Renal impairment after spontaneous bacterial peritonitis: incidence and prognosis.

BACKGROUND/AIMS: Spontaneous bacterial peritonitis (SBP) is an important complication in cirrhotic patients. The aim of the present study was to assess the incidence, predictive factors and prognosis for renal impairment (RI) after SBP in cirrhotic patients from southern Brazil. METHODS: Of the 1030 hospitalizations evaluated, 114 episodes of SBP were diagnosed in 94 patients (mean age 49 years; 76.59% men). SBP diagnosis was established when the ascitic fluid polymorphonuclear cell count was equal to or greater than 250 cells/mm3. Five cases were excluded. The variables assessed as possible predictors of steady or progressive RI were blood urea nitrogen and creatinine levels before the diagnosis of SBP; type of infection, antibiotic prophylaxis, first episode or recurrent SBP, presence of gastrointestinal bleeding and hepatic encephalopathy during hospitalization, SBP resolution, Child-Pugh classification, levels of blood pressure, ascitic fluid and blood polymorphonuclear cell count, bacteriological data (positive and negative ascitic fluid culture), albumin, bilirubin, sodium and prothrombin time at the moment of diagnosis. RESULTS: The incidence of SBP was 11.07%. In 61 (55.96%) episodes, SBP was associated with RI (transient in 57.37%; steady in 19.67%; and progressive in 22.95%). The mortality rate associated with progressive RI was 100%; 58.33% with steady RI; and 2.85% with transient RI. The mortality rate in patients with or without RI was 36.07% and 6.25%, respectively (P<0.001). The level of creatinine (greater than or equal to 1.3mg/dL) before the diagnosis of SBP and the rate of infection resolution were the only predictors of RI in the multivariate analysis. CONCLUSIONS: RI after SBP is a common complication, and indicates a poor prognosis for this infection. High levels of creatinine before infection and the rate of infection resolution are independent predictors of RI.     

Regulation of neurotransmitter enzyme by quisqualate subtype glutamate receptors in cultured cerebellar and hippocampal neurons

The possible involvement of ionotropic and metabotropic quisqualate (QA) receptors in neuronal plasticity was studied in cultured glutamtergic cerebellar or hippocampal cells in terms of the specific activity of phosphate-activated glutaminase, an enzyme important in the synthesis of the putative neurotransmitter pool of glutamate. When cerebellar of hippocampal neurons were treated with QA, it elevated the specific activity of glutaminase in a dose-dependent manner. The half-maximal effect was obtained at about 0.1 μM, the maximum increase was at about 1 μM, but levels higher than 10 μM QA produced progressive reduction in glutaminase activity. In contrast, QA had little effects on the activities of lactate dehydrogenase and aspartate aminotransferase and the amount of protein, indicating that the increase in glutaminase was relatively specific. The QA-mediated increase in glutaminase was mimicked by the ionotropic QA receptor agonist -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA; EC₅₀, about 0.5 μM), but not by the metabotropic QA receptor agonist trans-(±)-1-aino-cyclopentyl-1,3,dicarboxyalte (t-ACPD; up to 0.5 mM). The specific ionotropic QA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) inhibited QA- and AMPA-mediated increases in glutaminase activity in a dose-dependent manner, whereas other glutamate receptor antagonists, -2-amino-5-phosphonovalerate, γ- -glutamyl aminomethyl sulphonic acid and γ- -glutamyl diethyl ester were ineffective. The elevation of neurotransmitter enzyme was Ca²⁺-dependent. The increase in Ca²⁺ influx essentially through the activation of L-type voltage-operated Ca²⁺ channels, and not the mobilization of internal Ca²⁺ stores, was responsible for these QA receptor-mediated long-term plastic changes in hippocampal and cerebellar neurons.     

PaO2 increases with coughing in patients with chronic lung disease

We considered if the cyanosis frequently observed during a cough attack in patients with chronic lung disease was due to worsening hypoxemia. To investigate the effects of cough on PaO2, we measured arterial blood gases before and after a voluntary coughing period of 45 sec, in 11 patients with Interstitial Lung Disease (ILD) and 14 patients with Chronic Obstructive Lung Disease (COPD). All patients significantly increased (p less than 0.05) their PaO2 (COPD: from 49 +/- 2 to 60 +/- 2 mmHg; ILD from 44 +/- 2 to 51 +/- 3 mmHg, mean +/- SD) and decreased their PaCO2. We conclude that stable patients with COPD and ILD increase their PaO2 with coughing most likely due to hyperventilation. The cyanosis observed could be due to peripheral circulatory effects of coughing.     

