Ductal adenocarcinoma of the prostate

BACKGROUND:

Ductal or endometrioid adenocarcinoma of the prostate may be a subtype of prostate cancer that is amenable to aggressive local therapeutic strategies. The authors of this report investigated the clinical outcome of patients who had prostate ductal adenocarcinoma after primary radical prostatectomy or radiotherapy.

METHODS:

The clinical features of 108 patients with locally confined or advanced prostate ductal adenocarcinoma who had undergone primary radical prostatectomy (surgical group, n = 76 men) or no surgery (nonsurgical group, n = 32 men) were evaluated retrospectively. Clinical records were reviewed, and Gleason scores, clinical/pathologic stages, and preoperative prostate‐specific antigen levels were examined. The clinical features that were assessed included local recurrence, distant metastasis, and progression‐free and overall survival after primary therapy.

RESULTS:

In the surgical group, patients who had pure ductal prostate cancer survived longer (median, 13.8 years; 95% confidence interval [CI], from 13.8 years to not attained) than patients who had mixed ductal prostate cancer (median, 8.9 years; 95% CI, from 7.1 years to not attained; P = .05). In addition, the median time to local progression was shorter (2.8 years vs 4.9 years) and the median time to distant metastasis was longer (3.9 years vs 2.0 years) for patients who had pure ductal adenocarcinoma than for patients who had mixed ductal adenocarcinoma of the prostate after surgery, respectively.

CONCLUSIONS:

The results of this preliminary study suggested that pure ductal prostate adenocarcinoma tends to pursue an indolent clinical course and poses an increased risk for local recurrence. Local control (particularly prostatectomy) may improve the clinical outcome of patients with pure prostate ductal adenocarcinoma. These results need to be confirmed in prospective studies. Cancer 2009. © 2009 American Cancer Society.     

Growth rate of multiple intracranial hydatid cysts assessed by CT from the time of embolisation

We report the case of a 25-year-old man with multiple bilateral hydatid cysts of the brain in whom we were able to assess the growth rate of the cysts on repeated examination. On average, the cysts increased in diameter by 1 cm per month. Received: 1 April 1996 Accepted: 1 October 1997     

Time-dependent oxidative stress effects of percutaneous nephrolithotomy

Aim of this study was to investigate the effects of operation time of percutaneous nephrolithotomy (PCNL) on renal function and hemodynamic response. Thirty-four patients (14 male, 20 female) with normal renal function who underwent unilateral single-tract PCNL between December 2010 and June 2011 were included in the study. The age, sex, stone size, grade of hydronephrosis, operative time, access pole, shock number of lithotripter, complications, stone-free rate, and hemodynamic parameters during operation were recorded. Total blood count and oxidative stress parameters such as paraoxonase 1 (PON1), total antioxidant status (TAS), total oxidant status (TOS), and malonyldialdehyde (MDA) levels were examined before the operation as baseline levels and then at 30, 60, 90, and 120 min during the operation. The mean age of the patients was 31.4 ± 18.8 (9–66 years) years. Mean stone size was 35.5 ± 15.6 mm. Mean serum BUN and creatinine did not change postoperatively (p > 0.05), whereas mean WBC and 24-h urine cortisol were positively and hematocrite were negatively changed significantly (p < 0.05). Oxidative stress parameters such as PON1 and TAS showed statistically significant decreases, while TOS and MDA showed statistically significant increases with increased operation time, especially after 1 h (p < 0.005). A bivariate correlation test showed correlation between oxidative stress parameters and operation time (p = 0.002), but no correlation was found between oxidative stress parameters and other parameters (p > 0.05). Oxidative stress and response to it increased with increasing operative time during a PCNL procedure, especially after 1 h. Further studies with a larger and longer series should be performed to clarify this issue further.     

Incidence of iodine deficiency in patients presenting with goitre--discrepancy between clinical and ultrasonographic evaluation of the thyroid: comparison of patients with and without autoimmune thyroiditis--clinical, hormonal and urinary iodine excretion studies

In endemic areas iodine deficiency, and in iodine sufficient regions autoimmune thyroiditis, is the first aetiological factor for goitre. The aims of this study were to determine the incidence of iodine deficiency and autoimmune thyroiditis in patients presenting with goitre, to compare clinical and ultrasonographic assessment of thyroid size and to investigate the relationship between iodine and autoimmune thyroiditis. Patients diagnosed with goitre clinically (n = 204) were evaluated by their anthropometric measurements, ultrasonographic examination of the thyroid gland, thyroid function and TRH stimulation tests, thyroid autoantibodies and morning urinary iodine measurements. Thyroid volumes were evaluated according to three different reference criteria. Incidences of iodine deficiency and autoimmune thyroiditis were 54% and 17%. The incidences of iodine deficiency and excess were not significantly different in the autoimmune group (n = 35) compared to the non-autoimmune group (n = 169). In the autoimmune group, urinary iodine concentration correlated positively with serum thyroid hormones (FT3 r = 0.42, TT3 r = 0.38, TT4 r = 0.34) and negatively with serum TSH levels (r = 0.45). There were discrepancies between clinical and ultrasonographic evaluation of goitre, and between different reference criteria. This study revealed that iodine deficiency is still the first aetiological factor for goitre in our region and failed to show a relationship between iodine intake and autoimmune thyroid disease.     

