the diagnostic strategies for the patients with recurrent VAO. Further studies are necessary to explore the pharmacologic intervention method to decrease APAs and prevent VAO in HD patients.
Antibodies, Anticardiolipin* ; Antibodies, Antiphospholipid ; Arteriovenous Fistula ; Blood Platelets ; Blood Pressure ; Dialysis ; Enzyme-Linked Immunosorbent Assay ; Erythropoietin ; Heparin ; Humans ; Kidney Failure, Chronic ; Lupus Coagulation Inhibitor* ; Platelet Count ; Renal Dialysis* ; Retrospective Studies ; Risk Factors ; Thrombosis

No abstract available.
Arteriovenous Fistula*

No abstract available.
Achilles Tendon*