Postpartum amenorrhoea-galactorrhoea associated with hyperprolactinaemia and pituitary enlargement in primary hypothyroidism.

We report a 36-year-old woman with primary hypothyroidism revealed by postpartum amenorrhoea-galactorrhoea associated with hyperprolactinaemia and suprasellar pituitary enlargement on magnetic resonance imaging (MRI). On thyroid hormone replacement therapy all clinical, biochemical, radiological and endocrine abnormalities disappeared. Hyperplasia of pituitary thyrotrophs and/or lactotrophs seems to be responsible for the pituitary enlargement seen on MRI.

Endotoxin-induced liver damage in rats is minimized by beta 2-adrenoceptor stimulation.

OBJECTIVE AND DESIGN: To investigate the effects of beta(2)-adrenoceptor (beta(2)-AR) stimulation on endotoxin-induced liver damage and systemic cytokine levels in rats. SUBJECTS: Standard male Wistar rats. TREATMENT: A disease-model of lipopolysaccharide (LPS)-induced acute systemic inflammation was used. The beta(2)-selective AR agonist clenbuterol was administered before, during, and after LPS-challenge to investigate its effects on the acute inflammatory response and associated liver-failure. METHODS: The following parameters have been measured in plasma: TNF alpha, IL-1 beta, IL-6, IL-10, AST, ALT, and Bilirubin. Liver histological examination was performed to look for changes in tissue morphology. RESULTS: Administration of clenbuterol (p.o.) one hour before, or intravenous at the same time as LPS-challenge resulted in a marked reduction of plasma levels of TNF alpha, IL-1 beta, and IL-6. A change both in plasma-level and in time-concentration profile of the anti-inflammatory cytokine IL-10 was found. Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. Clenbuterol administration after LPS challenge failed to inhibit TNF alpha-release but reduced liver-damage. Simultaneous use of the beta(2)-AR antagonist propranolol augmented LPS-induced liver failure, suggesting a role of endogenous adrenoceptor-agonists in prevention of organ-failure during systemic inflammation. CONCLUSIONS: The results indicate that a selective beta(2)-AR agonist might be used as an additional therapeutic agent in the clinic for the treatment of (acute) systemic inflammatory disorders in order to reduce or prevent subsequent liver failure.

[Recurrent attacks of angioedema ascribed to the use of estrogen preparations and a pregnancy (hereditary angioedema type 3)]. / Recidiverende aanvallen van angio-oedeem toegeschreven aan het gebruik van oestrogeenpreparaten en aan zwangerschap (hereditair angio-oedeem type 3).

A woman experienced recurrent attacks of angioedema from the age of 17 to 21 years and these appeared to be associated with the use of oestrogens. After stopping the medication her complaints disappeared, but they returned during her first pregnancy. Angioedema is a serious condition, which can lead to acute abdominal symptoms, oedema of the upper respiratory tract and death by asphyxiation. The most well-known cause is hereditary angioedema, an autosomal dominant disorder that is characterized by deficiency of C1 esterase inhibitor (C1-INH). Recently, a new type of hereditary angioedema (type 3) has been reported that occurs exclusively in women and is characterised by oestrogen dependency (both endogenous and exogenous), normal C1-INH concentrations and severe attacks of angioedema, which are clinically indistinguishable from the classic form.

Oedema disease is associated with metabolic acidosis and small intestinal acidosis.

Limited information is available about the pathogenesis and pathophysiology of oedema disease (OD). Oedema disease is caused by specific enterotoxemic Escherichia coli (SLTIIv-toxin producing) strains; however, the same strains are also found in non-afflicted pigs. Furthermore, it is unclear how the 80 kDa SLTIIv-toxin can pass the intestinal barrier. In the present paper, piglets showing signs of acute OD were anaesthetised, instrumented and cardiovascular and intestinal parameters were determined at 0, 1, 2 and 3 hours. Healthy piglets from the same herd were used as a control. Cardiac output, blood pH and bicarbonate, small intestinal intramucosal pH, and (pulmonary) blood pressure were significantly lower in OD-pigs than in control pigs. It is concluded that OD is associated with metabolic and intestinal acidosis. Intestinal acidosis is known to increase macromolecular permeability. This suggests that once OD has developed, influx of SLTIIv-toxin into the blood stream is facilitated, thus perpetuating the disease. Since intestinal permeability appears to be central in OD, it is argued that post-weaning events increase intestinal permeability and predispose individuals to OD.

Asystole during combination chemotherapy for non-Hodgkin's lymphoma: the acute tumor lysis syndrome.

The acute tumor lysis syndrome is a rare condition that has most frequently been documented in patients with rapidly dividing myeloproliferative and lymphoproliferative malignancies. It is characterized by the development of hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, acute renal failure and metabolic acidosis, as a result of massive tumor cell destruction, usually secondary to effective cytotoxic treatment. We want to present the case history of a 62-year-old woman who died from cardiorespiratory arrest during combination chemotherapy for non-Hodgkin's lymphoma due to acute tumor lysis syndrome. Despite general preventive measures, severe electrolyte abnormalities developed within 18 h of the start of chemotherapy. The general guidelines for the management of this potentially fatal oncologic emergency are discussed, with special emphasis on the pathogenetic mechanisms and risk factors in our patient.

