No abstract

We report a 21-year-old white male with Kallman’s syndrome (gonadotropic hypogonadism, hyposmia and sensorineural hearing loss) with extensive brain calcification, demonstrated for the first time by computed tomography. The pattern and anatomic distribution of the extensive brain calcification is nonspecific, being indistinguishable from those seen in other causes of brain calcification (principally diseases related to a disturbance in calcium metabolism), despite the normal serum calcium levels found in this patient. This syndrome, therefore, should be considered along with Cockayne’s, Kearns-Sayre and Down’s syndromes, tuberous sclerosis, carbonic anhydrase II deficiency, congenital mental deficiency and idiopathic familial basal ganglia calcification as another developmental cause of brain calcification, which usually show no disturbance in serum calcium level.

Seven infants in congestive heart failure underwent high dose angiocardiography for diagnosis of severe congenital heart disease and subsequently displayed delayed opacification of the gallbladder. Biliary excretion of sufficient volume to opacify the gallbladder occurred despite structurally normal kidneys and no evidence of renal failure. Decreased renal clearance of contrast due to generalized diminution of glomerular filtration is postulated. The high doses of contrast and slow renal clearance allowed a relatively increased rate of hepatobiliary excretion and subsequent observation of the opacified gallbladder on abdominal radiographs. This phenomenon may not be as uncommon as is generally thought but its timing and location often do not allow an opportunity to make this observation.