A case with Listeria meningitis during administration of mycophenolate mofetil for pemphigus vulgaris

© 2007 The Authors 1447 JEADV 2007, 21, 1413–1450 Journal compilation © 2007 European Academy of Dermatology and Venereology (0.3 g/L). Electroencephalography did not show any aftermath neither aetiological element at the morning after crisis. Blood amounts of cortisol, TSH, IGF1, insulin, C peptide, glucagon, ACTH, and PTH were normal. Due to the severity of the symptoms and the risk of death, the patient was transferred to an intensive care unit. The situation was complicated by a respiratory distress syndrome due to an inhalation pneumopathy. The patient was treated with antibiotics, and sedation by midazolam chlorhydrate and sufentanil, with cisatracurium, was done. All symptoms resolved. One month later, burning pain was attenuated, and there was no relapse of convulsive, hallucinatory, or dysautonomic symptoms. Hence, this patient presented with severe neurological complications. Hypothermia, orthostatic hypotension, hypoglycaemia, and bradyarythmia may be considered as symptoms of an autonomic peripheral neuropathy. We cannot be sure that these complications are directly due erythermalgia, but this patient did not take any drug and did not suffer from any endocrinological disease, and there are many arguments to suggest that sympathetic neurones are involved in erythermalgia. On the contrary, epilepsy attack seems to be secondary to hypoglycaemia, and hallucinations are probably related to insomnia. Some cases of familial epilepsy have been related to mutations of voltage-gated sodium channels. But Nav1.7 channels are not expressed by central neurons and their role in the genesis of epilepsy in our patient is probably irrelevant. Dysautonomic symptoms have never been observed in primary erythermalgia. Two cases of erythermalgia in the course of inherited sensory neuropathies have been reported. Some adrenergic abnormalities were detected in patients with erythermalgia. Erythermalgia is due to a small-fibre neuropathy involving C-fibres, as shown by microneurography sympathetic skin response test and thermoregulatory sweat testing. Nav1.7 mutations are known to depolarise resting membrane potential in cells that express the mutant channels. These mutations render sensory neurones hyperexcitable and sympathetic neurones hypoexcitable. Our observation is the clinical confirmation of these data.