Pheochromocytoma

We present a series of 11 patients with pheochromozytomas. We recommend screening for a catecholamine-producing tumor for every patient with hypertension. Screening and diagnosis are based on demonstration of an increased catecholamine production or -excretion. In our laboratory determination of urinary vanillin-mandelic-acid proved to be quite accurate. As 6 of our 11 pheochromozytomas were found extra-adrenally preoperative evaluation with regard to localization of these tumors appears as sound practice. According to our experience no single examination can be favoured. Therefore localization of these tumors is best accomplished by multiple diagnostic procedures. Morbidity and mortality depend directly upon preoperative recognition of a catecholamine-producing tumor and thus according management. We were able to gather data on 8 of 10 surviving patients 4--13 years postoperatively. Six of these are normotensive without any treatment.     

A highly sensitive C-terminal specific radioimmunoassay for human parathormone as a routine method (author's transl)

The basis for the radioimmunoassay of parathormone (PTH) as a routine method is a new sheep antiserum and a labelled PTH stabilised by a modification of the purification technique. The antiserum is obtained by immunisation with pig and cattle parathormone, it is C-terminal specific and is used in the assay in a final dilution of 1:35000. The affinity to human PTH is markedly greater than of the antisera used up to now. Two purification steps of 125J labelled bovine PTH lead to a tracer with a nonspecific binding of approximately 5% which increases to approximately 10% within 6 weeks. All normal sera investigated so far were measurable quantitatively (normal range 0.7 to 2.5 mul/equiv.). The lower sensitivity range was at 0.3 mul/equiv. All patients with chronic renal insufficiency and dialysis patients have an increased PTH concentration (3.9 to greater than 20 mul/equiv.). This also applies to patients with primary hyperparathyroidism (2.9 to greater than 20 mul/equiv.).     

Trichinosis causing extensive ventricular mural endocarditis with superimposed thrombosis. Evidence that severe eosinophilia damages endocardium

Clinical and morphologic observations are described in a 46 year old woman with fatal trichinosis. Attention is called to the occurrence of extensive ventricular endocardial damage with superimposed thrombosis; Evidence is presented to indicate that the most likely cause of the endocardial damage is the associated eosinophilia. The mechanism by which eosinophils damage endocardium, however, remains obscure.     

Pathogenesis of renal calculi in distal renal tubular acidosis. Possible role of parathyroid hormone

Elevated circulating levels of immunoreactive parathyroid hormone (PTH), hypercalciuria and renal calculi were found in 3 patients with distal renal tubular acidosis (RTA). Treatment with alkali resulted in a fall of PTH toward normal and a reduction in urinary calcium, but the frequency of urolithiasis was unchanged. In one patient in whom prolonged follow-up was possible, a subtotal parathyroidectomy was performed. This was followed by virtual cessation of stone formation despite persistence of the acidification defect. This study suggests that RTA may be associated with secondary hyperparathyroidism and that the consequent elevation in PTH may play a contributory role in the pathogenesis of renal calculi.     

Therapeutic approach to a cerebrovascular accident

The therapeutic approach to vascular lesions, which in fact represents the effective prevention of potential or recurrent brain damage, is discussed. The following problems are considered: asymptomatic localized vascular bruit; transient ischemic attack; minor strokes; progressive strokes; total strokes; and hemorrhages. Supportive therapy in the patient with brain damage is presented.     

Complete atrioventricular block and acute pancreatitis

A new, specific haemolytic assay for C2 is described using EAC43 (Antrypol) cells and serum deficient in C4 and C2 from a patient with hereditary angio-oedema. The method is simple and the results in pathological and normal sera correlate well with those obtained using the EA and C2-deficient serum method.