Chronic tophaceous gout in the elderly.

Gout in the elderly seems to represent a special subgroup. The presentation is often atypical and drug treatment poses special difficulties. We present two elderly patients with large subcutaneous tophi leading to grotesque deformities. Their clinical features, risk factors, diagnosis and treatment are discussed. Although the appearance and radiographic changes caused by tophi are characteristic, the definitive diagnosis of tophaceous gout is made by aspiration and crystal analysis, as is illustrated by colour photographs.

Pneumomediastinum: an unusual complication of bronchial asthma in a young man.

We report a patient with bronchial asthma who presented with pneumomediastinum, pneumopericardium, pneumoretroperitoneum, pneumorrhachis and extensive subcutaneous emphysema, after a period of coughing. Pathogenesis, diagnostic procedures and treatment of pneumomediastinum and its complications are discussed.

[Meningo-encephalitis and hydrocephalus caused by Epstein-Barr virus]. / Meningo-encefalitis en hydrocefalus veroorzaakt door Epstein-Barr-virus.

In a 35-year-old woman who presented with acute somnolence, confusion and slow irregular breathing, Epstein-Barr virus (EBV) meningoencephalitis was diagnosed after serological testing and a polymerase chain reaction of the cerebrospinal fluid. She developed papilloedema and bilateral nervus abducens paresis. A CT scan showed generalized oedema of the brain and triventricular hydrocephalus. Treatment with a ventriculoperitoneal shunt and ganciclovir led to complete recovery. Meningoencephalitis is a not uncommon, yet rarely reported complication of infectious mononucleosis. It usually runs a mild course with spontaneous and full recovery. Hydrocephalus secondary to aqueduct stenosis is a complication of Epstein-Barr virus (EBV) meningoencephalitis which has not been reported in adults before. The disease should be considered whenever the clinical condition deteriorates or neurological symptoms increase.

The potential role of hemofiltration in the treatment of patients with septic shock and multiple organ dysfunction syndrome.

Hemofiltration may improve the hemodynamics of septic shock and the survival of multiple organ dysfunction syndrome patients. The pros and cons of this statement are reviewed and the practical implications are discussed.

High volume hemofiltration improves hemodynamics and survival of pigs exposed to gut ischemia and reperfusion.

This study assesses the influence of high volume continuous hemofiltration on hemodynamics of pigs subjected to bowel ischemia/reperfusion. Twelve anesthetized and ventilated pigs were studied for 60 min during clamping of the superior mesenteric artery (SMA) and subsequently for 90 min after release of the clamp, while measuring global hemodynamics, SMA flow, and jejunal pCO2. They were randomly divided into two groups: pigs in "control" group were subjected to SMA clamping only. Pigs in "hemofiltered" group received zero-balanced, high volume, veno-venous hemofiltration with the removal of 6000 ml of ultrafiltrate/h, starting 30 min before clamping until 90 min after removal of the SMA clamp. Thereafter, pigs were allowed to awake and sacrificed after 24 h for macroscopic assessment of bowel damage. The drop in cardiac output (CO) during SMA clamping in the hemofiltered group was 2.5 +/- .3 L/min (mean +/- SE) (1.1/4.0; 95% confidence interval) smaller than in the control group. At the end of the experiment, mean arterial pressure (MAP) in the hemofiltered group was 33 +/- 6 (19/48) mmHg higher than in the control group, CO was 2.0 +/- .2 (1.2/2.8) L/min higher in the hemofiltered group. After 60 min of SMA clamping, left ventricular stroke work in the hemofiltered group was 35 +/- 4 (14/56) g higher than in the control group, and higher by 33 +/- 3 (21/46) g at 90 min after release of the SMA clamp. The mean pulmonary artery pressure, right atrial pressure, pulmonary artery wedge pressure, SMA flow and bowel wall pCO2 at different time points did not differ between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Infusion of ultrafiltrate from endotoxemic pigs depresses myocardial performance in normal pigs.

We previously showed a beneficial effect of hemofiltration on hemodynamics of endotoxic shock pigs. To test the hypothesis that this effect of hemofiltration is caused by convective removal of factors that adversely affect hemodynamics during endotoxemia, we infused ultrafiltrate from endotoxic shock pigs into healthy pigs. Their hemodynamics were compared with those of pigs who were infused with ultrafiltrate from healthy pigs. Twelve anesthetized and ventilated pigs were hemodynamically monitored for 150 minutes following the infusion of 2 L of ultrafiltrate from 12 donor pigs. The acceptor pigs were randomly divided into two groups; group 1 received ultrafiltrate from pigs who were hemofiltered after the infusion of 0.5 mg/kg endotoxin over 30 minutes; group 2 served as a control group, receiving ultrafiltrate from healthy donor pigs. Group 1 showed a decrease in mean arterial pressure of 28 +/- 7 mm Hg (mean +/- SEM) versus an increase of 17 +/- 3 mm Hg in group 2 (P < 0.4). Mean pulmonary artery pressure increased more in group 1 than in group 2 (9 +/- 2 mm Hg versus 1 +/- 1 mm Hg, P < .04). The decrease in cardiac output in group 1 was greater than in group 2 (3.3 +/- 0.2 L/min v 0.3 +/- 0.3 L/min, P < .02) and was due to a decrease in stroke volume. The decrease in right ventricular ejection fraction was also greater (0.15 +/- 0.02 v 0.01 +/- 0.00, P < .01). Systemic vascular resistance, right atrial pressure, right ventricular end-diastolic volume, pulmonary wedge pressure and heart rate did not differ between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of hemofiltration in the critically-ill intensive care unit patient: present and future.

