Predictors of long-term survival in patients with gallbladder cancer

The aim of this study was to examine the predictors of long-term survival (>24 months) in patients with gall bladder cancer. A retrospective review of 117 cases of gall bladder cancer resected between 1989 and 2000. The resections included 80 simple cholecystectomies and 37 extended procedures. Patients with survival >24 months (n=44) were compared with those having survival <24 months (n=73) for 17 prognostic factors. Overall median survival was 16 months with a 5-year survival of 27%. T status (P=.000) and adjuvant chemoradiotherapy (P=.001) were independent predictors of long-term survival. Survival advantage was seen in T3N+ve disease (P=.007) with extended procedures. Complete (R0) resection was attained in 30 patients with a 5-year survival advantage of 30% as compared with incomplete (R1) resection (P=.0002). Adjuvant chemoradiotherapy improved survival in simple cholecystectomy group (P=.0008) but no advantage was seen after extended procedures. Stage III (P=.001) and node-positive disease (P=.0005) had significant benefit with adjuvant therapy. Poor differentiation and vascular invasion were associated with poor long-term survival. R0 resection was associated with prolonged survival. Extended procedures improved survival in patients with T3N+ve disease. Addition of chemoradiotherapy made significant improvement in long-term survival in stage III and node-positive lesions and in patients undergoing simple cholecystectomy. R0 resection predicted long-term survival in gall bladder cancer. T3 N+ve disease had better survival after extended procedures. Adjuvant chemoradiotherapy improved survival in stage III and node-positive disease. Poor differentiation and vascular invasion were adverse predictors of survival.     

Experience with the P.A.S.-PORT Venous Access Device in Patients with Gynecologic Malignancies

Experience with the P.A.S.-PORT, a peripherally implanted central venous access device, is evaluated in a retrospective review of 154 patients from July 1991 to June 1994. Blood could not be aspirated from six patients. Complications included temporary minor thrombophlebitis in seven patients (4.5%), symptomatic axillary or subclavian vein thrombosis in five patients (3.2%), clotted port in two patients (1.2%), port pocket cellulitis in two patients (1.2%), and fungal sepsis in two patients (1.2%). In six patients (3.8%) the P.A.S.-PORT had to be removed because of complications. The P.A.S.-PORT facilitated delivery of chemotherapy, parenteral nutrition, blood products, antibiotics, hydration, and blood sampling. It was demonstrated that the P.A.S.-PORT may be inserted and used with a low incidence of complications in gynecologic cancer patients.     

Magnetic resonance imaging of third cranial nerve palsy and trigeminal sensory loss caused by herpes zoster.

A 44-year-old man with right-sided herpes zoster ophthalmicus (HZO) developed ipsilateral third and sixth cranial nerve palsies and first-division trigeminal (fifth cranial nerve) sensory loss. MRI revealed contrast enhancement of the cisternal and cavernous portions of the third cranial nerve and high signal on a FLAIR sequence within the ipsilateral medulla at the presumed location of the trigeminal nucleus and tract. To our knowledge, this is the first report of the combination of these imaging findings in HZO.     

Changes in spinal cord injury-induced gene expression in rat are strain-dependent.

BACKGROUND AND CONTEXT: The functional recovery of animals subject to experimental spinal cord injury (SCI) is dependent on the injury model as well as the species and strain of animal used. Previous studies have shown differences in rates and degree of recovery between rats of different strains. PURPOSE: We sought to explore the hypothesis that differences in gene expression are associated with differences in functional recovery. STUDY DESIGN/SETTING: Laboratory study involving cohorts of three different strains of rat. METHODS: We used the Impactor device to produce identical spinal cord contusion injuries in groups of Long Evans, Sprague-Dawley, and Lewis rats (10 each). The functional recovery of animals was assessed using the Basso, Beattie, and Bresnahan rating scale. Six weeks after injury, rats were killed and the spinal cords were harvested for deoxyribonucleic acid microarray analysis. Changes in gene expression compared with intraspecies controls (3 each) were assessed at the region of injury and at a rostral segment of the spinal cord. Selected genes were also studied with real-time polymerase chain reaction. RESULTS: We found that different strains tended to exhibit different patterns of functional recovery. There were differences between the strains in terms of gene expression. CONCLUSIONS: These results emphasize the importance of testing novel therapies for SCI in a variety of animal species before introduction into human trials. Further research into the influence of several gene products on functional recovery is needed.     

Bile duct injury repair: when? what? who?

