Biomedical subjects

D Thierman-Duffaud

Publications and source records attributed to D Thierman-Duffaud.

10 recordsLinked to original sources

PubMed1992

[Acute hepatitis caused by wild germander. Hepatotoxicity of herbal remedies. Two cases].

While interest in herbal therapy is clearly increasing in Western countries, there are few available data about hepatotoxicity of herbal remedies. We report on two women who had severe acute hepatocellular liver injury occurring within one to two months of treatment with Wild Germander (Teucrium chamaedrys L.), a herbal medicine for losing weight. Clinical course was favorable after the treatment was discontinued. Involuntary rechallenge in one case resulted in reappearance of symptoms of liver injury. When a patient presents with unexplained hepatic abnormalities, it may be worthwhile to consider non-orthodox self-treatment with herbal remedy as a potential cause. Only systematic observation will provide a clear picture of the incidence of liver injury caused by herbal medicines.

Acute Disease↗

PubMed1989

A comparison of metoclopramide and trimebutine on small bowel motility in humans.

Trimebutine meleate and metoclopramide increase small bowel motility. The present manometric study of the human normal interdigestive duodeno-jejunal motility demonstrated two different pharmacological effects in 15 healthy volunteers. Trimebutine constantly induced a premature phase 3 activity (0.81 +/- 0.4 min after a 100-mg intravenous injection) with patterns similar to spontaneous phase 3. Metoclopramide increased the motility index (contractile activity) during phase 2 without inducing a premature phase 3. No significant variations in plasma motilin concentration were noticed after either trimebutine or metoclopramide. The pancreatic polypeptide concentration rose significantly after metoclopramide injection.

Adult↗

PubMed1987

Induction of phase 3 of the migrating motor complex in human small intestine by trimebutine.

The effects of trimebutine, a drug used in the treatment of various gastrointestinal motility disorders, have been investigated fed and fasted healthy subjects. Duodenojejunal motility was recorded manometrically with a 4-lumen probe. Trimebutine 50 or 100 mg was injected i.v. 3 or 25 min after observing a spontaneous Phase 3 complex in the fasted state. Other experiments were done in the postprandial state and after intravenous naloxone 0.8 mg. In the fasted state, trimebutine 100 mg, injected 25 min after a spontaneous Phase 3 complex consistently induced a premature Phase 3 complex. The mean duration of the migrating motor complex cycle decreased from 86.4 +/- 10.8 min to 32.5 +/- 1.0 min. Trimebutine 50 mg injected 3 and 25 min after a spontaneous Phase 3 complex did not significantly modify the periodicity of the migrating motor complex. Trimebutine 100 mg initiated Phase 3-like activity in the post-prandial state. Previous intravenous administration of naloxone 0.8 mg (Narcan) suppressed the stimulatory action of TMB. Thus, trimebutine is able to modify the motility pattern in the small intestine of man, possibly by acting at opioid receptors.

Adult↗

PubMed1987

[Effect of trimebutine on the motility of the normal human small intestines: mechanism of action].

The effects of intravenous trimebutine (TMB) on duodenojejunal motility were investigated in normal subjects in fed and fasted states. The motility was recorded manometrically. In the fasting state TMB 100 mg, 25 min after a spontaneous phase 3 (P3) constantly induced a premature P3. The mean period (means +/- SE) of the migrating motor complex (MMC) cycle decreased from 84 +/- 10.9 to 32.5 +/- 1.0 min. TMB 50 mg, 3 and 25 min after a spontaneous P3 did not significantly modify the periodicity of MMC. TMB 100 mg initiated P3-like activity in post-prandial state. Previous administration of a low dose of naloxone suppressed the stimulating action of TMB. After a TMB injection the motilin plasma level did not vary; a brief increated of PP plasma level was observed. It may be concluded that in the human small intestine TMB included a typical modification of the motility pattern. Opiate receptors might be involved.

Adult↗

PubMed1983

[Involvement of the peripheral and pyramidal nervous system in Crohn disease. Determining role of folic acid deficiency].

We report on the case of a 16-year-old male patient who presented with a peripheral neuropathy remarkable by the severity of pain, the proximal involvement and the association with an underlying myelopathy. All these symptoms coincided with an acute exacerbation of Crohn disease (regional enteritis) involving mainly the duodenojejunal segment, and were ascribed to a major folic acid deficiency, with total recovery following supplementation. In this connection we recall the various neurological symptoms induced by folic acid deficiency. We point out how difficult it is to prove the responsibility of such deficiencies in the production of neurologic diseases, mainly because of the possible intrication with other pathogenic factors: combined deficiencies or direct action of the factor responsible for the deficiency on the nervous system. Guidelines for solving these difficulties are suggested.

Adolescent↗

PubMed1981