Spontaneous Regression of Budd-Chiari Syndrome (Hepatic Venous Occlusion) in a Young Female

ABSTRACT. Hultcrantz R, Angelin B, Einarsson K, Friman L (Departments of Internal Medicine and Roentgenology, Serafimer Hospital, and Department of Internal Medicine, Huddinge University Hospital, Karolinska Institute, Stockholm, Sweden). Spontaneous regression of Budd-Chiari syndrome (hepatic venous occlusion) in a young female. Acta Med Scand 1987; 221:503–7. A case of occlusion of the hepatic veins in an 18-year-old girl is presented. The onset was sudden with massive ascites and markedly impaired general condition. The diagnosis was based on liver biopsy and angiograms of the caval and hepatic veins as well as of the celiac artery. No predisposing factors could be found. The patient was treated conservatively with laparo-centesis and diuretics. Clear improvement was seen after two weeks, and after four weeks she had no ascites and could be discharged. All liver function tests were then normalized. After three months, all diuretics could be withdrawn, and in the following 11 years she has remained completely recovered. The case illustrates that also widespread thrombi of the hepatic veins may sometimes rapidly dissolve spontaneously, with apparent total reconstitution of hepatic function. This case is unusual since previously reported cases have had high mortality rates and, in surviving cases, operative procedures or large doses of diuretics have been required to control the ascites.     

Inadequate Erythropoietin Response to Anaemia in HIV Patients: Relationship to Serum Levels of Tumour Necrosis Factor-Alpha, Interleukin-6 and Their Soluble receptors

Severe anaemia is a frequent complication in advanced HIV infection. In our study we investigated the interaction between cytokine network, HIV infection and erythropoietin (Epo) response with increasing anaemia levels. No correlations could be established between circulating tumour necrosis factor (TNF)-alpha and any of the examined parameters. However, a negative correlation was found between haemoglobin values and soluble TNF receptor levels (sTNF-R-I: r  = −0.54; P  < 0.001; sTNF-R II: r  = −0.47; P  < 0.001) as well as interleukin-6 levels ( r  = −0.29; P  < 0.001). In contrast, no significant increase in log[Epo], counterbalancing haemoglobin decline and paralleling the rise in sTNF receptors, was found. In patients classified as stage III, according to the Centers for Disease Control (CDC) classification, the erythropoietin response was significantly more impaired than in patients from CDC groups I and II ( P  < 0.001). The results of this study suggest that similar to its action in vitro , activation of the TNF/TNF-R system may impair erythropoietin production in HIV-associated anaemia. Due to the brief half-life of TNF-α, this activation is particularly reflected by elevations of soluble TNF receptor levels.     

Should nitrous oxide be discontinued before desflurane after anaesthesia with desflurane/N2O?

Background : The appearance of hypoxaemia immediately after anaesthesia with nitrous oxide may be partially explained by diffusion hypoxia. This study was undertaken to evaluate circulatory and respiratory variables during emergence after desflurane/nitrous oxide anaesthesia, and whether there are any differences depending on which gas is discontinued first. Methods : 20 patients were studied after gynaecological laparoscopic surgery. The depth of anaesthesia was reduced 10 min prior to the emergence by stopping the administration of one of the two inhalational agents. Desflurane was discontinued first in Group 1, nitrous oxide in Group 2. Ventilation was controlled with E'C0₂ maintained at 5% until the administration of the second anaesthetic gas was discontinued. Thereafter, the patients breathed spontaneously. Results : The PaC0₂ at which the respiratory drive reappeared after controlled normoventilation was similar in both groups, 6.1–6.5 kPa, and extubation was performed after 10–11 min. At extubarion, the end–tidal C0₂ and total MAC were similar in the groups, about 6.2 vol% and 0.16, respectively. Mean arterial blood pressure was significantly higher in Group 1. The cardiac output increased in both groups from about 6 1/min at the conclusion of anaesthesia to 9.0 and 7.6 1/min at 15 min in the recovery period. End–tidal O₂ decreased and CO₂ increased in both groups during the first 10 min in the recovery period. pH was reduced at 15 and 30 min in both groups. Conclusion : Irrespective of which agent was discontinued first, there was an increase in cardiac output, decrease in oxygenation and a modest acidosis in the first 30–min recovery period. The only significant difference between the groups was in mean arterial blood pressure in the early emergence phase with a greater MAP when N₂O had been used until the conclusion of anaesthesia.     

