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Philippe Hantson

Publications and source records attributed to Philippe Hantson.

At least 19 recordsLinked to original sources
PubMed2006

Pneumoproteins as markers of paraquat lung injury: a clinical case.

OBJECTIVE: To describe the changes in lung-specific secretory proteins in biological fluids in a fatal case of paraquat ingestion and to present immunostaining data obtained on postmortem lung tissue specimens. METHODS: A 20-year-old man committed suicide by ingesting 100ml of a 20% paraquat solution. Surfactant associated proteins A (SP-A), B (SP-B) and Clara cell 16kDa protein (CC16) were determined in the serum and on broncho-alveloar lavage performed 18h after admission. Renal failure progressed rapidly and the patient died from refractory hypoxia. Immunostaining studies using antibodies directed against CC16, SP-A and SP-B were performed on postmortem lung tissue specimens. RESULTS: Serum CC16 seemed to increase gradually with the progression of renal impairment. Serum SP-A and SP-B levels increased before any significant changes in pulmonary gas exchanges. The immunostaining study showed that the labeling for SP-A and SP-B was reduced or absent following paraquat toxicity, while Clara cells were relatively preserved. CONCLUSIONS: The elevation of serum CC16 with paraquat toxicity is probably mainly related to a reduced renal clearance. The increase of serum SP-A and SP-B could reflect an increased lung to blood leakage, independently of the alteration of the renal function.

Acute Kidney Injury↗
PubMed2006

Bilateral carotid-cavernous fistula following head trauma: Possible worsening of brain injury following balloon catheter occlusion?

A 68-year-old woman developed right pulsatile exophtalmos in the early course of facial and head trauma. Investigations by visual evoked potentials suggested the presence of a bilateral prechiasmatic lesion. Intraocular pressure rapidly increased and a high-flow carotid-cavernous fistula was evident at carotid angiography. Immediately after the treatment of the right fistula by balloon embolisation, a systolic bruit was noted over the left eyeball and angiography disclosed the presence of a left carotid-cavernous fistula that was treated by the same approach. The patient developed brain oedema leading to death and we postulated that reestablishment of normal cerebral perfusion after abrupt closure of the fistulas may have played a deleterious role.

Aged↗
PubMed2006

Electrocardiographic changes with segmental akinesia after chloral hydrate overdose.

We report a case of deliberate ingestion of 12.5 g chloral hydrate in a 25-year-old psychiatric patient. Coma and life-threatening ventricular dysrhythmias were observed soon after ingestion. Repeated electrocardiographic examination was consistent with ischemic changes appearing on day 3. They were associated with segmental abnormal left ventricular wall motion by echocardiography. A coronary angiogram was performed and was normal. Toxic metabolites of chloral hydrate, trichloroethanol and trichloroacetic acid were found in the urine until day 7. This case illustrates that with halogenated aliphatic hydrocarbons, sustained changes in cardiac contractility may occur in addition to early life-threatening ventricular dysrhythmias.

Adult↗
PubMed2006

Prolonged unconsciousness in a patient on automated peritoneal dialysis.

A 79-year-old man with end-stage renal disease treated by automated peritoneal dialysis was referred to the emergency department for altered consciousness. The first investigations, including toxicology screening, failed to reveal the precise etiology. The patient was treated for a possible seizure. After the progression of central nervous system depression with bradypnea, the patient was intubated and mechanically ventilated. It appeared later on that he had ingested by mistake one of his wife's medications, baclofen. Baclofen was detected in the blood sampled on admission at a level above the therapeutic range. Baclofen is mainly excreted by the kidney. A short-term administration of low-dose of baclofen is not effectively removed by peritoneal dialysis and may result in prolonged but reversible coma.

Aged↗
PubMed2006

The value of morphological neuroimaging after acute exposure to toxic substances.

Many toxic agents induce brain dysfunction and/or lesions. Modern neuroimaging techniques, such as CT and more recently magnetic resonance imaging (MRI), are able to demonstrate toxic brain lesions at both early and delayed phases of disease progression. In the early phase, neuroimaging enables the detection of acutely injured brain areas responsible for sudden onset of neurological dysfunction, but the severity and the extension of brain lesions on neuroimages do not necessarily parallel the severity of the clinical status. In the chronic phase, when neurological dysfunction has become permanent, neuroimaging allows precise identification of neuroanatomical sequelae that do not necessarily match the severity of the chronic neurological impairment. Papers in the medical imaging literature have dealt mainly with the brain changes induced by 'chronic exposure' to toxic substances such as solvents or heavy metals. This article selectively reviews the main radiological changes observed on CT/magnetic resonance (MR) neuroimages after 'acute exposure' to industrial products (methanol [methyl alcohol], ethylene glycol), environmental agents (cyanide, carbon monoxide), pharmaceuticals (insulin, valproic acid) and illicit substances (heroin, cocaine). Different kinds of lesions, which lack specificity for toxic injury, can be observed on radiological images, but deep grey matter lesions with symmetrical distribution throughout basal ganglia are most often seen. However, such findings have also been reported after anoxic-ischaemic insults or during severe metabolic disturbances. Lesions in the white matter may also be present in the case of acute exposure to toxic agents. The true prognostic value of toxic-induced brain changes in the acute phase in CT or MR studies is unclear, although serial MRI may add new information as may quantitative or molecular imaging techniques such as the MR diffusion-weighted imaging or MR spectroscopy.

