Graves disease (GD) can lead to complications such as cardiac arrhythmia and heart failure. Although dilated cardiomyopathy (DCMP) has been occasionally reported in adults with GD, it is rare in children. We present the case of a 32-month-old boy with DCMP due to GD. He presented with irritability, vomiting, and diarrhea. He also had a history of weight loss over the past few months. On physical examination, he had tachycardia without fever, a mild diffuse goiter, and hepatomegaly. The chest radiograph showed cardiomegaly with pulmonary edema, while the echocardiography revealed a dilated left ventricle with an ejection fraction (EF) of 28%. The thyroid function test (TFT) showed elevated serum T3 and decreased thyroid stimulating hormone (TSH) levels. The TSH receptor autoantibody titer was elevated. He was diagnosed with DCMP with GD; treatment with methylprednisolone, diuretics, inotropics, and methimazole was initiated. The EF improved after the TFT normalized. At follow-up several months later, although the TFT results again showed evidence of hyperthyroidism, his EF had not deteriorated. His cardiac function continues to remain normal 1.5 months after treatment was started, although he still has elevated T3 and high TSH receptor antibody titer levels due to poor compliance with drug therapy. To summarize, we report a young child with GD-induced DCMP who recovered completely with medical therapy and, even though the hyperthyroidism recurred several months later, there was no relapse of the DCMP.
Adult ; Arrhythmias, Cardiac ; Cardiomegaly ; Cardiomyopathy, Dilated* ; Child* ; Child, Preschool ; Compliance ; Deoxycytidine Monophosphate ; Diarrhea ; Diuretics ; Drug Therapy ; Echocardiography ; Fever ; Follow-Up Studies ; Goiter ; Graves Disease* ; Heart Failure ; Heart Ventricles ; Hepatomegaly ; Humans ; Hyperthyroidism ; Male ; Methimazole ; Methylprednisolone ; Physical Examination ; Pulmonary Edema ; Radiography, Thoracic ; Receptors, Thyrotropin ; Recurrence ; Tachycardia ; Thyroid Function Tests ; Thyrotropin ; Vomiting ; Weight Loss

Graves disease (GD) can lead to complications such as cardiac arrhythmia and heart failure. Although dilated cardiomyopathy (DCMP) has been occasionally reported in adults with GD, it is rare in children. We present the case of a 32-month-old boy with DCMP due to GD. He presented with irritability, vomiting, and diarrhea. He also had a history of weight loss over the past few months. On physical examination, he had tachycardia without fever, a mild diffuse goiter, and hepatomegaly. The chest radiograph showed cardiomegaly with pulmonary edema, while the echocardiography revealed a dilated left ventricle with an ejection fraction (EF) of 28%. The thyroid function test (TFT) showed elevated serum T3 and decreased thyroid stimulating hormone (TSH) levels. The TSH receptor autoantibody titer was elevated. He was diagnosed with DCMP with GD; treatment with methylprednisolone, diuretics, inotropics, and methimazole was initiated. The EF improved after the TFT normalized. At follow-up several months later, although the TFT results again showed evidence of hyperthyroidism, his EF had not deteriorated. His cardiac function continues to remain normal 1.5 months after treatment was started, although he still has elevated T3 and high TSH receptor antibody titer levels due to poor compliance with drug therapy. To summarize, we report a young child with GD-induced DCMP who recovered completely with medical therapy and, even though the hyperthyroidism recurred several months later, there was no relapse of the DCMP.
Adult ; Arrhythmias, Cardiac ; Cardiomegaly ; Cardiomyopathy, Dilated* ; Child* ; Child, Preschool ; Compliance ; Deoxycytidine Monophosphate ; Diarrhea ; Diuretics ; Drug Therapy ; Echocardiography ; Fever ; Follow-Up Studies ; Goiter ; Graves Disease* ; Heart Failure ; Heart Ventricles ; Hepatomegaly ; Humans ; Hyperthyroidism ; Male ; Methimazole ; Methylprednisolone ; Physical Examination ; Pulmonary Edema ; Radiography, Thoracic ; Receptors, Thyrotropin ; Recurrence ; Tachycardia ; Thyroid Function Tests ; Thyrotropin ; Vomiting ; Weight Loss