Laparoscopic cholecystectomy is associated with a two-to-four times higher risk of bile duct injury (BDI) than open cholecystectomy. BDI can lead to significant morbidity and even mortality. The first priority in BDI is to control peritoneal and biliary sepsis and to convert an acute BDI to a controlled external biliary fistula (EBF) — this can be achieved by endoscopic and/ or radiological intervention in most cases. This should be followed by assessment of the extent of injury — both biliary and vascular. Immediate management of BDI recognized during cholecystectomy depends on the type of injury, the condition of the patient, and the experience of the surgeon. For BDI recognized after cholecystectomy, early repair is not recommended, as the results are poor. The EBF may evolve into a benign biliary stricture (BBS), which should be electively repaired by a Roux-en-Y hepatico-jejunostomy. The use of an endoscopic stent as definitive management of BDI is not recommended. Long-term follow-up is essential after the repair of a BBS, as recurrence can occur several years after repair. Recurrent BBS is best treated with endoscopic balloon dilatation. Excellent early and long-term results can be obtained in specialized units at tertiary care referral centers.     

The rising trend of invasive zygomycosis in patients with uncontrolled diabetes mellitus.

Zygomycosis is an emerging infection worldwide. A study was conducted to understand its spectrum in the Indian scenario. All patients diagnosed for invasive zygomycosis at a tertiary care center in north India from 2000-2004, were retrospectively analyzed. A total of 178 cases (mean average of 35.6 cases/year) of zygomycosis were diagnosed. Rhino-orbito-cerebral type (54.5%) was the commonest presentation followed by cutaneous (14.6%), disseminated (9.0%), and gastrointestinal (8.4%) zygomycosis. Renal and pulmonary zygomycosis were seen in 6.7% patients each. Uncontrolled diabetes mellitus (in 73.6% of cases) was the significant risk factor in all types (Odds Ratio 1.5-8.0) except renal zygomycosis. Breach of skin was the risk factor in 46.2% patients with cutaneous zygomycosis. However, no risk factor could be detected in 11.8% patients. Antemortem diagnosis was possible in 83.7% cases. The commonest (61.5%) isolate was Rhizopus oryzae followed by Apophysomyces elegans in 27% patients. Combination of debridement surgery and amphotericin B therapy was significantly better in survival of the patients (P<0.005) than amphotericin B alone (79.6% vs. 51.7% survival). Thus, a rising trend of invasive zygomycosis was observed in patients with uncontrolled diabetes mellitus in India. Consistent diagnosis of renal zygomycosis in apparently healthy hosts and the emergence of A. elegans in India demand further study.     

Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

The initial response of liver cells to insulin is mediated through exocytosis of Cl⁻ channel-containing vesicles and a subsequent opening of plasma membrane Cl⁻ channels. Intracellular accumulation of fatty acids leads to profound defects in metabolism, and is closely associated with insulin resistance. It is not known whether the activity of Cl⁻ channels is altered in insulin resistance and by which mechanisms. We studied the effects of fatty acid accumulation on Cl⁻ channel opening in a model liver cell line. Overnight treatment with amiodarone increased the fat content by ∼2-fold, and the rates of gluconeogenesis by ∼5-fold. The ability of insulin to suppress gluconeogenesis was markedly reduced indicating that amiodarone treatment induces insulin resistance. Western blot analysis showed that these cells express the same number of insulin receptors as control cells. However, insulin failed to activate exocytosis and Cl⁻ channel opening. These inhibitory effects were mimicked in control cells by exposures to arachidonic acid (15 μ m ). Further studies demonstrated that fatty acids stimulate the PKC activity, and inhibition of PKC partially restored exocytosis and Cl⁻ channel opening in insulin-resistant cells. Accordingly, activation of PKC with PMA in control cells potently inhibited the insulin responses. These results suggest that stimulation of PKC activity in insulin resistance contributes to the inhibition of cellular responses to insulin in liver cells.     

Natural killer cell differentiation: insights from knockout and transgenic mouse models and in vitro systems

Summary: In the last few years, the routine development of knockout and transgenic mice and the ease with which rare progenitor populations can be isolated from hematopoietic organs and cultured in vitro has facilitated significant advances in understanding the lineage and development of natural killer (NK) cells. Fluorescence-activated cell sorter analyses have identified a common lymphoid progenitor capable of giving rise to NK, T, and B cells, confirming the lymphoid origin of NK cells. Knockout and transgenic mouse models have pointed to an absolutely critical role for signals sent through the interleukin (IL)-2/lS receptor β (CD 122) chain and common γ (γc) chain for NK development. Such signals are likely relayed inside the cell by the tyrosine kinase Jak3, which associates with γc. Recently developed IL-15 and IL-15 receptor a knockout mice have pinpointed IL-15 as the mediator of this signal. Other mouse models have indicated an unexpected role for flt3 ligand in early NK-cell development as well as minor roles for stem cell factor and IL-7 in expanding NK-cell progenitor numbers. Finally, in vitro culture systems have proven useful in identifying the point in NK development at which each of these signals is critical.