The early variation of left ventricular twisting function in patients with lymphoma received anthracycline therapy assessed by three-dimensional speckle tracking echocardiography.

BACKGROUND: Anthracycline-induced cardiotoxicity remains a significant and unresolved issue in patients receiving chemotherapy. The aim of this study was to evaluate left ventricular (LV) twisting function by three-dimensional speckle tracking echocardiography (3D-STE) in patients with lymphoma after anthracycline therapy. METHODS: One hundred and one patients with newly diagnosed diffuse large B-cell lymphoma who had planned to receive anthracycline chemotherapy were enrolled. LV apical rotation, basal rotation, twist, torsion, time to peak apical rotation and time to peak basal rotation were measured by 3D-STE at baseline, after the completion of two cycles and four cycles of the regimen, respectively. Apical-basal rotation delay was calculated as the difference between time to basal and time to apical rotation. RESULTS: The results showed that LV apical rotation, basal rotation, twist and torsion declined progressively during the whole procedure (baseline vs. two and four cycles of the regimen, apical rotation: 12.5 ± ± 4.5° vs. 8.8 ± 3.6° vs. 6.0 ± 3.2°; basal rotation: -7.7 ± 3.0° vs. -5.9 ± 2.6° vs. -4.4 ± 2.5°; twist: 20.0 ± 6.4° vs. 14.5 ± 5.1° vs. 9.8 ± 4.5°; torsion: 2.9 ± 0.9°/cm vs. 2.1 ± 0.9°/cm vs. 1.4 ± 0.7°/cm; all p < 0.01). Furthermore, apical-basal rotation delay increased significantly after two cycles as well as after four cycles of the regimen (38.3 ± 67.9 ms vs. 66.7 ± 73.9 ms vs. 92.6 ± 96.9 ms; p < 0.01). CONCLUSIONS: LV twisting function deteriorated in the early stage of anthracycline therapy in patients with lymphoma, which could be detected by 3D-STE sensitively.

[Adverse effects of treatment with psychotropic drugs in the elderly - special risks, protective mechanisms, prognosis]. / Unerwünschte Wirkungen unter Therapie mit Psychopharmaka im Alter - Spezielle Risiken, Schutzmechanismen, Prognosen.

Due to their multimorbidity elderly patients take multiple medications, which increase the risks of adverse side effects. In this patient group, main aim of treatment is to achieve an optimal quality of live. Unwanted effects of drugs and of drug combinations (polypharmacy) have carefully to be checked.

Left ventricular twisting and untwisting motion in childhood cancer survivors.

BACKGROUND: Anthracycline has been shown to degrade titin that plays a role in myocardial twisting and untwisting. This study aimed to test the hypothesis that left ventricular (LV) twisting and untwisting motion may be altered in children after anthracycline therapy. METHODS: Thirty-six childhood leukemia survivors aged 15.6 ± 5.5 years and 20 healthy controls aged 16.8 ± 7.7 years (P = 0.54) were studied. LV twisting and untwisting motion was determined using speckle tracking imaging, whereas LV ejection fraction and systolic and diastolic mitral annular velocities were determined respectively by three-dimensional and tissue-Doppler echocardiography. RESULTS: Compared with controls, patients had significantly lower LV ejection fraction (P = 0.01) but similar systolic and diastolic mitral annular velocities (all P > 0.05). Their peak LV torsion (P = 0.003), systolic twisting velocity (P < 0.001), and diastolic untwisting velocity (P = 0.04) were significantly lower than controls, which could be attributable to their reduced apical rotation (P = 0.03) and apical untwisting rate (P = 0.002). For the whole cohort, LV systolic torsion and twisting velocity correlated significantly with apical untwisting rate (P < 0.001) and LV diastolic untwisting velocity (P < 0.001). In patients, none of the twisting or untwisting parameters were found to correlate with cumulative anthracycline dose (all P > 0.05). Twenty-eight (78%) patients had LV ejection fractions ≥50%. Although their systolic and diastolic mitral annular velocities were similar to those of controls, their peak LV torsion (P = 0.005), apical untwisting rate (P = 0.01), and LV systolic twisting velocity (P = 0.001) remained significantly lower. CONCLUSION: Impairment of LV twisting and untwisting motion is evident in children after anthracycline therapy, even in those with "normal" LV ejection fractions.