Acute Disease↗
PubMed2005

Invasive aspergillosis in association with criminal arsenic poisoning.

A 26-year-old man suffered acute arsenic poisoning after a poisoning attempt. He developed multiple organ failure including encephalopathy, bleeding disorders, pancreatitis, renal and hepatocellular impairment. Generalized erythroderma also developed within one week after admission. The developed acute respiratory distress syndrome and Aspergillus fumigatus was isolated from the endotracheal aspirate. Despite intensive care support, antidote administration and various epuration techniques, the patient died on day 26 from subarachnoid bleeding. An autopsy was obtained and the concentration of arsenic was determined in different tissues. Multiple abscesses due to Aspergillus fumigatus were seen in the lungs, myocardium and kidneys. This uncommon complication in a previously immunocompetent patient could be related to impaired immunity directly caused by arsenic poisoning.

Adult↗
PubMed2005

Acute liver failure with renal impairment related to the abuse of senna anthraquinone glycosides.

OBJECTIVE: To report a case of chronic ingestion of very large amounts of senna fruits as an herbal tea, possibly leading to severe hepatotoxicity. CASE SUMMARY: A 52-year-old woman who had ingested, for >3 years, one liter of an herbal tea each day made from a bag containing 70 g of dry senna fruits, developed acute hepatic failure and renal impairment requiring intensive care therapy. The severity of the hepatic failure was reflected by the increase in prothrombin time (international normalized ratio >7) and the development of encephalopathy. Liver transplantation was discussed, but the patient ultimately recovered with supportive therapy. Renal impairment was consistent with proximal tubular acidosis, also with marked polyuria refractory to vasopressin administration. Suprisingly, large amounts of cadmium were transiently recovered in the urine. DISCUSSION: Cassia acutifolia and angustifolia plants are widely used as laxatives. Their chronic abuse may be associated with serious manifestations, including fluid and electrolyte loss, with chronic diarrhea. Severe hepatotoxicity is unusual, but could be explained by the exposure of the liver to unusual amounts of toxic metabolites of anthraquinone glycosides (sennosides). An objective causality assessment suggests that hepatotoxicity was possibly related to senna laxative abuse. Regarding nephrotoxicity, there are no available human data on sennosides, while experimental models suggest that anthraquinone derivatives may also accumulate in the kidneys. The finding of high urinary concentrations of cadmium would suggest contamination of the herbal tea by metals, but this hypothesis could not be verified. CONCLUSIONS: Ingestion of large doses of senna laxatives may expose people to the risk of hepatotoxicity.

Acidosis↗
PubMed2005

Analysis of two imported cases of yellow fever infection from Ivory Coast and The Gambia to Germany and Belgium.

BACKGROUND: Yellow fever remains one of the great burdens for public health in the endemic regions in Africa and South America. The under reporting of yellow fever cases in the respective regions and lack of international interest leads to an underestimation of the constant danger in these areas. Non-vaccinated travelers take a high risk without the effective protection of YFV 17D vaccination. OBJECTIVES: Two YF cases were imported to Europe in the last 4 years. We characterized two yellow fever virus (YFV) isolates from severely infected patients coming back from Africa, Ivory Coast and The Gambia, by genome sequencing and phylogenetic analysis. STUDY DESIGN: The virus infections in different organs were analyzed with pathological, immunohistological, electronmicroscopical and quantitative real-time PCR methods. RESULTS AND CONCLUSION: High virus loads in spleen and liver (2.4 x 10 (6) to 3 x 10 (7)GE/mL) demonstrated by real time PCR show massive virus replication leading to extraordinary progression of the disease in these patients. Immunohistological and electronmicroscopical analysis confirms virus particles in liver tissue. In all other organs no virus could be detected. A fast, specific and sensitive virus PCR detection is recommended for diagnostic of acute infections. The further sequence alignments show that the new isolates belong to the type II West African strain with great homology to over 40-year old YF isolates from Senegal and Ghana. The divergence observed was on average 3.3%, ranging from 0.0% to 5.0% in the coding region of Gambia 2001 strain and 2.9 %, ranging from 0.0% to 4.3% in the coding region of the Ivory C 1999 strain. Most mutations (5.0%/4.3%, respectively) occurred in the envelope protein.

Base Sequence↗
PubMed2005

Electrocardiographic changes after head trauma.

