The overall prognosis and survival of patients with advanced gastric cancer is generally poor. One of the most powerful predictors of outcomes in gastric cancer surgery is an R0 resection. However, the extent of the required surgical resection and the additional benefit of multivisceral resection (MVR) are controversial.
Methods
Electronic literature searches were conducted using Medline, EMBASE, and the Cochrane Central Register of Controlled Trials from January 1, 1998 to December 31, 2009. All search titles and abstracts were independently rated for relevance by a minimum of two reviewers.
Results
Seventeen studies were included in this review. Among the 1343 patients who underwent MVR, overall complication rates ranged from 11.8 to 90.5%. Perioperative mortality was found to be 0–15%. Pathological T4 disease was confirmed in 28.8–89% of patients. R0 resection and extent of nodal involvement were important predictors of survival in patients undergoing MVR. Patient outcomes may also be affected by the number of organs resected.
Conclusions
Gastrectomy with MVR can be safely pursued in patients with locally advanced gastric cancer to achieve an R0 resection. MVR may not be beneficial in patients with extensive nodal disease.
Gastric perforation is a rare presentation of gastric cancer and is thought to be a predictor of advanced disease and, thus, poor prognosis. Guidelines do not exist for the optimal management strategy. We aimed to identify, review, and summarize the literature pertaining to perforation in the setting of gastric cancer.
Methods
A qualitative, systematic review of the literature was performed from January 1, 1985, to January 1, 2010. Searches of MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were performed using search terms related to gastric cancer surgery. Abstracts were examined by two independent reviewers and a standardized data collection tool was used to extract relevant data points. Summary tables were created.
Results
Nine articles were included. Perforation was reported to occur in fewer than 5% of gastric cancer patients. Preoperative diagnosis of a gastric cancer was rated and occurred in 14–57% of patients in the papers reviewed. Mortality rates for emergency gastrectomy ranged from 0 to 50% and for simple closure procedures the rates ranged from 8 to 100%. Patients able to receive an R0 gastrectomy demonstrated better long-term survival (median 75 months, 50% 5-year) compared with patients who had simple closure procedures.
Conclusions
Gastric cancer patients presenting with a gastric perforation demonstrate improved overall survival with an R0 resection; however, implementation of this management technique is complicated by infrequent preoperative gastric cancer diagnosis, and inability to perform an oncologic resection due to patient instability and intra-abdominal contamination.
Variegate porphyria (VP) is a low penetrance, autosomal dominant disorder
that results from partial deficiency of protoporphyrinogen oxidase (PPOX)
activity caused by mutation in the PPOX gene. The rare homozygous variant
of VP is characterized by severe PPOX deficiency, onset of
photosensitization by porphyrins in early childhood, skeletal abnormalities
of the hand and, less constantly, short stature, mental retardation and
convulsions. We have identified PPOX mutations on both alleles of five of
the 11 unrelated patients with homozygous VP reported to date. Two patients
were homoallelic for missense mutations (D349A and A433P), while three were
heteroallelic. Functional analysis by prokaryotic expression showed that
the D349A and A433P and one missense mutation in each of the three
heteroallelic patients (G358R in two patients and A219KANA) preserved some
PPOX activity (9.5-25% of wild-type). Mutations on the other allele of the
heteroallelic patients abolished or markedly decreased activity. There was
no relation between genotype assessed by functional analysis and the
presence or severity of non-cutaneous manifestations. The mutations were
absent from 104 unrelated patients with autosomal dominant VP. Our findings
define the molecular pathology of homozygous VP and suggest that mild PPOX
mutations occur in the general population but have very low or no clinical
penetrance in heterozygotes.
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The autosomal dominant myopathy facioscapulohumeral muscular dystrophy
(FSHD) is causally related to a short Eco RI fragment detected by probe
p13E-11. This remnant fragment is the result of a deletion of an integral
number of tandemly arrayed 3.3 kb repeat units (D4Z4) on 4q35. Despite
intensive efforts, no transcribed sequences have been identified within
this array. Previously, we have shown that these repeats on 4q35 have been
exchanged for a similar highly homologous repeat locus on 10q26 in 20% of
the population and that a short chromosome 10-like array on 4q35 also
results in FSHD. Here, we describe the hybrid structure of some of these
repeat arrays, reflecting additional sub-telomeric instability. In three
healthy individuals carrying a 4-like repeat on chromosome 10 or vice
versa, one repeat array was shown to consist of hybrid clusters of
4-derived and 10-derived repeat units. Moreover, employing pulsed field gel
electrophoresis analysis, we identified two unrelated individuals carrying
deletions of a chromosomal segment (p13E-11) proximal to the repeat locus.
These deletions were not associated with FSHD. In one of these cases,
however, an expansion of the deletion into the repeat array was observed in
one of his children suffering from FSHD. These data provide additional
evidence for instability of this sub-telomeric region and suggests that the
length of the repeat, and not its intrinsic properties, is crucial to FSHD.
Moreover, they are in agreement with the hypothesis that FSHD is caused by
a position effect in which the repeat structure influences the expression
of genes nearby. Therefore, the region deleted proximal to the repeat locus
in healthy individuals can be instrumental to refine the critical region
for FSHD1.
