Chylous ascites in cirrhosis: A case report and review of the literature

Chylous ascites is an uncommon clinical entity which results from the accumulation of fat, predominantly chylomicrons, in the ascitic fluid. Conventional treatment methods are unsatisfactory. A patient is reported with chylous ascites associated with cirrhosis and portal hypertension in whom the ascites, the renal insufficiency and the fluid and electrolyte disturbances were corrected by the insertion of a Denver peritoneovenous shunt.     

ANTIDIURETIC HORMONE IN BRONCHOGENIC CARCINOMA

Immunoactive antidiuretic hormone (ADH) was measured by radioimmunoassay in the plasma, lung tumours and metastatic tumours of nineteen patients with bronchogenic carcinoma. Ten patients had hyponatraemia and carcinoma of the small oat cell type. Plasma ADH measured in nine of these patients ranged from 11--270 pg/ml and was elevated above the normal range (4.6--6.2 pg/ml) in all subjects. ADH-immunoreactive material was detectable in all primary lung tumours (range 9--1080 pg/mg wet weight, n = 7) and metastases (range 5--63 pg/mg wet weight, n = 9) obtained from the hyponatraemic patients. A statistical relationship existed between plasma and tumour ADH concentration in six patients where both measurements were performed. Three patients had small cell carcinomas (two oat cell and one anaplastic) without overt hyponatraemia. ADH-like material was detectable in the lung tumours (18 and 1.1 pg/mg wet weight) and liver metastases (4 and 1.0 pg/mg wet weight) of two patients but not in the third. Four of the remaining patients had squamous cell carcinomas and two had adenocarcinomas. None had hyponatraemia. ADH-like material was undetectable in all lung tumours, metastatic tumours and uninvolved tissue from these patients. ADH extracted from the pituitaries of four patients ranged from 6400--13200 pg/mg wet weight. ADH immunoreactive extracts of six lung tumours and nine metastases (all oat cell) showed the same pattern on elution from a Sephadex G-25 column. A large peak, which made up 65% of the total activity, was eluted in the same position as synthetic arginine vasopressin and contained comparable amounts of immunoreactive and bioactive ADH. Two smaller peaks (8 and 27% of total activity) were eluted in positions of higher molecular weight and contained more immunoreactive than bioactive ADH. In contrast, three of four pituitary extracts showed only a single peak which eluted in the same position as marker vasopressin.     

NYCTOHEMERAL VARIATION AND SUPPRESSIBILITY OF PLASMA ACTH IN VARIOUS STAGES OF CUSHING''S DISEASE

In order to define nyctohemeral plasma ACTH secretory patterns, frequency plasma ACTH samples were obtained in seven patients with untreated Cushing's disease (i.e. pituitary-dependent Cushing's syndrome), five Cushing's patients treated by bilateral adrenalectomy, four of whom had Nelson's syndrome, and one patient with 21-hydroxylase deficiency (congenital adrenal hyperplasia). A nyctohemeral rhythm of plasma ACTH concentration was apparent in the one patient with the adrenogenital syndrome but not in those with Nelson's syndrome or Cushing's disease. The effect of graded doses of dexamethasone, 2,8 or 32 mg per 24 h period, on plasma ACTH concentrations was studied in patients with untreated or treated Cushing's disease or Nelson's syndrome. In all of these hypercorticotrophic states, the mean plasma ACTH concentraton was not significantly affected by the smallest dose of dexamethasone, was partially suppressed by the intermediate dose, and further suppressed by the largest dose. In contrst, the patient with congenital adrenal hyperplasia and elevated plasma ACTH concentrations showed complete suppression of plasma ACTH levels following the smallest dose of dexamethasone. These findings indicate that there is resistance to ACTH suppression by dexamethasone in all stages of Cushing's disease and suggest that negative feedback of glucocorticoids may be involved in the pathogenesis of this disease.     

Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement.
Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N-acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide.
Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration-dependent effect of sodium channel blockade on defibrillation energy requirements in patients.     