Parathyroid Hormone-Related Protein and its Receptor in Human Glial Tumors

Summary  Objective. Parathyroid hormone-related protein (PTHrP) and its mRNA have been found to be expressed in a variety of human tumors including breast, prostate, colon, lung, renal and ovarian cancers. The purpose of this study is to evaluate the expression of PTH/PTHrP receptor and ligand in human glial tumors.  Methods. We examined the coexpression of PTH/PTHrP receptor and ligand in 73 glial tumors of different histological grades and 4 nonneoplastic human brain specimens and three glioblastoma cell lines, by using Western Blot analysis and immunohistochemical analysis.  Results. PTHrP and PTH/PTHrP receptors were shown in the neurons, reactive astrocytes and the endothelial cells of normal brain tissue as well as tumor cells, reactive astrocytes and vasculature of nonneoplastic tissue. They were expressed at higher levels in pure astrocytic tumors as compared to tumors with oligodendroglial components.  Conclusion. PTH/PTHrP receptor and PTHrP ligand are co-expressed in human glial tumors. There increased expression suggests an autocrine and/or paracrine loop may exist.     

Experience with long-term glucocorticoid treatment in congenital adrenal hyperplasia: growth pattern compared with genetic height potential

OBJECTIVE: Long-term replacement treatment with high doses of steroids in congenital adrenal hyperplasia (CAH) is known to have a negative influence on growth. We evaluated the effects of long-term steroid treatment in patients with classical CAH on height development in relation to genetic height potential. PATIENTS AND METHODS: Twenty-three patients with CAH (16 females, 7 males, mean age: 9.8 +/- 3.5 years) were included in this longitudinal study. The effect of steroid treatment on growth was determined by monitoring patients for 8.61 +/- 3.46 years (2-17 years) while they were treated with hydrocortisone at a mean dosage of 17.64 +/- 3.60 mg/m2/day. The height standard deviation scores (Ht-SDS), target Ht-SDS, and corrected Ht-SDS for target height was calculated for all patients. Predicted adult height according to bone age was calculated and it was determined whether height was developing according to the genetic height potential. In addition, patients were grouped as 'tight control' or 'poor control' according to their mean serum 17OH-progesterone or ACTH levels while on treatment. We evaluated whether height development was different for the tight and poor control groups. RESULTS: The mean chronological age of our patients at the time of the study was 9.89 +/- 3.53 years, Ht-SDS -0.77 +/- 1.57, target height (TH) 161.03 +/- 6.54 cm, TH-SDS -0.60 +/- 0.90, predicted height (PH) 157.2 +/- 11.16 cm, PH-SDS -1.1 +/- 1.69, and corrected Ht-SDS -0.75 +/- 1.14. There was no significant difference between the actual Ht-SDS and TH-SDS of our patients (p >0.05) but the corrected Ht-SDS was less than zero. Only 28.5% of our patients had normal height according to their genetic potential while 71.5% were shorter than their genetic height potential. While the Ht-SDS and corrected Ht-SDS were similar in the tight and poor metabolic control groups, the predicted height was significantly greater in the tight control group. CONCLUSION: We demonstrated that a hydrocortisone dose of 17.64 +/- 3.60 mg/m2/day in classical CAH had a negative influence on height development for genetic height potential in 8.5 years of follow-up and that it is necessary to use the lowest possible steroid dosage by individualizing the dose.     

Syndrome of congenital adrenocortical unresponsiveness to ACTH. Report of six patients

Familial glucocorticoid deficiency (FGD) or unresponsiveness to ACTH at the receptor level is a rare autosomal recessive hereditary syndrome characterized by a low cortisol level despite high serum ACTH concentration. Aldosterone levels are normal. The clinical entity generally presents in the first year of life with skin hyperpigmentation and hypoglycemic convulsions. Cortisol response to exogenous ACTH is also absent. Unresponsiveness to ACTH may be due to a mutation in the ACTH receptor; sometimes no mutation is found. We discuss the clinical and laboratory findings and genetic studies in six patients with a diagnosis of FGD. A homozygous V142L mutation was detected in three of the patients and a homozygous D103N mutation was detected in two patients.