Successful Treatment of Renal Infiltration Complicated by Atypical Hemolytic Uremic Syndrome in a Leukemic Child.

Renal infiltration in children with acute leukemia has been reported previously; however, it has rarely been described in association with atypical hemolytic uremic syndrome (aHUS). We present a case of 9-year-old boy who developed life-threatening aHUS in the 1st week of Burkitt leukemia/lymphoma diagnosis with renal infiltration. Complete resolution of aHUS was achieved after therapeutic plasma exchange. This is an uncommon complication of Burkitt leukemia/lymphoma in a pediatric case.

THYROID MALIGNANCY RISK OF INCIDENTAL THYROID NODULES IN PATIENTS WITH NON-THYROID CANCER.

CONTEXT: Thyroid incidentaloma is a common disorder in endocrinology practice. Current literature regarding the risk of thyroid cancer in incidentalomas found in patients with non-thyroid cancer is limited. OBJECTIVE: The aim of the present study was to investigate the frequency of thyroid malignancy in thyroid incidentalomas detected in patients with non-thyroid cancer. DESIGN: Case control study. SUBJECTS AND METHODS: The database of 287 thyroid nodules from 161 patients with a history of non-thyroid cancer followed between 2008 and 2014 were retrospectively evaluated. RESULTS: From 287 thyroid nodules, 69.7 % had a benign final cytology. Thyroid cancer detected in one nodule while follicular neoplasia detected in 4 nodules, atypia of unknown significance (AUS) detected in 10 nodules, Hurthle cell neoplasia detected in 5 nodules and suspicious for malignancy detected in 6 nodules according to fine needle aspiration biopsy results. Metastasis of the non-thyroid cancer to the thyroid gland was detected in 4 nodules. Twenty seven nodules from 15 patients were removed with surgery. There were 3 malignant nodules found after surgery (1 papillary, 1 follicular and 1 medullary cancer). In addition to these three thyroid cancers, two patients with benign nodules had co-incidental thyroid cancer detected after surgery. Finally, 11.1 % of thyroid nodules which underwent thyroid surgery had malignant histopathology except for co-incidental and metastatic cancers. CONCLUSIONS: The frequency of thyroid malignancy seems not to be substantially increased in incidental thyroid nodules detected in patients with non-thyroid cancer when these patients were evaluated in nodule-based approach.

The role of urodynamic studies in the diagnosis and treatment of patients with spina bifida.

AIM: Spina bifida (SB) is a congenital deformity that is frequently seen in infancy. Surgical treatment and clinical follow-up of patients with the diagnosis of SB are important to provide education to the patients and their relatives, to increase patient survival, to ensure that they have a more comfortable life. Neuro-urological problems are highly important for the patients in terms of both social and medical. MATERIALS AND METHODS: The medical records of patients who underwent surgery for SB and tethered cord syndrome at our clinic in the past year were retrospectively evaluated. The results of urodynamic studies of the patients were evaluated. The results of patients who underwent control urodynamic studies during the follow-up period were compared with the previous results, and their clinical courses were determined. RESULTS: The most frequent urodynamic changes in patients were hyperactive detrusor activity and detrusor sphincter dyssynergy preoperatively. CONCLUSION: A significant improvement was observed when the results of postoperative urodynamic studies were evaluated in patients who underwent surgery for tethered cord.

Comparison of nephron-protective effects of enalapril and GLP analogues (exenatide) in diabetic nephropathy.

BACKGROUND: One of the major concerns is a nephropathy in diabetes, which applies many different kinds of medicines. However, required level of the treatment of renal disease has not been achieved. AIM: To investigate and compare the effect of the enalapril and the exenatide on diabetic nephropathy in rats developed diabetes by streptozosin. MATERIAL AND METHODS: 32 male Sprague Dawley rats were divided into 4 groups: (1) Control, (2) Diabetic (DM), (3) DM+ Enalapril, and (4) DM+ exenatide groups. Then, the animals were euthanized and their blood samples were collected by cardiac puncture for blood glucose; blood urea nitrogen (BUN), creatinin, and nephrectomy were performed for histopathologic examination, and urine samples were taken on stick for proteinuria. RESULTS: Administration of the enalapril or the exenatide in diabetic rats resulted in a significant reduction both fibronectin, induced nitric oxide synthase (i-NOS) expression in glomerular area and urine protein levels. It was shown that both of enalapril and exenatide protected the renal glomerulus more than diabetic group in the nephropathy histopathologically. CONCLUSION: The beneficial effects of enalapril and exenatide which reduces fibronectin, i-NOS expression and urine protein levels or increases recovery of glomerules, might be used for preventing the harmful effects of diabetic nephropathy.

