Pilot study of changes in stretched penile length 3 months after radical retropubic prostatectomy.

OBJECTIVES: To evaluate changes in stretched penile length after radical retropubic prostatectomy (RRP) in a prospective penile measurement study because an occasional complaint from patients after RRP is that their penis is shortened. METHODS: Thirty-one patients undergoing RRP by one surgeon were enrolled. The same physician completed measurements with a paper ruler to the nearest 0.5 cm. The stretched penile length was measured from the tip of the glans to the pubopenile skin junction. The measurements were taken in the preoperative holding area before the patient received anesthetic medication for the RRP and again 3 months postoperatively. The reliability and reproducibility of this measurement were confirmed. RESULTS: All 31 patients were measured at 3 months postoperatively. Of the 31 patients, 22 (71%) had a decrease in stretched penile length (range 0.5 to 4.0 cm). Seven were shortened 0.5 cm, 11 were shortened 1.0 to 2.0 cm, and 4 were shortened more than 2.0 cm. Five patients had no change, and in four the penile length was longer (range 0.5 to 1.0 cm). CONCLUSIONS: The results of this pilot study appear to show that the stretched penile length decreases after RRP at 3 months of follow-up in most men; 48% (15 of 31) had considerable shortening greater than 1.0 cm. If confirmed by other investigators, the cause of this change needs to be elucidated.

Use of tolterodine in children with dysfunctional voiding: an initial report.

PURPOSE: Tolterodine was recently approved for the treatment of incontinence and overactive bladder in adults, and has fewer side effects than oxybutynin. We evaluated the safety and efficacy of tolterodine in children with dysfunctional voiding. MATERIALS AND METHODS: We retrospectively reviewed our experience with 30 pediatric patients treated with tolterodine for a primary diagnosis of dysfunctional voiding. Patients were treated with adult doses of tolterodine and behavioral modifications. Standard definitions determined by the International Children's Continence Society were adapted to designate final treatment outcomes on medication as cured-greater than 90% reduction in wetting episodes, improved-greater than 50% reduction or failed-less than 50% reduction. RESULTS: The children were 4 to 17 years old (mean age 8.7) and were treated with tolterodine for an average of 5.2 months. The final dose was 1 mg. twice daily in 1, 2 mg. twice daily in 27 and 4 mg. twice daily in 2 patients. Wetting episodes were cured in 10 (33%), improved in 12 (40%), and failed to show improvement in 8 (27%) cases. Four patients (13.3%) reported side effects and only 1 discontinued the medication due to diarrhea. There were no reports of hyperpyrexia, flushing or intolerance to sunshine and outdoor temperature. CONCLUSIONS: Our results demonstrate that tolterodine at adult doses without titration can be used safely to decrease wetting episodes in children with dysfunctional voiding. Controlled clinical trials should be completed to evaluate further efficacy and safety in children.

Prenatally diagnosed autosomal recessive polycystic kidney disease: initial postnatal management.

We report a case of autosomal recessive polycystic kidney disease (ARPKD). A presumptive diagnosis was made after a late-term prenatal ultrasound revealed hypoplastic lungs, massive polycystic kidneys, and oligohydramnios. A full-term baby girl was delivered vaginally. Respiratory distress required intubation. Twelve hours after birth, she underwent bilateral nephrectomy and peritoneal dialysis catheter placement. The average kidney size was 150 g and 9.25 cm. Pathologic examination confirmed ARPKD. Peritoneal dialysis was started on the third day of life. The baby had no gross neurologic deficit. At 6 months of age, she was growing well, and the mother was a candidate to be a living-related kidney donor.

Priming of human polymorphonuclear leukocytes with granulocyte-macrophage colony-stimulating factor involves protein kinase C rather than enhanced calcium mobilisation.