We report the case of a patient who developed, a few days after a closed head injury, marked electrocardiographic changes mimicking an acute coronary event, in the absence of actual cardiac damage. The electrocardiographic changes were fully reversible, paralleling the neurologic status. Neuroimaging examinations excluded subarachnoid hemorrhage or space-occupying hematoma, but demonstrated diffuse axonal injury using susceptibility-weighted magnetic resonance techniques. This kind of traumatic brain injury thus may be responsible for a pseudo-acute myocardial ischemic syndrome.

Adult↗
PubMed2005

[Biological and pathological data in a case of yellow fever imported from the Gambia].

A 47-year-old woman developed fever and asthenia 1 week after having traveled to Gambia. Four days after the first symptoms, she was transferred to the intensive care unit. She was in poor general condition, with anuria and jaundice. Liver function tests showed severely disturbed function and the diagnosis of yellow fever infection was made by RT-PCR in this patient who had not been vaccinated. Encephalopathy appeared on day 7 and death occurred on day 8 due to massive gastrointestinal bleeding. At autopsy, extensive panlobular liver necrosis was observed together with the presence of numerous Councilman bodies in the three hepatic zones.

Anuria↗
PubMed2005

Recurrent seizure and sustained encephalopathy associated with dimethylsulfoxide-preserved stem cell infusion.

We report the case of a patient who received two infusions of dimethylsulfoxide (DMSO) cryopreserved autologous peripheral blood progenitor cells (PBPCs) after myeloablative chemotherapy for a relapsing lymphoma. A 49-year-old man presented an episode of tonic-clonic seizure over a few minutes after the start of each infusion and developed a profound and sustained but reversible encephalopathy with coma after the second infusion. The patient's neurological condition correlated well with the electrophysiological findings (electroencephalogram and multimodality evoked potentials) and, to a lesser extent, with the radiological abnormalities (magnetic resonance imaging). Severe but reversible neurological complications may occur with the infusion of PBPCs cryopreserved with DMSO.

Cryopreservation↗
PubMed2005

Propofol infusion syndrome associated with short-term large-dose infusion during surgical anesthesia in an adult.

In this case report we describe a case of propofol infusion syndrome in an adult after a short-term infusion of large-dose propofol during a neurosurgical procedure. Large-dose propofol (9 mg.kg(-1).h(-1)) was given for only 3 h during surgery and was followed by a small-dose infusion (2.3 mg.kg(-1).h(-1)) for 20 h postoperatively. The patient had also received large doses of methylprednisolone. He developed a marked lactic acidosis with mild biological signs of renal impairment and rhabdomyolysis but no cardiocirculatory failure. There were no other evident causes of lactic acidosis as documented by laboratory data. We believe this is the first report of reversible lactic acidosis associated with a short duration of large-dose propofol anesthesia.

Acidosis, Lactic↗
PubMed2004

[Organ procurement after poisoning].

BACKGROUND: There is an increasing gap between the number of patients on the waiting list and the number of transplanted patients. In France, more than 10000 patients waited for an organ transplantation in 2002. Due to the graft shortage, "marginal" donors are now considered. The patients who present brain death after accidental or voluntary poisoning belong to this category. EPIDEMIOLOGY: The data available from European or North American organ procurement organisations show that poisoned donors represent about 1% of all organ donors. It seems likely that a significant number of poisoned patients are not referred because poisoning is regarded as a contraindication to organ donation. When organ procurement can be achieved, the results expressed as recipient survival or graft survival are quite encouraging. TOXIC PRODUCTS: The most frequently involved toxins are either drugs (psychotropic agents, analgesics...), illicit substances, or environmental agents (gases, alcohols...). The literature data are discussed; some issues remain controversial. PRACTICAL APPROACH: Several criteria have to be applied when poisoned patients are considered as potential organ donors. Besides a firm diagnosis of "brain death", the knowledge of the "target organs" of poisoning is of paramount importance, together with careful analysis of the toxicokinetics and toxicodynamics. In most cases, routine biological and morphological data are sufficient to assess graft function.

Graft Survival↗
PubMed2004

Comparison of clinical, magnetic resonance and evoked potentials data in a case of valproic-acid-related hyperammonemic coma.

Magnetic resonance (MR) multimodality evoked potentials (MEPs) and clinical findings were correlated in a 47-year-old epileptic man in whom parenteral valproic acid (VPA) therapy induced severe comatose hyperammonemic encephalopathy without biological signs of hepatotoxicity (or hepatocytic dysfunction). Although the plasma VPA level remained within a normal therapeutic range, the ammoniemia increased to a toxic peak level at 411 micromol/l 24 h after symptom onset, requiring VPA therapy discontinuation. Brain MR monitoring demonstrated early cytotoxic edema evolving into delayed vasogenic edema and final brain atrophy. Concomitantly to abnormalities within the brainstem on MR images, an increase in brainstem conduction at MEPs and clinical disturbance of brainstem reflexes were observed at the initial phase of the disease course. Later, the resolution of the MR and MEPs abnormalities paralleled the clinical recovery of the reflexes.

Atrophy↗