Incision wound healing activity of pine bark extract containing topical formulations: a study with histopathological and biochemical analyses in albino rats.

The present study was designed to identify and compare the in vivo wound healing capacity of a bark extract from Pinus brutia and Pycnogenol in an incision wound model in rats. O/W cream formulations were prepared incorporating 2% Pycnogenol and P. brutia bark extract. The rats were divided into three groups (n = 8). Subsequently placebo and test formulations were applied to animals once a day from day "0" until the 9th day. Malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were studied in addition to histopathological examinations. Treatment with F. brutia extract containing cream inhibited lipid peroxidation by a 35% decrease in MDA and 46.8% increase in SOD activity, whereas 19.3% decrease in MDA and 34.7% increase in SOD activity were attained with Pynogenol compared to control. The histological data revealed a better performance of P. brutia extract enriched formulation in terms of degeneration of hair roots, increased vascularization and a decrease in necrotic area. Consequently, a high wound healing activity was observed in animals treated with P. brutia extract significantly accelerating the wound healing process.

Does pantoprazole protect against reperfusion injury following myocardial ischemia in rats?

BACKGROUND: Myocardial ischemia is inadequate perfusion due to reduced blood flow. Sudden onset of reperfusion could result with damage to the myocytes that have not been affected during ischemia called ischemia reperfusion (I/R) injury. Extracellular accumulation of H+ ions resulting in tissue acidosis is one of the underlying mechanisms. Inhibition of myocardial H+/K+-ATPase, namely proton pump, may lead to intracellular acidification via decreasing the extracellular H+ transport. AIM: The aim of this study is to investigate the effects of a proton pump inhibitor pantoprazole in intact rat I/R models. MATERIALS AND METHODS: A total of 30 adult male Wistar albino rats weighing 200-300 g were studied. Rats were allocated into four groups: sham (n=6), ischemia (n=8), control (n=8), and pantoprazole (n=8). Left anterior descending coronary artery was occluded for 30 minutes and then reperfused for two hours. Pantoprazole was administered via jugular vein at the dose of 9 mg/kg starting from 30 minutes before ischemia, to the first 30 minutes of reperfusion. Haemodynamic parameters were recorded and serum CK-MB levels were measured. After reperfusion, heart was removed for the measurement of myocardial infarct size. Myocardial infarct area was measured using triphenyltetrazolium chloride (TTC) staining technique. Myocardial infarction size were expressed as the percentage of the total left ventricular weight. RESULTS: Compared with other groups, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in pantoprazole group (p < 0.008). CONCLUSIONS: Pantoprazole preconditioning induces delayed cardioprotection in intact rat I/R model, which may be triggered via H+/K+-ATPase ion channels.

Q-VD-OPh, a pancaspase inhibitor, reduces trauma-induced apoptosis and improves the recovery of hind-limb function in rats after spinal cord injury.