This study aims to elucidate the mechanisms by which dexmedetomidine alleviates pulmonary edema in rats with acute lung injury induced by lipopolysaccharide (LPS). Male Wistar rats were randomly divided into five groups: normal saline control (NS) group, receiving intravenous 0.9% normal saline (5 mL/kg); LPS group, receiving intravenous LPS (10 mg/kg); small-dose dexmedetomidine (S) group, treated with a small dose of dexmedetomidine (0.5 μg · kg(-1) · h(-1)); medium-dose dexmedetomidine (M) group, treated with a medium dose of dexmedetomidine (2.5 μg · kg(-1) · h(-1)); high-dose dexmedetomidine (H) group, treated with a high dose of dexmedetomidine (5 μg · kg(-1) · h(-1)). The rats were sacrificed 6 h after intravenous injection of LPS or NS, and the lungs were removed for evaluating histological characteristics and determining the lung wet/dry weight ratio (W/D). The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the lung tissues were assessed by enzyme- linked immunosorbent assay (ELISA). The mRNA and protein expression levels of aquaporin-1 (AQP1) and aquaporin-5 (AQP5) were detected by RT-PCR, immunohistochemistry, and Western blotting. The lung tissues from the LPS groups were significantly damaged, which were less pronounced in the H group but not in the small-dose dexmedetomidine group or medium-dose dexmedetomidine group. The W/D and the concentrations of TNF-α and IL-1β in the pulmonary tissues were increased in the LPS group as compared with those in NS group, which were reduced in the H group but not in S group or M group (P<0.01). The expression of AQP1 and AQP5 was lower in the LPS group than in the NS group, and significantly increased in the H group but not in the S group or M group (P<0.01). Our findings suggest that dexmedetomidine may alleviate pulmonary edema by increasing the expression of AQP-1 and AQP-5.
Acute Lung Injury ; chemically induced ; drug therapy ; genetics ; pathology ; Adrenergic alpha-2 Receptor Agonists ; pharmacology ; Animals ; Aquaporin 1 ; agonists ; genetics ; immunology ; Aquaporin 5 ; agonists ; genetics ; immunology ; Dexmedetomidine ; pharmacology ; Dose-Response Relationship, Drug ; Drug Administration Schedule ; Gene Expression Regulation ; Injections, Intravenous ; Interleukin-1beta ; antagonists & inhibitors ; genetics ; immunology ; Lipopolysaccharides ; Lung ; drug effects ; immunology ; pathology ; Male ; Organ Size ; drug effects ; Pulmonary Edema ; chemically induced ; drug therapy ; genetics ; pathology ; Rats ; Rats, Wistar ; Signal Transduction ; Transcription, Genetic ; Tumor Necrosis Factor-alpha ; antagonists & inhibitors ; genetics ; immunology

In the present study, we analyzed the role of Ginkgo biloba extract in lipopolysaccharide(LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS. G. biloba extract (12 and 24 mg·kg(-1)) and dexamethasone (2 mg·kg(-1)), as a positive control, were given by i.p. injection. The cells in the bronchoalveolar lavage fluid (BALF) were counted. The degree of animal lung edema was evaluated by measuring the wet/dry weight ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-a, interleukin-1b, and interleukin-6, were assayed by enzyme-linked immunosorbent assay. Pathological changes of lung tissues were observed by H&E staining. The levels of NF-κB p65 and COX-2 expression were detected by Western blotting. Compared to the LPS group, the treatment with the G. biloba extract at 12 and 24 mg·kg(-1) markedly attenuated the inflammatory cell numbers in the BALF, decreased NF-κB p65 and COX-2 expression, and improved SOD activity, and inhibited MPO activity. The histological changes of the lungs were also significantly improved. The results indicated that G. biloba extract has a protective effect on LPS-induced acute lung injury in mice. The protective mechanism of G. biloba extract may be partly attributed to the inhibition of NF-κB p65 and COX-2 activation.
Acute Lung Injury ; chemically induced ; drug therapy ; metabolism ; Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Cell Count ; Cyclooxygenase 2 ; genetics ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Gene Expression ; drug effects ; Ginkgo biloba ; chemistry ; Interleukin-1beta ; analysis ; Interleukin-6 ; analysis ; Lipopolysaccharides ; Lung ; immunology ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Peroxidase ; metabolism ; Phytotherapy ; Plant Extracts ; pharmacology ; Pulmonary Edema ; Superoxide Dismutase ; metabolism ; Transcription Factor RelA ; genetics ; metabolism ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo observe and study the effects of sivelestat on acute lung injury in dogs with severe burn-blast combined injury.