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The dose response and pharmacokinetics of orally administered calcitriol were investigated in normal humans. In one protocol, six volunteers received calcitriol 0.25 micrograms twice a day, 0.5 micrograms daily, and 0.5 micrograms twice a day, in successive weeks. Peak plasma levels of 1,25(OH)2D occurred 4 to 8 hours after ingestion of a single dose of 0.5 micrograms, with a return to baseline within 24 hours. The 8:00 AM calcitriol plasma levels were raised only when the drug was given twice daily. Urinary calcium excretion (UCa) was significantly increased from 199 +/- 19 mg/24 hr during the control period to similar levels of 302 +/- 26 mg/24 hr after 0.25 microgram twice a day and 284 +/- 31 mg/24 hr after 0.50 microgram daily. With 0.50 microgram twice a day, UCa was 417 +/- 36 mg/24 hr, a value greater than after the lower doses (p less than 0.05). In another protocol, fourteen volunteers received calcitriol 0.25 microgram, 0.5 microgram, and 1.0 microgram twice a day each for 14 days with intervening control periods of 2 weeks. A dose-related response in urinary calcium/creatinine excretion occurred. Thus, UCa (milligrams calcium per milligram creatinine) increased with calcitriol from 0.13 +/- 0.014 mg to 0.15 +/- 0.018 mg with 0.25 microgram twice a day, from 0.13 +/- 0.010 mg to 0.22 +/- 0.022 mg with 0.5 microgram twice a day, and from 0.12 +/- 0.012 mg to 0.23 +/- 0.012 mg with 1 microgram twice a day (p less than 0.05 with 0.25 microgram, p less than 0.01 with 0.5 and 1 microgram twice a day).(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
To evaluate the radiographic manifestations of the response of intrathoracic metastases to and the toxicity of interleukin-2 (IL-2) therapy, the chest radiographs and computed tomographic scans of 43 patients receiving 103 cycles of IL-2 treatment and lymphokine-activated killer cells for advanced renal cell carcinoma were reviewed. Among these 43 patients, 31 could be assessed for response of metastatic disease: Complete response was seen in one (3%), partial response in 11 (36%), mixed response in nine (29%), progressive disease in five (16%), and stable disease in five (16%). In 103 treatment cycles radiographic evidence of toxicity included pleural effusions (45.6%), pulmonary edema (21.4%), increased cardiothoracic ratio (16.5%), increased azygos vein diameter (9.7%), pericardial effusion (5.8%), and hilar lymphadenopathy (1.0%). These toxic effects could be distinguished from metastatic disease by a temporal relationship to treatment cycles. A favorable response to IL-2 therapy was significantly correlated (P less than .001) with the presence of pleural effusions. 相似文献
While the use of magnesium-containing compounds is usually contraindicated in dialysis patients, the risk of toxicity from hypermagnesemia can be reduced by lowering the magnesium concentration in dialysate. We examined the effects of a magnesium-free dialysate on both serum magnesium level and the peritoneal removal rate of magnesium over 12 weeks in 25 stable patients undergoing continuous ambulatory peritoneal dialysis (CAPD). After 2 weeks, the serum magnesium level decreased from 2.2 to 1.9 mg/dL (0.9 to 0.8 mmol/L) (P less than .02) and the peritoneal removal rate increased from 66 to 83 mg/d (2.8 to 3.5 mmol/d) (P less than .05), with both values remaining stable thereafter. There was a strong association between these parameters (r = -0.62, P less than .05), suggesting that the serum magnesium level decreased as a result of the initial increased peritoneal removal rate. For an additional 4-week period, a subgroup of nine patients received magnesium-containing, phosphate binding agents instead of those containing only aluminum. During this phase, serum inorganic phosphorus was well controlled. The serum magnesium level increased only from 1.8 to 2.5 mg/dL (0.7 to 1.0 mmol/L) (P less than .05), due in great part to the concomitant 41% rise in peritoneal magnesium removal from 91 to 128 mg/d (3.8 to 5.3 mmol/d) (P less than .05). No toxicity was noted during the entire 16-week study period, nor did serum calcium change. Thus, serum magnesium levels remained within an acceptable range as magnesium-containing phosphate binders were given through the use of magnesium-free peritoneal dialysate.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
To examine the effect of prolonged metabolic acidosis on the responsiveness of end organs to PTH, we measured the changes in serum ionized calcium and the urinary excretion of calcium and phosphorus in response to a 10-h infusion of parathyroid extract (PTE) before and after 9 days of metabolic acidosis. During the first hours of PTE infusion, the increases in ionized calcium were slower during acidosis, but the maximal increments in ionized calcium (0.5 +/- 0.1 and 0.4 +/- 0.1 mg/dl, respectively) were not different. Moreover, the PTE-induced increments in the fractional excretion of phosphate during acidosis and the control study were not different. Fractional excretion of calcium before the infusion of PTE was higher in acidosis than in control (3.7 +/- 0.3% compared to 0.8 +/- 0.3%; P less than 0.01). However, at 10 h of the infusion, when the maximal effect of PTE was observed, the fractional excretions of calcium in control and acidosis were not significantly different. These data suggest that prolonged metabolic acidosis has little or no effect on bone or renal responsiveness to PTH. 相似文献
