Biomedical subjects

J D Tempe

Publications and source records attributed to J D Tempe.

At least 37 records · Page 2Linked to original sources

PubMed1976

[Hyperosmolar comatose states].

A recently determined entity, hyperosmolar coma is a good example of a clinical candition attributable to a fundamental alteration, namely extracellular hyperosmolarity. The principal stages in its history are summarised. The laws governing osmosis are recalled and the various features of the sndrome are studied. Attention is drawn to the clinical peculiarities (skin dehydration), biological features (record glycaemia value), and EEG data noted in 17 cases treated in a resuscitation centre over a period of seven years, along with the treatment employed-this being still a matter of debate. Reference is also made to 52 cases of acute drunkenness in a study of the relation between blood alcohol values and plasma hyperosmolarity.

Adult↗

PubMed1976

[Angioneurotic hereditary edema. 3 faimilial cases].

The study involved three families with hane. This disorder differs from the simple condition by its preferential visceral localisation (digestive and, above all, the glottis), its hereditary nature and the existence of a biological abnormality affecting the serum complement system (absence of enzyme activity of C1 esterase inhibitor in the serum of sufferers). The cases reported illustrate the serious prognosis of this condition (four deaths by asphyxia in one family) in the absence of specific therapy. This disorder, although rare, represents a fundamental problem in general pathology by virtue of the enzymatic, immunological and genetic processes which it involves.

Adolescent↗

PubMed1976

[Hyperosmolar Coma].

For some little time it has been known that hyperosmolar coma is a clinical condition which may arise from various causes and yet is based on a fundamental pathophysiological disturbance: extracellular hyperosmolarity, usually accompanied by hyperglycemia or hypernatremia. The clinical and biological picture is easily recognizable and requires immediate and massive rehydration with hypotonic solutions. Many pathological uncertainties still exist, but one thing is certain and of great importance: in many cases, hyperosmolar coma is the result of errors or negligence: for this reason it is essential know this syndrome so that it may be better avoided.

Adult↗

PubMed1975

[Hereditary coproporphyria. 7 cases].

Hereditary coprophyria, known since 1955, is a rare variety of hepatic porphyria. The clinical picture is similar to that of acute intermittent porphyria with certain minor differences; neurological manifestations being rarer in particular. The essential biological characteristic is the massive excretion, in the urine and faeces, of coproporphyrins whilst the excretion of porphobilinogen and delta-amino-laevulinic acid is only slightly increased. As in acute intermittent porphyria, certain medications have an adverse effect, especially the barbiturates. The exact nature of the biochemical lesion is not understood but its hereditary nature has been demonstrated. 25 families have been reported in the literature up to the present time. The authors report two cases of hereditary coproporphyria with peripheral paralysis and respiratory failure, the outcome being fatal in one case. Study of the families led to the discovery of 3 other cases in the second family and 2 latent forms in the first.

Adolescent↗

PubMed1974