We describe two cases of right hyperglycemia hemichorea (HGHC) with identical Tc-99m TRODAT-1/ Tc-99m ECD scan findings. While the brain MRI showed signal alterations within the left putamen, there was evidence of hyperperfusion on Tc-99m TRODAT-1 but hypoperfusion on Tc-99m ECD within the left putamen, in association with hyperperfusion within left thalamus on Tc-99m ECD. The discrepancy between the Tc-99m TRODAT-1 and Tc-99m ECD scan provides insight into the imbalance between direct and indirect circuits along the nigrostriatal pathway, as the fundamental genesis of HGHC. Furthermore, the hyperperfusion at the left thalamus represents thalamic disinhibition secondary to loss of pallidal negative control, which ultimately leads to HGHC through re-entrant outflow to the motor cortex.
Hyperglycemia

We report a 22-year-old man with a solid mass in the right proximal leg, which was furned out to be a gossypiboma. MR imaging revealed a well-defined mass lesion that showed intermediate signal intensity at T1-weighted imaging (T1WI) and slightly high signal intensity at T2-weighted imaging (T2WI). Wavy, low-signal-intensity stripes were visible within the fluid-filled central cavity. At surgical exploration, a sponge, retained after previous knee surgery, was discovered, and it was found that a granuloma had developed. Pathologic examination revealed granulomatous inflammation, with lymphocyte and giant cell infiltration. The presence of wavy, low-signal-intensity gauze fibers at T2WI may be a characteristic MR appearance of gossypiboma.

BACKGROUNDProactive infection control management is crucial in preventing the introduction of multiple drug resistant organisms in the healthcare setting. In Hong Kong, where vancomycin-resistant enterococci (VRE) endemicity is not yet established, contact tracing and screening, together with other infection control measures are essential in limiting intra- and inter-hospital transmission. The objective of this study was to illustrate the control measures used to eradicate a VRE outbreak in a hospital network in Hong Kong.

METHODSWe described an outbreak of VRE in a healthcare region in Hong Kong, involving a University affiliated hospital and a convalescent hospital of 1600 and 550 beds respectively. Computer-assisted analysis was utilized to facilitate contact tracing, followed by VRE screening using chromogenic agar. Multi-locus sequence typing (MLST) was performed to assess the clonality of the VRE strains isolated. A case-control study was conducted to identify the risk factors for nosocomial acquisition of VRE.

RESULTSBetween November 26 and December 17, 2011, 11 patients (1 exogenous case and 10 secondary cases) in two hospitals with VRE colonization were detected during our outbreak investigation and screening for 361 contact patients, resulting in a clinical attack rate of 2.8% (10/361). There were 8 males and 3 females with a median age of 78 years (range, 40 - 87 years). MLST confirmed sequence type ST414 in all isolates. Case-control analysis demonstrated that VRE positive cases had a significantly longer cumulative length of stay (P < 0.001), a higher proportion with chronic cerebral and cardiopulmonary conditions (P = 0.001), underlying malignancies (P < 0.001), and presence of urinary catheter (P < 0.001), wound or ulcer (P < 0.001), and a greater proportion of these patients were receiving β-lactam/β-lactamase inhibitors (P = 0.009), carbapenem group (P < 0.001), fluoroquinolones (P = 0.003), or vancomycin (P = 0.001) when compared with the controls.

CONCLUSIONExtensive contact tracing and screening with a "search-and-confine" strategy was a successful tool for outbreak control in our healthcare region.

Aged ; Aged, 80 and over ; Enterococcus faecium ; growth & development ; pathogenicity ; Female ; Gram-Positive Bacterial Infections ; epidemiology ; prevention & control ; Hong Kong ; epidemiology ; Humans ; Male ; Middle Aged ; Vancomycin Resistance

BACKGROUNDVon Hippel-Lindau (VHL) syndrome is an autosomal dominant familial cancer syndrome predisposing the affected individuals to multiple tumours in various organs. The genetic basis of VHL in Southern Chinese is largely unknown. In this study, we characterized the mutation spectrum of VHL in nine unrelated Southern Chinese families.

METHODSNine probands with clinical features of VHL, two symptomatic and eight asymptomatic family members were included in this study. Prenatal diagnosis was performed twice for one proband. Two probands had only isolated bilateral phaeochromocytoma. The VHL gene was screened for mutations by polymerase chain reaction, direct sequencing and multiplex ligation-dependent probe amplification (MLPA).

RESULTSThe nine probands and the two symptomatic family members carried heterozygous germline mutations. Eight different VHL mutations were identified in the nine probands. One splicing mutation, NM_000551.2: c.463+1G > T, was novel. The other seven VHL mutations, c.233A > G [p.Asn78Ser], c.239G > T [p.Ser80Ile], c.319C > G [p.Arg107Gly], c.481C > T [p.Arg161X], c.482G > A [p.Arg161Gln], c.499C > T [p.Arg167Trp] and an exon 2 deletion, had been previously reported. Three asymptomatic family members were positive for the mutation and the other five tested negative. In prenatal diagnosis, the fetuses were positive for the mutation.

CONCLUSIONSGenetic analysis could accurately confirm VHL syndrome in patients with isolated tumours such as sporadic phaeochromocytoma or epididymal papillary cystadenoma. Mutation detection in asymptomatic family members allows regular tumour surveillance and early intervention to improve their prognosis. DNA-based diagnosis can have an important impact on clinical management for VHL families.

Asian Continental Ancestry Group ; DNA Mutational Analysis ; Humans ; Polymerase Chain Reaction ; Sequence Analysis, DNA ; Von Hippel-Lindau Tumor Suppressor Protein ; genetics ; von Hippel-Lindau Disease ; genetics