BACKGROUND: Various caspases have been implicated in the development of secondary damage after spinal cord injury (SCI). Anticaspase therapy that targets only one caspase has been investigated in a variety of in vitro and in vivo studies. This study examined the neuroprotective effects of Q-VD-OPh, a pan-caspase inhibitor, in a rat model of SCI. METHODS: Thirty Wistar albino rats were divided into 3 groups of 10 each: the sham-operated controls (group 1), the trauma-created controls (group 2), and the QVD- OPh-treated rats (group 3). An SCI (a trauma of 40 g-cm) was produced at the thoracic level (T8-T10) by the weight-drop technique. The response to injury and the neuroprotective effects of Q-VD-OPh were investigated by histopathologic examination and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) 24 hours and 5 days after trauma. The inclined plane technique of Rivlin and Tator and a modified version of Tarlov's grading scale were used to assess the functional status of the rats 24 hours, 3 days, and 5 days after injury. RESULTS: Twenty-four hours after trauma, light microscopic examination of a specimen taken from group 2 rats revealed hemorrhage, necrosis, vascular thrombi, and edema. Group 3 tissue samples showed similar features at that time. Twenty-four hours after trauma, the mean apoptotic cell number was 4.47 +/- 0.35 cells in group 2 and 1.58 +/- 0.33 in group 3. Five days after injury, the mean apoptotic cell count was 4.35 +/- 0.47 in group 2 and 1.25 +/- 0.34 in group 3. Thus the number of TUNEL-positive cells in an injured spinal cord was greatly reduced by treatment with Q-VDOPh. The neurologic function scores (both the inclined plane performance and motor grading scores) were significantly better in the Q-VD-OPh-treated group than in the trauma-created control group. CONCLUSION: The marked antiapoptotic properties of Q-VD-OPh due to the inhibition of all caspases render it a promising novel agent. A therapeutic strategy using Q-VD-OPh may eventually lead to the effective treatment of SCI in humans.

Q-VD-OPh, a pancaspase inhibitor, reduces trauma-induced apoptosis and improvesthe recovery of hind-limb function in rats after spinal cord injury

Background. Various caspases have been implicatedin the development of secondary damage after spinalcord injury (SCI). Anticaspase therapy that targets onlyone caspase has been investigated in a variety of in vitroand in vivo studies. This study examined the neuroprotectiveeffects of Q-VD-OPh, a pan-caspase inhibitor, ina rat model of SCI.Methods. Thirty Wistar albino rats were divided into3 groups of 10 each: the sham-operated controls (group1), the trauma-created controls (group 2), and the QVD-OPh–treated rats (group 3). An SCI (a trauma of40 g-cm) was produced at the thoracic level (T8-T10) bythe weight-drop technique. The response to injury andthe neuroprotective effects of Q-VD-OPh were investigatedby histopathologic examination and terminaldeoxynucleotidyl transferase dUTP nick-end labeling(TUNEL) 24 hours and 5 days after trauma. The inclinedplane technique of Rivlin and Tator and a modifiedversion of Tarlov’s grading scale were used to assess thefunctional status of the rats 24 hours, 3 days, and 5 daysafter injury.Results. Twenty-four hours after trauma, lightmicroscopic examination of a specimen taken fromgroup 2 rats revealed hemorrhage, necrosis, vascularthrombi, and edema. Group 3 tissue samples showedsimilar features at that time. Twenty-four hours aftertrauma, the mean apoptotic cell number was 4.47 ± 0.35cells in group 2 and 1.58 ± 0.33 in group 3. Five daysafter injury, the mean apoptotic cell count was 4.35 ±0.47 in group 2 and 1.25 ± 0.34 in group 3. Thus thenumber of TUNEL-positive cells in an injured spinalcord was greatly reduced by treatment with Q-VDOPh.The neurologic function scores (both the inclinedplane performance and motor grading scores) were significantlybetter in the Q-VD-OPh–treated (AU)

Introducción. En el desarrollo de daño secundario tras lesión medular están implicadas diversas caspasas.La terapia anti-caspasas ha utilizado como diana una sola caspasa que ha sido investigada en una gran variedad de estudios tanto in-vitro como in-vivo. Estos estudios han examinado el efecto neuroprotector delQ-VD-PPh, un inhibidor pan-caspasa, en un modelo delesión medular en rata. Material y métodos. Se dividieron 30 ratas Wistar entres grupos de 10 ratas cada uno: una lesión medulartraumática (con un trauma de 40 g-cm) se realizó anivel torácico grupo control (grupo 1), grupo traumacontrol (grupo 2) y el grupo de ratas tratadas con QVD-OPh (grupo 3) se realizó a nivel torácico (T8-T10) mediante la técnica de caída de peso. La respuesta a la lesión y los efectos neuroprotectores de Q-VD-OPh se valoraron mediante el examen histopatológico y la técnica de TUNEL 24 horas y 5 días tras el traumatismo. Se usó la prueba del plano inclinado de Rivlin y Tatory una versión modificada de la escala de Tarlov paravalorar el resultado funcional de las ratas 24 horas, 3 días y 5 días tras la lesión. Resultado. Veinticuatro horas tras la lesión, el estudio histopatológico de las secciones obtenidas del grupo 2 revelaron hemorragia, necrosis, trombos vasculares y edema. Las secciones obtenidos del grupo 3 mostraron hallazgos similares en ese momento. 24 horas tras lalesión el número de células apoptóticas fue 4.47 ± 0.35en el grupo 2 y 1.58 ± 0.33 en el grupo 3. Cinco días trasla lesión el número medio de células apoptóticas fue de4.35 ± 0.47 en el grupo 2 y de 1.25 ± 0.34 en el grupo 3. De esta forma el número de células TUNEL positivas enla médula dañada se redujo de forma considerable conel tratamiento con Q-VD-OPh (AU)

