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We report a peculiar case of radiocontrast induced anaphylactoid shock following an intravenous pyelography, which was announced by an hyperacute bilateral parotid enlargement as the sole prodrome. From a review of the literature, two clinical presentation of iodide-induced sialadenitis are individualized according to their pathogenesis. In patients with normally functioning kidneys, the occurrence of a sialadenitis after a short delay (5 minutes to 24 hours) evokes an anaphylactoid mechanism. In patients with renal function impairment, the role played by extrarenal excretory pathways of iodinated compounds and especially the salivary glands, results in a delayed onset (1 to 5 days) of the sialadenitis due to an effect of toxicity.

The effect of chronic nicotine consumption on the morphology of the rat parotid gland was investigated. After nicotine-loading for 90 days with an average serum nicotine concentration of 78 +/- 10 ng/ml a significant increase of acinar cell volume was observed. The acinar cells contained an increased number of enlarged light, immature secretory granules. These findings were confirmed by morphometric analysis. Further an increase of the granular endoplasmatic reticulum, an enlargement of the Golgi complexes and an oedematous swelling of intraglandular autonomous nerves were found. Similar findings have been observed in the parotid gland of animals and also of humans chronically treated with the beta-adrenergic drugs aludrin and isoproterenol, and have been termed "sialadenosis". It seems likely that the observed morphological alterations are caused by a stimulation of glandular beta-adrenoceptors via a nicotine-induced release of catecholamines from the adrenals.

We report a case of bilateral submandibular and parotid sialadenitis subsequent to the injection of 100 ml of iopamidol (Niopam 370, Bracco) for an intravenous urogram. Iodide 'mumps' has previously been reported as a rare sequela of ionic contrast media injection. It is a mild and short lived condition, usually requiring no treatment.

Acute suppurative parotitis is a possible consequence of poisoning by organophosphates (E 605). The endogenous accumulation of acetylcholine results--as in the acute pancreatitis caused by poisoning with organophosphates--in massive hyperemia and an increased secretory activity with leakage of saliva into the tissue, in an activation of the kallikrein-kinin system, the phospholipase A2, and, ultimately, in toxic tissue lesions caused by lysolecithin and the superoxide-radical anion. In spite of antibiotic therapy this is followed by bacterial inflammation. Treatment consists in the administration of aprotinin (Trasylol) and corticosteroids. In the case of abscess formation surgical drainage is necessary.

Mechanical trauma of rat parotid gland led to an increase in the size of the gland (due to edema) with simultaneous activation of unspecific proteases, which were estimated at pH 7.6 using casein as a substrate. Administration of kallikrein-like salivary enzyme salivain into non-traumatized parotid gland caused also the same alterations. Complex application of two factors (trauma and salivain) resulted in distinct increase of the gland edema and the proteolytic activity. Administration of trasilol (inhibitor of proteases) decreased the pathogenic effects of salivain. After administration of salivain the alkaline phosphatase activity was shown to decrease in the parotid salivary gland.

Acute thyrotoxicosis following the ingestion of massive doses of thyroid hormone may pose diagnostic problems when the intoxication is clandestine, and may endanger life. The authors report here the case of a previously euthyroid young woman. The outcome was favourable, though assisted ventilation was required for a number of days. The particular features of this case (relatively low blood thyroxinelevels, anaemia and thrombocytopaenia following regression of the thyrotoxicosis, presence of parotid swelling) are discussed in the context of data from the literature.