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Biomedical subjects

J D Tempe

Publications and source records attributed to J D Tempe.

13 recordsLinked to original sources
PubMed1979

[Immunoallergic acute haemolysis, thrombocytopaenia and acute renal insufficiency due to treatment with catechines (author's transl)].

The authors report the case of a 25-year-old patient who during discontinuous treatment with a venotropic agent containing catechines suffered from intravascular haemolysis, thrombocytopaenia and acute renal failure, the course of which was favourable with treatment by haemodialysis. Renal biopsy revealed lesions of acute tubulonephritis with a slight interstitial reaction but without immune deposits. The demonstration in the serum and on the red cells of the patient of anti-catechine antibodies confirmed the immunoallergic nature of the haemolysis. The existence of crossed allergy with another venotropic agent, leucocyanide, led to suspicion of the localisation of the antigenic site on the 3-4 dihydroxyphenyl portion of the catechine molecule.

Acute Kidney Injury↗
PubMed1979

Acute immunoallergic hemolysis with acute renal failure induced by catechin.

A young woman, 25 years old, being treated for her veinous system with EucatexR (a drug including catechins) presented an acute intravascular hemolysis with an acute renal failure. The finding of anti-Eucatex and anti-catechins antibodies in the serum and on the red cells of the patient proved the immuno-allergic nature of this hemolysis. A renal biopsy showed lesions of acute tubular nephritis but no immune depots. The patient recovered after a treatment by hemodialysis.

Acute Kidney Injury↗
PubMed1979

Accidental acute mercury vapor poisoning.

Accidental acute mercury vapor poisoning in three persons is reported. Three hours after exposure, symptomatology began by chills, vomiting, diarrhea and chest pain. Two patients, respectively 67 and 77 year old, presented severe pulmonary edema, then neurological symptoms with tremor and coma. This toxic pulmonary edema, which entailed artificial ventilation, was followed in both cases by an acute interstitial pulmonary fibrosis which led to death respectively after six and sixteen days. In the third case (a thirty eight year old patient) a skin rash, erythematous and pustuliform was observed. Analysis for total mercury by flameless atomic absorption showed very high mercury levels in blood and urine of the three patients. The effect of treatment by Dimercaptopropanol on renal excretion of mercury was studied. Optic and electron microscopy of the lung of the two patients who died showed the pulmonary changes of acute interstitial fibrosis.

Adult↗
PubMed1978

[Inappropriate secretion of anti-diuretic hormone in a case of intermittent acute porphyria (author's transl)].

The authors report the case of a patient who presented, during two exacerbations of intermittent acute porphyria, a grave psychiatric syndrome secondary to severe hyponatraemia. The later was due to inappropriate secretion of anti-diuretic hormone confirmed by laboratory tests and the stimation of anti-diuretic activity in the urine. The course was favourable under the effects of symptomatic treatment including sodium supplements and fluid restriction. The anti-diuretic syndrome disappeared on each occasion without sequelae at the time of regression of the exacerbation of porphyria.

Acute Disease↗
PubMed1978

Acute interstitial pulmonary fibrosis. Comparative light and electron microscopic study of 19 cases. Pathogenic and therapeutic implications.

Comparative light and electron microscopic studies of the lung were performed in 19 cases of diffuse acute interstitial fibrosis with various etiologies. Our observations emphasize the relation between hyaline membranes (HM) and the evolution of fibrosis. HM formation is due to fibrinous exudates and epithelial necrosis. This phenomenon recurs during the evolution of the disease and appears to be responsible for new waves of fibrosis. Its pathogenesis (humoral or neurovascular ...) remains hypothetical. Modifications of the alveolar epithelium consecutive to septal fibrosis can be clearly distinguished from "fibrinoid necrosis" -type lesions, which results in HM. The formation of HM is accompanied by fibroblastic stimulation which proceeds in spite of epithelial regeneration. The exact stimulus for the proliferation and collagen hypersecretion of fibroblasts remains to be determined. The use, in association with corticosteroid treatment, of a structural analogue of L lysine, acexamic acid, to impede collagenesis reveals encouraging perspectives for improved therapy.

Acute Disease↗
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↗