Effects of GYKI 52466 on early vasospasm in rats.

OBJECTIVE: The pathogenesis and treatment of cerebral vasospasm (CV) after subarachnoid hemorrhage (SAH) remains a matter of discussion. The authors investigated the efficacy of GYKI 52466, a 2,3-benzodiazepine that is a selective and potent alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) receptor antagonist, in a rat femoral artery vasospasm model. METHODS: Twenty-seven Wistar albino rats were used in this study. The animals were divided into 3 groups of 9 animals each: sham-operated control (group 1), vasospasm group (group 2), and vasospasm-plus-treatment group (group 3). In groups 2 and 3, autologous blood (0.1 mL) was applied to a 1-cm segment of the femoral artery, which was then wrapped with a silicone cuff. One minute after blood application, the rats in group 3 received an intraperitoneal injection of 15 mg/kg GYKI 52466 every 12 h for 24 h. Responses to blood application and treatment were evaluated with light and electron microscopy examinations of femoral artery specimens at 72 h. RESULTS: On light microscope examination, the mean diameters of the arterial lumens in groups 1, 2, and 3 were 514.47+/-15.3, 317.63+/-12.1, and 503.91+/-9.6 microm, respectively. At 24 h, the mean arterial wall thickness in group 1 was 77.69+/-4.2 microm. This mean thickness in group 2 increased to 164.82+/-9.1 microm. After GYKI treatment in group 3, the mean arterial wall thickness measured 95.37+/-5.3 microm. In group 2 rats, electron microscopy demonstrated various changes including marked luminal narrowing and increased wall thickness in the femoral arterial wall. The most striking finding were the degenerative changes in the endothelium, which presented as a corrugated appearance of the internal elastic lamina. Rats in group 3 had endothelia that were slightly constricted and smooth muscle cells that were relaxed; changes in the vessel wall and internal elastic lamina were less prominent in these rats than in the rats of group 2. CONCLUSIONS: The results of the present study suggest that GYKI 52466 inhibited AMPA receptors and induced relaxation of smooth muscle cells in the wall of the femoral artery in a rat model. This substance may be a protective and therapeutic agent in the treatment of cerebral vasospasm.

Calpain inhibitor AK 295 inhibits calpain-induced apoptosis and improves neurologic function after traumatic spinal cord injury in rats.

BACKGROUND: An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. In this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model. METHODS: Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma. FINDINGS: Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotic cell numbers in groups 1 and 2 were zero and 4.57 +/- 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 +/- 0.34 cells, a value significantly lower than that in group 2 (P < .05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05). CONCLUSIONS: AK 295 inhibited apoptosis via calpaindependent pathways and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI.