Natural history of experimental pulmonary atelectasis in dogs with closed chest

In order to establish an animal model of pulmonary vasoconstriction we followed the time course of intrapulmonary shunt (Qs/Qt) in a canine model of lobar atelectasis with closed chest. Ten mongrel dogs were studied. Bronchial occlusion of the right lower lobe (RLL) was performed by inflating the balloon of a Foley catheter placed through a rigid bronchoscopy. Analysis of variance was used for statistical analysis. (15 minutes) After occlusion Qs/Qt reached its maximum increasing from 8.2 +/- 3.6 to 29.7 +/- 11.7% (p less than 0.05) and PaO2 decreased from 357 +/- 49 to 100 +/- 43 mm Hg (p less than 0.05). Afterwards, there was a progressive decline of Qs/QT accompanied by an also progressive increase in PaO2. At the end of the experiment (3 hrs post atelectasis) Qs/Qt was 11.2 +/- 4.9 and PaO2 251 +/- 124 mm Hg (p less than 0.05). Pulmonary vascular resistance increased post atelectasis from 439 +/- 168 to 598 +/- 256 d.s.cm-5 (p less than 0.05). Complete atelectasis of the RLL was confirmed postmortem. As the changes in Qs/Qt and PaO2 did not parallel the change in cardiac output we conclude that the mechanism of decrease in Qs/Qt was hypoxic vasoconstriction.     

HLA and Behçet's disease in Northern Spain: Their lack of correlation with arthritis pattern

Summary We have studied the characteristics of arthritis present in 32 patients with Behçet's disease (BD), and how this arthritis is related to the HLA markers class I. 84% of the patients presented arthritis, the most common being monoarthritis as the initial presentation, and oligoarthritis in subsequent episodes. In 63% of the cases, the development was in episodes of acute/subacute arthritis. We found statistically significant association between antigens B-5 and B-51, and the group with BD, with a relative risk of 3.89 and 4.71 respectively. The attempt to relate markers B-5, B-51 and B-27 to the presence of arthritis as well as to its manifestation and further development was not conclusive.     

Gastrinomas demonstrate amplification of the HER-2/neu proto-oncogene.

OBJECTIVE: This study determined whether genomic amplification of HER-2/neu or mutations of the p53 and ras genes were present in gastrinomas. SUMMARY BACKGROUND DATA: Amplification of HER-2/neu, a proto-oncogene related to the epidermal growth factor receptor, and mutation of the ras proto-oncogene and p53 tumor suppressor gene appear to play a role in the pathogenesis of some human cancers. Little is known about possible molecular alterations in gastrinomas, tumors that may be particularly virulent because of gastrin overproduction, resulting in the severe ulcer diathesis, the Zollinger-Ellison syndrome. METHODS: The differential polymerase chain reaction (PCR) procedure was used to detect amplification of the HER-2/neu gene in DNA samples from the novel human gastrinoma cell line (PT) and from paraffin-embedded samples of gastrinomas. Sequencing techniques were used to determine whether mutations of the p53 or ras (Ha-ras, N-ras, Ki-ras) genes were present. RESULTS: Amplification (> twofold) occurred in all gastrinoma tumor samples. Compared with normal pancreas or ileum, a 4- to 12-fold amplification of HER-2/neu was found in 3 gastrinomas, 3 to 3.3-fold in four samples and 2.1- to 2.4-fold in the remaining five tumors. A heterozygous point mutation in the p53 gene (codon 273) was found in a single sample; none of the gastrinomas contained a mutation of the ras genes. CONCLUSIONS: Amplification of the HER-2/neu gene, but not alterations of either p53 or ras, may be involved in the pathogenesis of gastrinomas. The unique PT cell line will be a useful model to further elucidate the molecular mechanisms that contribute to gastrinoma formation and growth.