The development of acute renal failure (ARF) in intensive care unit (ICU) patients carries a poor prognosis. Today, most cases are no longer an isolated organ dysfunction but are part of a multiple system organ failure syndrome. Recently developed renal replacement therapies allow adequate metabolic control, even in highly catabolic and hemodynamically unstable patients. Whether these newer continuous techniques have resulted in a better outcome of these patients is unclear. Recent data suggest a possible beneficial effect of hemofiltration on outcome of ICU patients and the course of human and experimental septic shock, which may be ascribed to the removal of inflammatory mediators. The purpose of this paper is to review the history of hemofiltration techniques and to assess their present and future role in the management of ICU patients. Although hemofiltration has been shown to improve hemodynamics of experimental septic shock, convincing evidence that hemofiltration improves outcome of ICU patients is lacking. Available data suggest that high ultrafiltrate volumes may be needed to achieve clinically important beneficial effects of hemofiltration in these patients. Prospective, randomized trials in homogeneous patient groups are needed to assess the role of hemofiltration in patients with septic shock or multiple system organ failure.

High volume hemofiltration improves right ventricular function in endotoxin-induced shock in the pig.

This study assessed the influence of continuous high volume hemofiltration on right ventricular function of pigs with endotoxin induced shock. Eighteen anesthetized and ventilated pigs were studied for 240 min after the start of infusion of 0.5 mg/kg endotoxin over 30 min. Right ventricular ejection fraction (RVEF) was measured by rapid response thermodilution technique. After endotoxin infusion, the pigs were randomly divided into 3 groups: group 1 as a control group, receiving endotoxin only, group 2 to observe the effects of zero balance high volume veno-venous hemofiltration with removal of ultrafiltrate at a rate of 6000 ml/h, and group 3 to evaluate the effect of the extracorporeal circuit itself on RVEF. The decline of RVEF in group 2 was less than in group 1 (0.04 +/- 0.02 vs 0.21 +/- 0.03 (mean +/- SEM); p less than 0.001). The decline of RVEF in group 3 (0.24 +/- 0.02) was more pronounced than that in group 1 (p less than 0.05). The differences in the course of RVEF between group 1 and group 2 could not be explained by differences in heart rate, preload or afterload. Cardiac output and mean arterial pressure were significantly higher in group 2 than in group 1 (p less than 0.01). It is concluded that in this model, high volume hemofiltration improves RVEF and cardiac performance by removal of vasoactive mediators, responsible for myocardial depression.

Hemodynamic aspects of multiple organ failure.

Multiple organ failure (MOF) secondary to sepsis is associated with a high mortality. A large body of evidence suggests that the disturbed relationship between oxygen supply and oxygen uptake plays an important role in the pathogenesis of MOF. The relationship between oxygen-supply dependency and MOF and the practical implications of the relationship are reviewed. It is concluded that, apart from the all-important eradication of the source of the sepsis, optimizing oxygen transport is the best method of preventing the development of MOF. Since the effects of hemodynamic and ventilatory treatments on oxygen uptake are often unpredictable, the impact of the treatments on oxygen uptake should be evaluated directly.

Albumin abuse in intensive care medicine.

Albumin is a much abused and expensive drug in intensive care units. One of the motivations for its use is the prevention of pulmonary edema by enhancing the colloid osmotic pressure (COP). Fear of pulmonary edema has led to the formation of a magic (arbitrary) albumin value varying from one intensive care unit to another. Many intensive care units start substituting albumin when it is below 25 g/l. The objective of this paper is to look at the rationale of this policy. Our results show that in intensive care patients, with a variety of primary diagnoses, a poor correlation exists between COP and serum albumin concentration (r = 0.56; p less than 0.001). To get an index of the colloid osmotic status of the I. C.-patient measuring albumin concentration is useless and COP should be measured instead. From 19 patients with a COP in the 15.0-20.0 mmHg range (corresponding albumin range: 12.0-25.0 g/l) and from 10 patients with a COP in the 11.6-15.0 mmHg range (corresponding albumin range 10.5-19.2 g/l) none developed pulmonary edema. It is questionable if expensive, scarce albumin is the drug of choice with which to increase COP, for the mean increase (+/- SD) in COP after infusion of 100 grams albumin is 2.2 (+/- 1.5) mmHg (p less than 0.001). Adopting a COP action level of 15 mmHg can lead to considerable savings.