Serum interleukin-8 in inflammatory bowel disease

To investigate the relationship between serum concentrations of interleukin-8 (IL-8) and disease activity in inflammatory bowel disease, serum IL-8 concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in 93 patients. Interleukin-8 levels were compared with plasma interleukin-6 (IL-6) levels in 80 of these patients. Interleukin-8 levels were also measured in ten patients with active Crohn's disease, before and after treatment with a defined formula polymeric diet. Of these patients, 70 out of 93 IL-8 concentrations were below the detection limit of the assay. Levels were higher in patients with active ulcerative colitis (median < 20 pg/mL, 75th centile value = 190) compared with inactive disease (median and 75th centile value < 20; P 0.05). Interleukin-8 concentrations correlated with a combined score for disease severity and extent (P= 0.01). Thirty-eight per cent (8/20) of patients with active Crohn's disease also had high levels of IL-8 but there was no significant difference between active and inactive disease. There was no correlation between serum IL-8 and plasma IL-6; on the contrary, very few patients had raised blood levels of both cytokines. In the diet treated group, serum IL-8 fell significantly after treatment (median = 37 pg/mL, range < 20–4615 before treatment, median < 20, range < 20–104 after treatment; P= 0.03). The results suggest that although IL-8 may be involved in the inflammatory process in inflammatory bowel disease, it is a poor marker of disease activity.     

Comparison of Complete and Incomplete Revascularization by Coronary Angioplasty for Unstable Angina

When a "culprit lesion" can be identified in a patient with unstable angina, it may be possible to achieve clinical improvement with incomplete revascularization. We analyzed actuarial survival free of an event (severe angina, myocardial infarction, coronary artery bypass graft, or death) at 6, 12, 18, and 24 months in 83 patients with multi-vessel disease and unstable angina who had undergone successful percutaneous transluminal coronary angioplasty (PTCA); revascularization was complete in 31 patients and incomplete in 52. Event-free survival in 85 patients with single-vessel disease and unstable angina who had undergone successful PTCA also was analyzed. Event-free survival at 24 months was worse in the multivessel disease patients than in the single-vessel disease patients (62% vs 85%; P = 0.001). Multivessel disease patients with complete revascularization had the same event-free survival as those with incomplete revascularization (63% vs 61%; P NS). Diagnostic angiograms revealed thrombus or an irregular ulcerated lesion in 42 of the multivessel disease patients. The event-free survival of these 42 patients was not different from that of the multivessel disease patients as a whole (64% vs 60%; P NS). We conclude that in patients with multivessel disease and unstable angina the event-free survival after PTCA is poorer than in patients with single-vessel disease and unstable angina. In the former patients, event-free survival does not necessarily depend on the completeness of revascularization. The outcome of patients who have intra-coronary thrombus or an irregular ulcerated lesion resembles the outcome of patients who lack these findings. (J Interven Cardiol: 1988:1:1)     

A Snapshot of Immunotherapy for Rheumatoid Arthritis

Apoptosis represents the cell's innate ability to self-destruct and is an important cellular response mechanism against virus infection. The purpose of this series of articles is to critically review significant advances in important areas of virology with respect to virus infection and its relationship with apoptosis. In the Introduction to the first issue (Intern. Rev. Imm., 22: 321–326, 2003), we dedicated these entire two issues to the memory of Dr. Lois K. Miller. Dr. Miller's Ph.D. advisor, Robert D. Wells, and two of her students, Rollie Clem and Lorena Passarelli, contributed touching remembrances of their associations with Dr. Miller. In the Introduction to this issue, an overview of key points of discussion detailed in each chapter of the two issues is provided. The future of the emerging field of viral apoptosis remains bright, indeed.     

Antigenic variation in Giardia lamblia: cellular and humoral immune response in a mouse model

Neonatal mice (CR:NIH:S) were infected with a cloned human isolate of Giardia lamblia (GS/M-83-H7) and the surface antigens of the intestinal trophozoites, as well as the cellular and humoral immune responses, were analysed during the course of infection. Infections in mice peaked 2-3 weeks after inoculation and were self-cured by day 42 post-infection (p.i.). The proportion of trophozoites expressing the Mr 72,000 surface antigen of the initial inoculum had decreased by day 12 and approached zero by day 22 p.i., similar to infections in humans. The predominant parasite-specific humoral response was an IgM- and IgG-isotype directed to the original Mr 72,000 surface antigen as well as other antigens. T-lymphocytes (predominantly LY4(CD4)+) isolated from Peyer's patches 12 days p.i. and later showed a significant proliferative response to Giardia lamblia antigens. Spleen and lymph node cells showed no lymphoproliferative response. T-cell blot analysis revealed the presence of dominant T-cell epitopes in the areas of Mr 200,000-75,000 and less than 50,000 polypeptides. No response was demonstrated in the Mr 72,000 region (migration site of the major surface antigen), suggesting T-cell dependent mechanisms are most likely not responsible for the surface antigen switch which occurred during the course of infection. This model infection can be used to study the role of immunological mechanisms in Giardia lamblia variant antigen switching and in the control of infections.