Calpain inhibitor AK 295 inhibits calpain-induced apoptosis and improves neurologicfunction after traumatic spinal cord injury in rats

Background: An increase in the level of intracellular calcium activates the calcium-dependent neutral protease calpain, which in turn leads to cellular dysfunction and cell death after an insult to the central nervous system. In this study, we evaluated the effect of a calpain inhibitor, AK 295, on spinal cord structure, neurologic function, and apoptosis after spinal cord injury (SCI) in a murine model. Methods: Thirty albino Wistar rats were divided into 3 groups of 10 each: the sham-operated control group (group 1), the spinal cord trauma group (group 2), and the spinal cord trauma plus AK 295 treatment group (group 3). After having received a combination of ketamine 60 mg/kg and xylazine 9 mg/kg to induce anesthesia, the rats in groups 2 and 3 were subjected to thoracic trauma by the weight drop technique (40 g-cm). One hour after having been subjected to that trauma, the rats in groups 2 and 3 were treated with an intraperitoneal injection of either dimethyl sulfoxide 2 mg/kg or AK 295 2 mg/kg. The effects of the injury and the efficacy of AK 295 were determined by an assessment of the TUNEL technique and the results of examination with a light microscope. The neurologic performance of 5 rats from group 2 and 5 from group 3 was assessed by means of the inclined plane technique and the modified Tarlov's motor grading scale 1, 3, and 5 days after spinal cord trauma. Findings: Light-microscopic examination of spinal cord specimens from group 2 revealed hemorrhage, edema, necrosis, and vascular thrombi 24 hours after trauma. Similar (but less prominent) features were seen in specimens obtained from group 3 rats. Twenty-four hours after injury, the mean apoptotic cell numbers in groups 1 and 2 were zero and 4.57 ± 0.37 cells, respectively. In group 3, the mean apoptotic cell number was 2.30 ± 0.34 cells, a value significantly lower than that in group 2 (P<.05). Five days after trauma, the injured rats in group 2 demonstrated significant motor dysfunction (P < .05). In comparison, the motor scores exhibited by group 3 rats were markedly better (P < .05). Conclusions: AK 295 inhibited apoptosis via calpaindependent pathways and provided neuroprotection and improved neurologic function in a rat model of SCI. To our knowledge, this is the first study to evaluate the use of AK 295, a calpain inhibitor, after SCI. Our data suggest that AK 295 might be a novel therapeutic compound for the neuroprotection of tissue and the recovery of function in patients with a SCI (AU)

Introducción: Una lesión en el sistema nervioso central origina un incremento en los niveles de calcio intracelular que activa la proteasa neutral calciodependiente calpaina, que a su vez conduce a la producción de disfunción y muerte celular. En este estudio evaluamos el efecto de un inhibidor de la calpaina, AK 295, sobre la estructura de la médula espinal, la función neurológica y apoptosis tras lesión medular en un modelo murino. Métodos: Treinta ratas Wistar se dividieron en tres grupos de 10 ratas cada uno: Un grupo control (grupo 1), un grupo sometido a trauma espinal (grupo 2) y un grupo de ratas a las que se sometió a trauma medular y tratamiento con AK 295 (grupo 3). Después de recibir una combinación de ketamina 60 mg/kg y xylazina 8 mg/kg para la inducción anestésica, las ratas del grupo 2 y 3 fueron sometidas a trauma medular torácico mediante la técnica de caída de peso (40 g-cm). Una hora después de haber sufrido el traumatismo, las ratas del grupo 2 y 3 fueron tratadas mediante una inyección intraperitoneal bien de dimetil-sulfóxido 2 mg/kg o de AK 295 2 mg/kg. Los efectos del traumatismo y la eficacia de AK 295 fueron determinados mediante la estimación de la técnica TUNEL y los resultados del examen del tejido mediante microscopía óptica. La función neurológica de 5 ratas del grupo 2 y 5 del grupo 3 fue estimada mediante la técnica del plano inclinado y la escala motora de Tarlov modificada a 1, 3 y 5 días desde el traumatismo medular. Resultados: El estudio mediante microscopía óptica de las preparaciones de médula espinal del grupo 2 demostró la existencia de hemorragia, edema, necrosis y trombosis vascular 24 horas tras el traumatismo. Hallazgos similares pero menos importantes se encontraron en las preparaciones procedentes del grupo 3. Veinticuatro horas tras el trauma, el número medio de células apoptóticas en los grupos 1 y 2 fueron cero y 4.57 ± 0.37 células respectivamente. En el grupo 3, el número medio de células apoptóticas fue de 2.30 ± 0.34 células, un valor significativamente menor que en el grupo 2 (p < 0.05). Cinco días tras el traumatismo, las ratas lesionadas en el grupo 2 demostraron una significativamente mayor disfunción neurológica (p < 0.05). En comparación, la puntuación motora que exhibieron las ratas del grupo 3 fue marcadamente mejor (p < 0.05). Conclusión: AK 295 inhibe la apoptosis a través de vías calpain-dependientes y provee neuroprotección y consigue una mejor función neurológica en el modelo de lesión medular traumática en la rata. En nuestro conocimiento, este es el primer estudio en evaluar el uso de AK 295, un inhibidor de la calpaina, tras lesión medular traumática. Nuestros datos sugieren que AK 295 podría ser un nuevo compuesto terapéutico capaz de ofrecer neuroprotección tisular y recuperación funcional en pacientes con lesión medular traumática (AU)

