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Pentachlorophenol (PCP) is a widely applied insecticide and fungicide, particularly in wood preservation. Significant amounts of this compound have been reported in human serum, adipose tissue and urine. PCP is even found in people not occupationally exposed to this toxin or not living in PCP-treated log-houses. Substantial concentrations of this possible neurotoxic agent were detected in the cerebrospinal fluid (CSF) of 16 neurologic patients as measured by a high resolution gas chromatographic method using electron capture detection. This is the first report on PCP levels in (human) CSF. The observed level in CSF ranged from 0.24 up to 2.03 micrograms/L (ppb), with an average value of 0.75 +/- 0.49. The cerebrospinal fluid level did not correlate with the serum PCP concentration nor with the protein level of the cerebrospinal fluid.

A patient is described with post-thyroidectomy hypoparathyroidism and basal ganglia calcifications. The patient presented with a tonic-clonic seizure. The calcifications shown on CT scan were extensive in the basal ganglia, the bifrontal periventricular white matter and even in the brainstem. The white matter with calcifications displayed a high signal intensity on MRI, probably due to a different stage of the calcifying process in the white matter than in the basal ganglia. A severe dystonic reaction was observed after phenothiazine therapy and is discussed.

Documentation of gastrointestinal lesions in Brucella infections is sparse. A case of Brucella melitensis type 3 infection accompanied by erosive lesions of the colon, observed by endoscopy and histopathologic examination, is reported. Such gastrointestinal lesions have not been described since 1934. Before 1934 only postmortem observations are recorded.

For many decades lead has been considered to be one of the causes of chronic renal failure. A critical analysis of the available epidemiological studies, however, indicates that the relationship between lead exposure and the development of chronic renal failure is largely circumstantial. Indeed, several aspects remain obscure: relative and absolute risk, risk factors, duration of exposure, pathology and diagnostic criteria. Moreover, methodological problems related to cohort selection (i.e. the 'Healthy worker effect'), study design and definition of renal dysfunction may limit the value of the epidemiological results. Although the available literature suggests that lead may play a direct or contributory role in the development of chronic renal failure it is concluded that additional detailed epidemiological studies are required.

Thromboembolic complications may occur in inflammatory bowel disease. Recently, we had the opportunity to observe a case of a cerebral arterial thrombosis in a young patient with active ulcerative colitis. Investigation of blood coagulation revealed a temporary Protein C, Protein S and Factor II deficiency. To our knowledge, this is the first reported case of a temporary Protein C and S deficiency in a patient with thrombosis and inflammatory bowel disease.

One of the major side effects of aminoglycoside antibiotics (AG) is ototoxicity. The authors review the literature revealing many controversies on every aspect of this side-effect. Although epidemiological studies have to face the problem of reliable evaluation techniques, the incidence of cochleo- and vestibulotoxic side-effects has been estimated at 7.5% for each. Netilmicin appears to be less ototoxic. No definite risk factors can be proposed, although age, length of therapy, bacteremia, fever, liver and renal dysfunction are probably very important parameters. Most pathological changes at the cochlear level follow a clear spatial sequence, showing unspecific, degenerative lesions, involving every structure of the cochlea. This makes it impossible to draw etiopathological conclusions. Recent pharmacokinetic studies have rejected the 'accumulation theory' of AGs in perilymph, while also in endolymph no accumulation can be found. Only a few data are available on inner ear tissue levels. Among the different pharmacodynamic hypotheses on the action of AGs, binding of the drug to acidic glycosaminoglycans in the stria vascularis, and interference by the drug with phosphoinositide metabolism in the hair cells seem to be of major importance.

This article describes a case of infective aortic valve endocarditis due to Fusarium oxysporum occurring 4 years after coronary artery bypass grafting. It is the first reported case of endocarditis caused by Fusarium.

Two cases of enterolithiasis of the small intestine are reported. In the first patient, enterolithiasis recurred two years after the discovery of an enterolith due to a stricture of the ileum. An enterolith was found in a huge jejunal diverticulum at post-mortem examination in the second patient. Incidence and diagnosis of enterolithiasis are briefly discussed.

We present the case of a 68-year-old man with a peculiar coincidence of cardiac pathologic findings: a huge left atrial myxoma, mitral insufficiency, a high degree atrioventricular block and three-vessel disease. The myxoma was vascularized from a dilated sinus arteriosus branch, giving rise to neovascularization at the base of the tumor. Blood from the neovascularization gathered into a large cavern which fistulated into the left atrium, responsible for a left-to-left cardiac shunt.

The occurrence of torsades de pointe is often associated with the use of drugs. We report three cases of amiodarone-induced torsades de pointe. Although a lot of amiodarone-induced torsades de pointe have been published, a review of all these cases and the underlying risk-factors has never been made.

Poisoning often affects the ear, nose, mouth and throat. Sialorrhea, stomatitis, oropharyngeal dryness, a burning sensation in the mouth, rhinitis and nasal septal perforation, hearing loss and vestibular disturbances can be the result of intoxications by poisonous plants, growing or used in Europe and the United States. This article has not the intention to be exhaustive, but to give a synopsis of this topic.