METHODSThirty-two male beagle dogs of clean grade were divided into 4 groups: uninjured group (U), combined injury control group (CIC), combined injury+low dose of sivelestat group (CI+LS), combined injury+high dose of sivelestat group (CI+HS), with 8 dogs in each group. Except for the dogs in group U which were not injured, the dogs in the other 3 groups were inflicted with severe burn-blast combined injury. According to the Parkland formula, the dogs in groups U and CIC were infused with physiological saline, and the dogs in groups CI+LS and CI+HS received sivelestat with the dosage of 0.5 and 2.0 mg·kg(-1)·h(-1) respectively in addition. The 24 h continuous intravenous infusion was carried out for 2 days. At post injury hour (PIH) 6, CT scanning was conducted to observe the lung damage. At PIH 2, 6, 12, 24, and 48, mean arterial pressure (MAP), respiratory rate (RR), extra vascular lung water (EVLW), pulmonary vascular permeability index (PVPI), PaO2, and PaCO2 were measured; the contents of neutrophil elastase (NE), IL-8, and TNF-α were determined by ELISA. At PIH 48, all the dogs were sacrificed, and the lung tissues were harvested to measure the wet to dry lung weight ratio. The same examination was carried out in the dogs of the group U at the same time points. Data were processed with analysis of variance of repeated measurement and LSD test.

RESULTS(1) CT images showed some exudative lesions in the dogs of groups CIC and CI+LS but not in the dogs of groups U and CI+HS. (2) No statistically significant differences were observed in MAP at each time point between every two groups (with P values above 0.05). The RR values in group U were significantly different from those of the other 3 groups at all time points (with P values below 0.05). The values of EVLW and PVPI in 3 combined injury groups were significantly different from those in group U at PIH 6, 12, 24, and 48 (with P values below 0.05). The values of RR and EVLW in group CI+LS were significantly different from those in group CI+HS at PIH 12, 24, and 48 (with P values below 0.05). The values of PVPI in group CI+LS were significantly different from those in group CI+HS at PIH 24 and 48 (with P values below 0.05). (3) The levels of PaO2 and PaCO2 showed significant differences between group U and the other 3 groups at each time point (with P values below 0.05). The levels of PaO2 in group CI+LS were significantly different from those in CI+HS group at PIH 12, 24, and 48 (with P values below 0.05). The level of PaCO2 showed significant differences between group CI+LS and group CI+HS at PIH 24 and 48 (with P values below 0.05). (4) The contents of NE (except for PIH 2), TNF-α, and IL-8 showed significant differences between group U and the other 3 groups at each time point (P < 0.05 or P < 0.01). At PIH 2, 6, 12, 24, and 48, the contents of NE in groups U, CIC, CI+LS, and CI+HS were respectively (69 ± 21), (83 ± 24), (80 ± 20), (75 ± 17), (72 ± 27) pg/mL; (66 ± 24), (196 ± 20), (231 ± 26), (252 ± 25), (266 ± 22) pg/mL ; (71 ± 22), (180 ± 27), (214 ± 21), (194 ± 24), (218 ± 20) pg/mL; (68 ± 22), (136 ± 24), (153 ± 22), (146 ± 26), (150 ± 28) pg/mL. NE values in group CI+HS were statistically different from those in groups CIC and CI+LS at PIH 6, 12, 24, and 48 (with P values below 0.05). The contents of TNF-α in group CI+LS were statistically different from those in groups CIC and CI+HS at PIH 24 and 48 (with P values below 0.05). The contents of IL-8 in group CI+LS were statistically different from those in group CI+HS at PIH 24 and 48 (with P values below 0.05). (5) At PIH 48, the wet to dry lung weight ratio of group CIC was statistically different from that in group CI+LS or group CI+HS (with P values below 0.05); there was also difference between group CI+LS and group CI+HS (P < 0.05).

