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Four patients with Felty's syndrome developed massive upper gastrointestinal bleeding due to oesophageal varices. The underlying hepatic pathology in all 4 was nodular regenerative hyperplasia. This appears to be a difficult histological diagnosis to make, having been initially reported as normal on percutaneous biopsy or as fibrosis or cirrhosis on wedge biopsy. This series brings the total number of cases reported in the English literature of this association to 12, suggesting a definite symptom complex. The portal hypertension seems to be due to a combination of increased splenic blood flow and postsinusoidal resistance. The clinical importance of this syndrome is that the appropriate therapy for bleeding oesophageal varices appears to be shunt procedure such as a splenorenal shunt with splenectomy, which should be well tolerated.

Summary The author first reviews, on the basis of personal and literature data, the main changes in three major parameters of potassium metabolism: serum potassium; daily urinary output of potassium; exchangeable potassium (Ke) at the three stages of the course of liver cirrhosis. The action of K-sparing diuretics (spironolactone, triamterene, amiloride) on these parameters is analysed. Although the introduction of these diuretics in our therapeutic armamentarium has resulted in a major advance, i.e. the quasi-total elimination of iatrogenic hypokalaemia and hypokalaemia-induced portacaval encephalopathy in the cirrhotic, the limits of their action on K metabolism are underlined: they may moderately enhance urinary K output; following cessation of their administration, a ‘rebound’ in urinary K output may be noted. Finally, Ke may still continue to decrease during their administration, indicating an aggravation of the underlying disease. It was also found that a rise in serum K and/or Ke during amiloride administration did not prevent the elevation of plasma renin activity usually induced by volume and/or Na depletion.

Summary The term ‘functional renal failure’ has been used to describe the renal failure developing in advanced cirrhosis in which tubular function and structure remain intact. It may develop spontaneously, in which case prognosis is poor, but may be secondary to gastro-intestinal haemorrhage or excessive use of diuretics, in which case correction of the precipitating factor leads to improvement in renal function. It is suggested that the renal failure is due to a reduction in effective circulating plasma volume.

A study of renal tubular acidification in two cirrhotic patients with functional renal failure and partly compensated metabolic acidosis. Unlike renal distal tubular acidosis, but alike what is seen in organic renal failure, renal acidification was nearly normal and could not account per se for the development of metabolic acidosis. The multiple cause of the association in the cirrhotic of hyperchloremia and hypobicarbonatemia are reviewed (respiratory alkalosis, metabolic acidosis due to renal failure, distal tubular acidosis) and the diagnostic procedures outlined.

The authors report the case of a 72 year old woman affected by gamma heavy chain disease in whom the heavy chain was detected in the serum and the urine as well. Further study of the paraprotein showed that it belonged to the gamma 1 subclass. This observation was unusual because of the presence of a 15 year-long peripheral neuropathy and the existence of various auto-antibodies, especially intrinsic factor antibody.

The discrepancy between the finding of hypernatremia--a manifestation of extra-cellular fluid depletion--and the presence of edema--a manifestation of increased ECF--is best explained by the patient's inability to mobilize edemas to compensate intra-vascular dehydratation. Treatment must start by the administration of hypotonic solutions, as hypernatremia is dangerous for the brain.

In 2 similar groups of alcoholic cirrhotics with definite hepatic failure, the results of the oral administration of 25-hydroxycholecalciferol and of vitamin d2 on calcemia and urinary calcium excretion were studied. 25-hydroxycholecalciferol definitely increases calcemia and urinary calcium excretion, this action being superior to that of vitamin D2. This action which occurs, at least in part, by an increase in intestinal calcium absorption, deomonstrated the true nature of the "hepatic block" of vitamin D2 in alcoholic cirrhosis and the value of the administration of 25-hydroxycholecalciferol.

Description of a Programme started in 1979. Its aim is to deliver reliable, scientifically established and target-oriented information. It comprises two activities. a) The preparation and diffusion of documents, the Technical Reviews (TRs) adjusted to the needs of 4 groups of users: physicians and university level workers; primary care workers; policy makers; mass media specialists. The TRs deal with major child health problems. They are in French, English and Spanish and can be freely circulated, translated and reproduced. b) The organisation of joint health and mass media specialists meetings (five have been held: two in Africa, two in Asia and one in Latin America). The methods used to develop the Programme and its future are considered.

The authors report 4 cases of carcinoma of the intestine, stomach, ovary and breast, association with monoclonal Ig. Clinical and laboratory analysis showed, in particular, that the immunoglobulin was present in small quantity and that there was no Bence-Jones protein in these 4 cases, that the bone marrow was little, or practically unmodified. The authors then discuss the nature, whether by chance or not, of this association the differential diagnosis with major monoclonal dysglobulinemia, e.g. myeloma or Waldenström's disease, and the significance in a cancer patient, of the discovery of Igmc. According to the authors, although in a few cases the tumour may induce development of a clone secreting Igmc, usually carcinoma and Igmc are independent from one another and are due to a common mechanism : reduction in cell immunity, according to Burnet.

Regencrative nodular hyperplasia (RHN) is a rare condition, the diagnosis of which is based upon histological findings. It is seen in Felty's syndrome with portal hypertension (PHT), as was the case in the patient reported here. This was a 72-year-old man, with long standing rheumatoid arthritis, hepatosplenomegaly, a neutrophil leucopaenia and oesophageal varices responsible for recurrent haematemeses. Despite a portocaval anastomosis, the patient died from postoperative acute hepatic failure. Histological study revealed changes in the hepatocytes and the reticulin system typical of RNH without cirrhosis. The relationship between Felty's syndrome and RHN, as well as the mechanism of the hypertension, are discussed in the light of cases from the literature.

A case is reported of heat stroke associating dehydration, anuria, muscle disorders and early hypercalcemia. All disorders disappeared within 48 hours with rehydration. Early hypercalcemia differs from late hypercalcemia reported at resumption of diuresis. Early hypercalcemia might result from blood concentration with hyperproteinemia and release of bone calcium under the action of PTH. Its prognosis is good, which is not the case of late hypercalcemia.