FDG-PET in suspected dementia with Lewy bodies: a case report.

BACKGROUND: Dementia with Lewy bodies (DLB) is still underdiagnosed or mistaken for other types of neurodegenerative diseases. Biomarkers such as 18-Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) can be helpful. CASE PRESENTATION: A 72-year-old gentleman presented with postural hypotension, hallucination, Parkinsonism and recurrent falls. He also had rapidly progressing cognitive impairment. CT and MRI brain showed atrophy of the frontal lobes with preservation of the hippocampi. FDG-PET was suggestive of DLB. He was subsequently treated with Rivastigmine, with significant improvement of his symptoms. CONCLUSION: This case highlights the challenges in diagnosis of an elderly patient with DLB, the use of neuro-imaging as a diagnostic biomarker, the avoidance of the use of antipsychotic and the response to pharmacological treatment with Rivastigmine after a probable diagnosis of DLB.

Mania following antidepressant discontinuation in depression: two case reports.

OBJECTIVE: Antidepressant-induced mania and an antidepressant discontinuation syndrome are well documented, whereas mania occurring after antidepressant cessation has been infrequently reported. METHOD: We describe antidepressant discontinuation-related mania in two Chinese patients, as well as a review of the literature on this phenomenon in unipolar depression. RESULTS: A 72-year-old man and a 65-year-old woman had late-onset depression with vascular risk factors, but no personal or family history of mood disorders. Manic symptoms started after stopping escitalopram and venlafaxine during depressive relapse, and resolved with the initiation of olanzapine and valproate. In the literature, 29 episodes of antidepressant discontinuation-related mania were reported. Tricyclic antidepressants were most frequently implicated, followed by selective serotonin reuptake inhibitors. There was spontaneous resolution of manic symptoms in half of the cases. CONCLUSION: This is the first report of antidepressant discontinuation-related mania in an Asian population, in the setting of late-onset depression. This phenomenon is rare and is amenable to standard treatment.

Mitochondrial D-loop polymorphisms and mitochondrial DNA content in childhood acute lymphoblastic leukemia.

The mitochondrial displacement loop (D-loop) controls mitochondrial expression, with mutations and mitochondrial DNA (mtDNA) content linked to oncogenesis. We investigated D-loop polymorphisms and mtDNA content in childhood acute lymphoblastic leukemia (ALL). The D-loop was sequenced in 251 children: precursor B ALL (n=114), with 76 paired remission/relapse samples; T-ALL (n=24); cord blood controls (n=113). The mtDNA copy number was analyzed using real-time quantitative polymerase chain reaction for 92 controls and 54 ALL patients at diagnosis and remission. Polymorphisms around H-strand replication origin (nucleotides 150 to 199) and conserved sequence block II (nucleotides 299 to 317) were associated with leukemia biology and treatment response. T-ALL patients were more likely to have longer nt303 poly-C tract. T199C polymorphism was associated with increased risk of ALL in Malays; T152C was more frequent in good responders. There was no difference in mtDNA content between diagnostic ALL samples and controls; however, there was significant decrease in mtDNA content after treatment, especially in samples with OH polymorphisms. Somatic mutations were found in 13% (9 of 76) of patients, suggesting a link to leukemogenesis. Our results suggest that polymorphisms impacting transcriptional control could affect mtDNA replication. Decrease in mtDNA content after treatment may confer susceptibility to chemotherapy and be a clue to the good prognosis of childhood ALL.

Minimal residual disease-guided treatment deintensification for children with acute lymphoblastic leukemia: results from the Malaysia-Singapore acute lymphoblastic leukemia 2003 study.

PURPOSE: To improve treatment outcome for childhood acute lymphoblastic leukemia (ALL), we designed the Malaysia-Singapore ALL 2003 study with treatment stratification based on presenting clinical and genetic features and minimal residual disease (MRD) levels measured by polymerase chain reaction targeting a single antigen-receptor gene rearrangement. PATIENTS AND METHODS: Five hundred fifty-six patients received risk-adapted therapy with a modified Berlin-Frankfurt-Münster-ALL treatment. High-risk ALL was defined by MRD ≥ 1 × 10(-3) at week 12 and/or poor prednisolone response, BCR-ABL1, MLL gene rearrangements, hypodiploid less than 45 chromosomes, or induction failure; standard-risk ALL was defined by MRD ≤ 1 × 10(-4) at weeks 5 and 12 and no extramedullary involvement or high-risk features. Intermediate-risk ALL included all remaining patients. RESULTS: Patients who lacked high-risk presenting features (85.7%) received remission induction therapy with dexamethasone, vincristine, and asparaginase, without anthracyclines. Six-year event-free survival (EFS) was 80.6% ± 3.5%; overall survival was 88.4% ± 3.1%. Standard-risk patients (n = 172; 31%) received significantly deintensified subsequent therapy without compromising EFS (93.2% ± 4.1%). High-risk patients (n = 101; 18%) had the worst EFS (51.8% ± 10%); EFS was 83.6% ± 4.9% in intermediate-risk patients (n = 283; 51%). CONCLUSION: Our results demonstrate significant progress over previous trials in the region. Three-drug remission-induction therapy combined with MRD-based risk stratification to identify poor responders is an effective strategy for childhood ALL.