Sixteen gauge needles improve specimen quality but not cancer detection rate in transrectal ultrasound-guided 10-core prostate biopsies.

Performance of 16 (16 g) (n=103) and 18 gauge (18 g) (n=101) biopsy needles in transrectal ultrasound (TRUS)-guided 10-core prostate biopsies were compared in terms of cancer detection and pre-defined specimen quality criteria in this prospective randomized study. Cancer detection rates of the two groups were similar, although the mean core volume of 16 g needles was almost twice that of 18 g needles. On the other hand, using 16 g needles significantly improved specimen quality by acquiring less empty cores, small cores and fragmented cores. There were no significant differences among the complication rates and VAS pain scores of the two groups. Sixteen gauge needles can safely be used in TRUS-guided prostate biopsies, as they improve specimen quality without increasing morbidity and patient discomfort.

Treatment effect of sibutramine compared to fluoxetine on leptin levels in polycystic ovary disease.

Weight reduction on its own is observed to cause improvement in some of the abnormalities seen in patients with polycystic ovary syndrome (PCOS). With respect to this observation, we studied the possible effects of different serotonin reuptake inhibitors (fluoxetine and sibutramine) on serum leptin levels that might play a role in the obesity component seen in patients with PCOS. In a random design, sixteen patients were assigned to fluoxetine and sibutramine for a period of 10 days. In both treatment groups, no significant differences were observed between pre-treatment and post-treatment values in insulin levels (p > 0.05). There was no significant difference between pretreatment and post-treatment serum leptin levels in the fluoxetine treatment group (p > 0.05). However, a significant reduction was observed in the serum leptin levels at the end of treatment in the sibutramine group (p < 0.05). The observed difference in the serum leptin response to the treatment effect of sibutramine compared to fluoxetine seems to be due to a mechanism independent of serotonin reuptake inhibition, possibly to the thermogenic effect of the sibutramine itself. Further studies with larger groups are warranted, to examine the mechanism of the weight-reducing effect of sibutramine. Detailed analyses of basal metabolic activity and change in serum leptin levels should be carried out.

Mitral valve vegetation and cerebral emboli in a primary antiphospholipid syndrome patient who had hepatitis C virus infection: report of a case and review of the literature.

We report the case of 36-year-old woman who came to us with a history of recurrent miscarriages and who was later diagnosed as having primary antiphospholipid syndrome (PAPS) and chronic hepatitis C virus (HCV) infection. The patient was referred to us with generalised seizures; cranial MRI revealed multiple embolic infarcts in both frontal lobes and a focal cortical infarct in the left frontoparietal lobe. Her echocardiography showed mitral valve vegetation and insufficiency. The patient was put on oral anticoagulant therapy and during her 8-month follow-up period no thrombotic events occurred. We report this case because it was the first in which PAPS, valvular disease, a cerebral embolic event and HCV infection were coexistent in the same patient. We also review other cases in which there was valvular vegetation and a cerebral ischaemic event associated with PAPS.

The effect of glucose-insulin-potassium solution on ventricular late potentials and heart rate variability in acute myocardial infarction.