Adnexal torsion following gonadotropin-releasing hormone analog therapy: a case report.

Adnexal torsion may occur in girls and adolescents. Often it is associated with ovarian diseases resulting in ovarian enlargement. Adnexal torsion may involve the ovary, fallopian tube or both, and the main symptom is acute pelvic pain. An 8-year-old girl complaining of acute pelvic and abdominal pain, who was previously diagnosed with precocious puberty and who received treatment with a GnRH analog, is reported. Ultrasound demonstrated a normal-sized uterus and bilaterally enlarged ovaries with multiple internal cysts. At laparotomy, we found a complete torsion in the right adnexa. The histological examination revealed massive edema associated with multiple antral follicles and reduction of the follicular reserve.

Adnexal torsion following gonadotropin-releasing hormone analog therapy: a case report

Torção anexial pode ocorrer em crianças e adolescentes do sexo feminino. Frequentemente está associada com doenças ovarianas que resultam em crescimento da gônada. A torção anexial pode comprometer os ovários isoladamente, as tubas uterinas ou ambos e o sintoma principal é dor pélvica aguda. Descrevemos um caso de dor pélvica aguda em uma menina de 8 anos de idade, com diagnóstico prévio de puberdade precoce e que estava em tratamento com análogo de GnRH. O exame ultra-sonográfico demonstrava útero de tamanho normal com ovários aumentados bilateralmente e múltiplos cistos. Na laparotomia foi encontrado torção completa do anexo direito. O exame histológico demonstrou edema maciço de ovário associado com múltiplos cistos antrais e redução da reserva folicular.

Effects of sex and hormonal status on astrocytic basic fibroblast growth factor-2 and tyrosine hydroxylase immunoreactivity after medial forebrain bundle 6-hydroxydopamine lesions of the midbrain dopamine neurons.

We examined astrocytic basic fibroblast growth factor immunoreactivity (FGF-2-IR) and tyrosine hydroxylase immunoreactivity (TH-IR) in the cell-body region of midbrain dopaminergic neurons after unilateral infusions of the neurotoxin 6-hydroxydopamine into the medial forebrain bundle in male and female rats. In addition, to determine whether neonatal exposure to gonadal hormones has consequences on the expression of astrocytic FGF-2 and cell loss in response to injury in adulthood, we studied the effects of these lesions in adult male and female rats that had been exposed or not to testosterone in the neonatal period. In both males and females there was a progressive loss of TH-expressing cells that peaked 5 weeks after the lesions. Females showed less loss of TH-expressing cells than males, but this effect was not estrogen dependent. Lesions led to an increase in expression of astrocytic FGF-2 that was greater in males than in females. Finally, it was found that, regardless of genetic sex, rats exposed to testosterone neonatally showed greater astrocytic FGF-2 expression after lesions than those not exposed, and that among those not exposed to testosterone, estrogen treatment had a modest protective effect. Analysis of behavior and striatal dopamine content showed that the percent of striatal dopamine depletion 14 days after the lesion correlated with the amount of behavioral asymmetry displayed by animals on all tests conducted after lesioning. In groups killed 2 and 5 weeks after the lesion, the amount of behavioral asymmetry correlated with the percent loss of TH-IR cells and with the percent increase in FGF-2-IR cells in the midbrain. These relationships were not evident in groups killed 3 and 7 days after the lesion, possibly because the changes in the number of FGF-2- and TH-IR cells were not fully manifested. The present findings show that hormonal events early in life can alter the response of midbrain dopamine neurons to insult and injury in adult life and suggest that the slow degeneration of these neurons may release signals triggering a sustained activation of adjacent astrocytes which, in turn, may lead to induction of astrocytic FGF-2.