Pretreatment of human polymorphonuclear leukocytes with the recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) enhances leukotriene biosynthesis in response to a receptor agonist (e.g. N-formyl-methionyl-leucyl-phenylalanine, fMLP) or a Ca(2+)-ionophore (e.g. ionomycin). This priming effect could be traced back to an elevated release of arachidonic acid from the phospholipid pools and hence an increased leukotriene biosynthesis by 5-lipoxygenase. Preincubation of polymorphonuclear leukocytes with GM-CSF did not influence the basal intracellular Ca2+ level and does not enhance cytosolic free calcium after stimulation with fMLP or ionomycin. Only a small increase in the second Ca2+ phase after receptor agonist stimulation was found. However, the Ca(2+)-threshold level necessary for the liberation of arachidonic acid by phospholipase A2 was decreased from 350-400 nM calcium in untreated cells to about 250 nM calcium in primed cells. This allows phospholipase A2 to be activated by a release of calcium from intracellular stores and by ionomycin concentrations which are ineffective in untreated cells. Protein biosynthesis inhibitors like actinomycin D (10 micrograms/ml) and cycloheximide (50 micrograms/ml) had no effect on the enhanced leukotriene biosynthesis in primed cells after stimulation with ionomycin. However, staurosporine (200 nM), an inhibitor of protein kinase C totally abolished the priming effect of GM-CSF after stimulation with ionomycin. The priming effect of GM-CSF could be mimicked by phorbol myristate acetate (PMA; 1 nM) and no additive or synergistic effect was found on leukotriene biosynthesis by simultaneous pretreatment with PMA and GM-CSF and stimulation with either fMLP or ionomycin. These results provide evidence that the enhanced arachidonic acid release in GM-CSF-primed polymorphonuclear leukocytes after stimulation with either fMLP or ionomycin involves activation of protein kinase C which, by a still unknown mechanism, reduces the Ca2+ requirement of phospholipase A2.

Regulation of leukotriene biosynthesis in human polymorphonuclear leukocytes.

Since the formation of leukotrienes in human polymorphonuclear leukocytes is Ca-dependent we have determined the Ca-pools involved and the enzymes affected. With PAF, fMLP and LTB4 as agonists the Ca-transients measured with Fura-2 showed the same height of the intracellular Ca-signal but an external Ca-component in decreasing magnitude. In parallel the activity of 5-lipoxygenase was also decreasing. 5-lipoxygenase was linearly dependent on Ca with saturation of around 350 nMol/l already provided by the release of intracellular Ca. Phospholipase A2, however, started to activate at about this concentration. Hence arachidonate is a limiting factor in stimulated leukocytes due to a limited influx of extracellular Ca.

The involvement of extracellular calcium in the formation of 5-lipoxygenase metabolites by human polymorphonuclear leukocytes.

We have addressed the question why in the presence of a Ca2+ ionophore human polymorphonuclear leukocytes generate leukotrienes in high yields, but in only low amounts after stimulation by receptor agonists like fMLF (fM, formylmethionine), leukotriene B4 or platelet-activating factor (PAF), although a significant release of intracellular calcium can be measured. Using ionomycin we can show that from the two enzymes involved, phospholipase A2 and 5-lipoxygenase, the first requires a threshold level of about 350-400 nM calcium whereas 5-lipoxygenase shows a linear dependence on calcium and saturates at this concentration. Our data indicate that the Ca2+ requirement of phospholipase A2 can only be met by an additional influx of extracellular calcium, whereas 5-lipoxygenase will operate already at levels provided by intracellular stores. Consequently, the complexing of extracellular calcium by EGTA stops phospholipase A2 activity immediately, whereas added arachidonate can be still adequately metabolized by intracellular Ca2+ release triggered by fMLF or PAF. Interestingly, PAF shows a stronger extracellular component in its Ca2+ transient than fMLF, and also generates more 5-lipoxygenase metabolites. However, a clear correlation between the amount of 5-lipoxygenase metabolites and the extracellular Ca2+ signal was lacking, since maximal activity was achieved before the bulk of the extracellular calcium was monitored. Ca2+ influx after PAF stimulation could be blocked after 2 min by EGTA, but a further increase in the formation of 5-lipoxygenase metabolites was observed. In contrast ionomycin-elicited 5-lipoxygenase activity could be stopped at any time shortly after EGTA addition.

[Destructive non-infectious spondyloarthropathy in chronic renal insufficiency]. / Destruierende, nicht-infektiöse Spondyloarthropathie bei chronischer Niereninsuffizienz.

The aetiology of destructive non-infectious spondylo-arthropathy has not been completely elucidated. Deposition of various crystals and of amyloid (beta-2-microglobulin) is a possible cause of this condition which has not been considered previously. The appearances of destructive non-infectious spondylo-arthropathy are illustrated by seven patients with renal insufficiency and on chronic haemodialysis; these were examined by conventional radiographs and by CT. It is possible to distinguish between the complete condition (five patients) and an early form (two patients). The differential diagnosis of the changes in the vertebral end-plates are discussed with reference to three further patients with chronic renal disease and on dialysis.

[Hyperostotic bone changes of the spine in diabetes mellitus]. / Hyperostotische Knochenveränderungen an der Wirbelsäule bei Diabetes mellitus.

The diffuse idiopathic skeletal hyperostosis, especially with manifestation at the vertebral column, is often associated with metabolic disorders, such as diabetes mellitus or hyperuricaemia. Clinical, pathogenetic and radiological aspects are discussed. Routine thoracic x-ray give important informations on the diagnosis of this osteoplastic diathesis.