Skeletal Muscle Adaptations to Physical Training in Type II (Non-insulin-dependent) Diabetes Mellitus

Seven middle-aged men with manifest type II diabetes mellitus underwent an endurance training programme for 10–15 weeks. The maximal aerobic capacity, as well as the endurance capacity, was improved by 10% (p<0.05). The intramuscular glycogen store increased by more than 80% (p<0.05) from 350 μmol/g dw (dry weight), and the activities of citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase increased by more than 50% (p<0.05) and 30% (p<0.05). The activity of glycogen synthase was decreased by approximately 20% (p<0.05), whereas lactate dehydrogenase remained unchanged. Capillaries/fibre and fibre area increased by more than 50% (p<0.05) and 30% (p<0.05) leaving the area of supply constant. Training did not influence fasting blood lipids and glucose, glycosylated hemoglobin, oral glucose tolerance, and insulin response to an oral glucose load measured 72 hours post-exercise. It is concluded that patients with manifest type II diabetes, as normoglycaemic individuals, adapt to physical training. However, no persistent effect on glucohomeostasis and lipaemia is produced by short-term training in the diabetic patients.     

Evening administration of melatonin and bright light: Interactions on the EEG during sleep and wakefulness

Both the pineal hormone melatonin and light exposure are considered to play a major role in the circadian regulation of sleep. In a placebo- controlled balanced cross-over design, we investigated the acute effects of exogenous melatonin (5 mg p.o. at 20.40 hours) with or without a 3-h bright light exposure (5000 lux from 21.00 hours–24.00 hours) on subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in healthy young men. The acute effects of melatonin, bright light and their interaction were measured on the first day (treatment day), possible circadian phase shifts were assessed on the post-treatment day. On the treatment day, the evening rise in subjective sleepiness was accelerated after melatonin and protracted during bright light exposure. These effects were also reflected in specific changes of EEG power density in the theta/alpha range during wakefulness. Melatonin shortened and bright light increased sleep latency. REMS latency was reduced after melatonin administration but bright light had no effect. Slow-wave sleep and slow-wave activity during the first non-rapid eye movement (NREMS) episode were suppressed after melatonin administration and rebounded in the second NREMS episode, independent of whether light was co-administered or not. Self rated sleep quality was better after melatonin administration whereas the awakening process was rated as more difficult after bright light. On the post-treatment day after evening bright light, the rise in sleepiness and the onset of sleep were delayed, independent of whether melatonin was co-administered or not. Thus, although acute bright light and melatonin administration affected subjective sleepiness, internal sleep structure and EEG power density during sleep and wakefulness in a additive manner, the phase shifting effect of a single evening bright light exposure could not be blocked by exogenous melatonin     

Coronary Sinus Isolation: No Myth But Reality

Coronary sinus (CS) has muscular connections with atria and is often targeted to complete left atrial ablation for curing atrial fibrillation; however, complete CS isolation is difficult to achieve with hard end points. We present a distinctive case of complete isolation of CS that had an unusual muscular connection. (PACE 2012; 35:e322–e324)     

Studies on the A, B, O(H) Blood Groups on Human Cells in Culture

HeLa cells were used in the mixed agglutination reaction to determineoptimal conditions for demonstrating blood group H activity by this method.The following parameters were studied in the mixed agglutination reaction:(1) derivation of cell line, (2) cell viability, (3) effects of antibody titer, (4)source and type of antibody.

Studies with primary human amnion cells indicated that over a 30-day period of cultivation in vitro there were losses in specific ABO blood groupactivity.

Addition of blood group precursors to establish human amnion celllines FL-J and F-D indicated that blood group B antigen could be synthesizedand maintained in vitro.

Submitted on September 8, 1964 Accepted on October 26, 1964     

Effects of etanercept on urine neopterin levels in patients with psoriasis in a controlled, open-label study

Neopterin is an immunological marker of cellular immune activation. Etanercept is a tumor necrosis factor-α (TNF-α) antagonist that decreases excessive levels of TNF-α associated with inflammatory disease down to physiological levels. The objective of this study was to investigate urine neopterin levels in psoriatic patients treated with etanercept, to study the effect of etanercept as a TNF-α blocker on urine neopterin levels. Urine neopterin levels and urine neopterin/creatinine ratios were measured by high-performance liquid chromatography in 22 patients with psoriasis before and after treatment with etanercept. Results were compared with a group of 20 healthy volunteers, and 20 patients with inflammatory skin diseases as control groups. Urine neopterin levels, neopterin/creatinine ratios and Psoriasis Area and Severity Index (PASI) scores were evaluated at baseline, and the 12th and 24th week after treatment. Urine neopterin levels were significantly elevated in the psoriatic group compared with control and inflammatory skin diseases groups ( P  < 0.05). Urine neopterin levels were significantly reduced after etanercept treatment. Statistically we did not find any correlation between neopterin levels and PASI scores. Our findings indicate that urine neopterin concentrations may reflect the disease activity in psoriasis, and may be used as a marker for monitoring disease activity and response to treatment with etanercept in psoriatic patients.