BACKGROUND: Blunted heart rate variability (HRV) and presence of ventricular late potentials (VLPs) are known to correlate with an increased risk of ventricular tachycardia and sudden cardiac death in acute myocardial infarction (AMI). In the present study, we investigated the effect of glucose-insulin-potassium (GIK) solution on the VLPs and HRV in AMI. METHODS: Seventy-two consecutive patients with first Q wave AMI were randomized to GIK solution and placebo. HRV analysis and ambulatory electrocardiographic recordings were taken in all patients between 24 and 48 h. Sub-maximal exercise testing and echocardiography were performed and signal-averaged electrocardiography (SAECG) was recorded before discharge. RESULTS: Total filtered QRS duration (FQRS: 102 +/- 7 versus 108 +/- 11 ms; P < 0.05), low-amplitude signal (LAS: 25 +/- 8 versus 32 +/- 11 ms; P < 0.01) and frequency of VLPs (21 versus 45%; P < 0.05) were found to be significantly lower while root-mean-square voltage of the terminal 40 ms of QRS (RMS-40: 45 +/- 18 versus 36 +/- 20 microV; P < 0.05), and left ventricular ejection fraction (EF: 55 +/- 6 versus 48 +/- 7; P < 0.05) were significantly higher in the GIK group when compared to placebo. During the hospital period, the presence and frequency of post-myocardial infarction angina were significantly lower in the GIK group (15 versus 29%, P < 0.05), whereas an insignificant decrease in frequency of ventricular arrhythmias was observed in these patients. On HRV analysis, there was no significant difference between two groups in either time domain (SD, SDNN, RMS-SD) or frequency domain (HF, LF, LF/HF ratio) parameters. CONCLUSION: GIK solution may be beneficial to VLPs, ischaemic events, and left ventricular systolic performance in the early period of AMI. This therapy has no significant effect on HRV in AMI patients.

Right ventricular aneurysm complicating right ventricular infarction.

Right ventricular (RV) involvement commonly occurs in patients with acute inferior myocardial infarction and is associated with high mortality and morbidity. RV dysfunction and dilatation commonly recover in survivors; chronic RV dyskinesia and failure are rare complications. This case report presents a patient in whom an isolated RV aneurysm complicates a RV involvement of acute inferior-posterior myocardial infarction.

The effects of trimetazidine on heart rate variability and signal-averaged electrocardiography in early period of acute myocardial infarction.

BACKGROUND: Acute myocardial infarction (AMI) is accompanied by electrophysiological changes in cardiovascular system as well as those in autonomic cardiac control. Heart rate variability (HRV) is depressed due to increased sympathetic activity and/or decreased parasympathetic activity following AMI. Moreover, the frequency of ventricular late potentials (VLP) is increased due to the electrophysiological changes. Based on the hypothesis that the treatments increasing HRV and decreasing the frequency of VLP can improve the prognosis of AMI, we investigated the short-term effects of trimetazidine (TMZ) on HRV and VLP in patients with AMI. METHODS: The study group consisted of 64 patients (men 49, mean age 55+/-12 years, range 26-70) suffering from first Q-wave AMI. Thirty-one of them were treated with conventional therapy (thrombolytic therapy, aspirin, beta-blocker, heparin and intravenous nitroglycerin) plus TMZ 20 mg tid. The remaining 33 patients served as controls. Holter monitorization between 24 and 48 h, echocardiography at average day 6 (range 4-7 days) and SAECG and sub-maximal exercise at average day 7 (range 6-9 days) were performed to all patients. RESULTS: While HRV parameters reflecting parasympathetic activity (SDSD: 43+/-16 ms-35+/-13 ms, RMSSD: 34+/-14 ms-27+/-8 ms, HF: 7.8+/-5 ms(2) -4.3+/-4 ms(2), P<0.05) were of significantly higher levels in TMZ group, the low frequency component mainly reflecting sympathetic activity (LF: 10+/-6 ms(2)-10+/-5 ms(2), P>0.05) was similar in both groups. In addition, LF/HF ratio showing sympatho-vagal balance was significantly decreased in TMZ group (1.5-3.0, P=0.005). About VLP, the mean FQRS (105+/-8 ms-107+/-10 ms), LAS (28+/-10 ms-30+/-11 ms) and RMS-40 (34+/-15 microV-41+/-12 microV) were not different in both two groups (P>0.05). CONCLUSION: Our results suggest that TMZ treatment causes changes in sympatho-vagal balance in favor of vagal activity by increasing parasympathetic activity in AMI at early period; however, no effect on VLP was observed.