CONCLUSIONSSivelestat, especially in a high dose, exerts a protective effect in acute lung injury after burn-blast combined injury through improving the index of blood gas analysis, ameliorating pulmonary edema, and lowering the production of pro-inflammatory mediators.

Acute Lung Injury ; complications ; drug therapy ; Animals ; Blood Gas Analysis ; Burns ; complications ; Capillary Permeability ; Dogs ; Extravascular Lung Water ; Glycine ; administration & dosage ; analogs & derivatives ; Infusions, Intravenous ; Interleukin-8 ; Male ; Pulmonary Edema ; etiology ; Serine Proteinase Inhibitors ; administration & dosage ; Sulfonamides ; administration & dosage ; Tumor Necrosis Factor-alpha

AIM: In a previous study, the anti-inflammatory effects of tectorigenin were disclosed. In this study, the anti-inflammatory effects of tectorigenin on acute lung injury using a lipopolysaccharide (LPS)-induced acute lung injury (ALI) mouse model were investigated METHOD: The cell-count in the bronchoalveolar lavage fluid (BALF) was measured. The animal lung edema degree was evaluated by the wet/dry weight (W/D) ratio. The superoxidase dismutase (SOD) activity and myeloperoxidase (MPO) activity was assayed using SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α (TNF-α), IL-1β, and IL-6 were assayed using an enzyme-linked immunosorbent assay method. Pathological changes of lung tissues were observed through HE staining. The inflammatory signal pathway related protein nuclear factor NF-κB p65 mRNA expression was measured by real-time PCR, and the protein level of NF-κB p65 was measured using Western blotting analysis. RESULTS: The data showed that treatment with the tectorigenin markedly attenuated the inflammatory cell numbers in the BALF, decreased nuclear factor NF-κB p65 mRNA level and protein level in the lungs, and improved SOD activity and inhibited MPO activity. Histological studies showed that tectorigenin substantially inhibited LPS-induced neutrophils in lung tissue compared with the model group. CONCLUSION The results indicated that tectorigenin had a protective effect on LPS-induced ALI in mice.
Acute Lung Injury ; chemically induced ; drug therapy ; pathology ; Animals ; Bronchoalveolar Lavage Fluid ; cytology ; Cell Count ; Female ; Inflammation ; drug therapy ; pathology ; Isoflavones ; therapeutic use ; Lipopolysaccharides ; Mice ; Mice, Inbred BALB C ; Peroxidase ; analysis ; Pulmonary Edema ; pathology ; Superoxide Dismutase ; analysis

