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Yellow nail syndrome is characterized by nail changes, respiratory disorders, and lymphedema. In a yellow nail patient with a skeletal titanium implant and with gold in her teeth, we found high levels of titanium in nail clippings. This study aims to examine the possible role of titanium in the genesis of the yellow nail syndrome. Nail clippings from patients with one or more features of the yellow nail syndrome were analyzed by energy dispersive X-ray fluorescence. Titanium was regularly found in finger nails in patients but not in control subjects. Visible nail changes were present in only half of the patients. Sinusitis with postnasal drip and cough was the most common complaint. The dominant source of titanium ions was titanium implants in the teeth or elsewhere. The titanium ions were released through the galvanic action of dental gold or amalgam or through the oxidative action of fluorides. In other patients the titanium was derived from titanium dioxide in drugs and confectionary. Stopping galvanic release of titanium ions or canceling exposure to titanium dioxide led to recovery. In one patient with a titanium implant, the symptoms recurred after renewed exposure to titanium. Yellow nail syndrome is caused by titanium

Mucosal biopsies from 48 patients with and 9 without amalgam tattoos were analysed with respect to their mercury content, distribution of mercury in the tissue, and histological tissue reactions. The distribution of mercury was assessed by autometallography (AMG), a silver amplification technique. The mercury content was determined by energy dispersive X-ray fluorescence (EDXRF), a multielemental analysis. Mercury was observed in connective tissue where it was confined to fibroblasts and macrophages, in vessel walls and in structures with the histological character of nerve fibres. A correlation was found between the histopathological tissue reaction, the type of mercury deposition, the intensity of the AMG reaction, and the mercury content. Mercury was also found in patients with amalgam dental fillings but without amalgam tattoos.

Summary:Previously symptomatic and permanently asymptomatic carriers of a gene mutation for acute intermittent porphyria as well as matched controls were screened with regard to a series of variables of possible relevance to the development of porphyric symptoms. The basis for the study was a concept of acute porphyria as a condition of a permanent system overload of oxidative stress, with long term effects on hepatic and renal tissue, and with instances of periodic overload of free radicals giving rise to acute neurologic involvement.Leukocyte concentrations of manganese, calcium, iron and zinc, as well as erythrocyte calcium differed between the groups, acute intermittent porphyria gene carriers, irrespective of previous porphyric illness, showing significantly higher levels than the controls.Manganese was found to be the most discriminative component of all the 78 variables investigated, accounting for about 98 per cent of the variance between the groups. An increment, by a factor of four, in cellular manganese is suggestive of an increase, in acute intermittent porphyria, of a manganese associated enzyme, e. g. glutamine synthetase, pyruvate carboxylase or mitochondrial Superoxide dismutase. The best fit into the model considered is provided by a theory focused on Superoxide dismutase, induced in response to Superoxide anion radical produced from aminolaevulinic acid. In porphyria gene carriers seemingly resistent to porphyric manifestations, an increase in potentially prooxidant cellular iron is matched by a proportional increment in manganese, i.e. presumably by a corresponding mitochondrial Superoxide dismutase induction. This mechanism is not operative in porphyric individuals prone to development of neuropsychiatric symptoms.In acute intermittent poiphyria with a history of porphyric illness there is a positive correlation between erythrocyte manganese and serum folate and a negative correlation between leukocyte ferrochelatase activity and serum cobalamin concentration. This may mirror a role of the cobalamin-folate system in the acute porphyric process.

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