BACKGROUND/AIMS: Cyclophosphamide (CP) is a promising treatment for severe cases of paraquat (PQ) poisoning. We investigated the effective dose of CP for mitigating PQ-induced lung injury. METHODS: Adult male Sprague-Dawley rats were allocated into five groups: control, PQ (35 mg/kg, intraperitoneal injection), and PQ + CP (1.5, 15, or 30 mg/kg). The dimensions of lung lesions were determined using X-ray microtomography (micro-CT), and histological changes and cytokine levels were recorded. RESULTS: The micro-CT results showed that 15 mg/kg CP was more effective than 1.5 mg/kg CP for treating PQ-induced lung injury. At a dose of 1.5 mg/kg, CP alleviated the histological evidence of inflammation and altered superoxide dismutase activity. Using 15 mg/kg CP reduced the elevated catalase activity and serum transforming growth factor (TGF)-beta1 level. CONCLUSIONS: A CP dose of > 15 mg/kg is effective for reducing the severity of PQ-induced lung injury as determined by histological and micro-CT tissue examination, possibly by modulating antioxidant enzyme and TGF-beta1 levels.
Animals ; Catalase/metabolism ; Cyclophosphamide/*pharmacology ; Cytokines/metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Immunosuppressive Agents/*pharmacology ; Inflammation Mediators/metabolism ; Lung/*drug effects/metabolism/pathology/radiography ; Lung Injury/chemically induced/diagnosis/*drug therapy/metabolism ; Male ; Oxidative Stress/drug effects ; *Paraquat ; Pulmonary Edema/chemically induced/diagnosis/*drug therapy/metabolism ; Rats ; Rats, Sprague-Dawley ; Severity of Illness Index ; Superoxide Dismutase/metabolism ; Transforming Growth Factor beta1/metabolism ; X-Ray Microtomography

No abstract available.
Animals ; Cyclophosphamide/*pharmacology ; Immunosuppressive Agents/*pharmacology ; Lung/*drug effects ; Lung Injury/*drug therapy ; Male ; *Paraquat ; Pulmonary Edema/*drug therapy

BACKGROUNDRapid reexpansion of collapsed lungs leads to reexpansion pulmonary edema (RPE). We aimed to investigate the effect of melatonin in the prevention of RPE formation.

METHODSWe used a Wistar rat model in which the left lung was collapsed by ligating the left bronchus for 48 hours and then reexpanded and ventilated for an additional 2 hours. Thirty minutes before reexpansion, we injected melatonin (10 mg/kg) or vehicle intraperitoneally. We compared the wet/dry ratio, oxygenation index, myeloperoxidase (MPO) activity, nitric oxide (NO), malondialdehyde (MDA) and interleukin 8 (IL-8) levels in the reexpanded lungs between untreated and treated animals.

RESULTSWe found that the wet/dry ratio of the melatonin group was significantly lower than that of the vehicle group, and the oxygenation index was higher in the melatonin group. Compared with the control, melatonin pretreatment significantly decreased the activities of IL-8, NO, MDA levels and MPO in lung tissues. Histopathology of reexpanded lungs showed that the melatonin pretreatment group had less pulmonary edema and less inflammatory cell infiltration.

CONCLUSIONMelatonin decreases pulmonary edema and improves oxygenation after reexpansion by attenuating oxidative stress and inhibiting pro-inflammatory cytokines.

Animals ; Cytokines ; metabolism ; Interleukin-8 ; metabolism ; Lung ; drug effects ; metabolism ; pathology ; Male ; Malondialdehyde ; metabolism ; Melatonin ; therapeutic use ; Nitric Oxide ; metabolism ; Oxidative Stress ; drug effects ; Peroxidase ; metabolism ; Pulmonary Edema ; drug therapy ; metabolism ; pathology ; Rats ; Rats, Wistar

Diabetes mellitus is responsible for diverse cardiovascular complications such as accelerated atherosclerosis, increased plaque burden and diffuse coronary lesions. It is also a major risk factor for myocardial infarction, stroke and peripheral vascular disease. Here, we present two cases. The first patient had subtle changes in the ECGs, with severe coronary artery disease requiring coronary artery bypass grafting, while the second had deep T wave inversion in the ECG and was found to have normal coronary arteries and nonischaemic cardiomyopathy. Although ECG failed to show the severity of the disease, it is invaluable as a simple, noninvasive test to aid in diagnosis. Our two cases stress the importance of a high index of suspicion and the low threshold for investigations in the diabetic population.
Aged ; Biomarkers ; analysis ; Combined Modality Therapy ; Coronary Angiography ; Coronary Artery Bypass ; Coronary Stenosis ; diagnosis ; therapy ; Diabetes Complications ; diagnosis ; drug therapy ; surgery ; Diagnosis, Differential ; Electrocardiography ; Humans ; Male ; Middle Aged ; Pulmonary Edema ; diagnosis ; therapy ; Radiography, Thoracic