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We present a case of a patient diagnosed in the 3rd trimester of pregnancy with a Krukenberg tumor being a metastasis of stomach cancer. Due to severe pre-eclampsia, the pregnancy was solved by Caesarean section, a female child was born with severe virilization.

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Adrenal incidentaloma (AI) is an asymptomatic mass localized in the adrenal gland, usually detected during diagnostic imaging performed due to other health issues than the suspected adrenal disease. It occurs in 2% of adults and 0,2% of children. Pediatric AI may cause many difficulties in the diagnostic processes. Neuroblastoma is one of the most common malignant tumors in children. Usually, it is localized in the medulla of the adrenal gland. Many patients do not have any symptoms, but some may present with fever, weariness, weight loss, pain, enlarging mass, etc. The majority of cases are high- risk and the survival rate is less than 50%. The diagnostic protocol consists of laboratory tests and radiological imagining. Treatment depends on the risk group that the patient is assigned to. Pheochromocytoma is a rare catecholamine-secreting tumor in children originating in the adrenal medulla. Most pediatric patients present with sustained hypertension. 60% of pheochromocytoma cases are sporadic. The surgical removal of the tumor through adrenalectomy is a standard procedure. To the group of pediatric adrenocortical tumors (ACT), benign adrenocortical adenoma (ACA) and malignant adrenocortical carcinoma (ACC) are included. ACA is found in only 20% of cases of ACT. Most of the patients present with signs of virilization, Cushing Syndrome, or both. The 5-years survival rate of ACC in the pediatric population is 46-55%. An adrenal incidentaloma is an unpredictable and possibly dangerous disorder in the pediatric population. Due to the rarity of the finding and their variety, there is not much data and clear recommendations about AI management. Doctors need to know about the prevalence of different types of adrenal tumors in the pediatric population based on age.

Patients suffering from endocrine disorders often present a wide profile of skin lesions. In hyperthyroidism we observe hair loss, lower leg myxedema and onycholysis or, in the case of hormone deficiency, generalized swelling of the skin, which becomes cold and pale. Primary hyperparathyroidism is revealed by pruritus, presence of chronic urticaria or deposition of amorphous calcium salts. In hypoparathyroidism, the skin is dry while the nails become very brittle. Skin lesions in diabetes include necrobiosis lipoidica, granuloma annulare, scleroderma-like diabetic edema and acanthosis nigricans. Overactive pituitary gland is often manifested as acromegaly with hypertrophy of soft tissue thickening and hypertrichosis. The skin in the early stages of hypopituitarism feels swollen, is pale yellow and oily, and finally becomes alabaster and dry. The characteristic features of Cushing syndrome are central obesity, lunar face, buffalo hump, and striae. In Addison’s disease we observe hyperpigmentation. Hyperandrogenism in women leads to acne, hirsutism and virilization.

Copyright of Review of Medicine / Przeglad Lekarski is the property of Wydawnictwo Przegld Lekarski / Publisher Medicine Review and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Hirsutism is the presence of terminal hairs in a male-like pattern in females, due to elevated male hormone levels. Females with hirsutism are often overweight and have metabolism disturbances as insulin resistance and impaired glucose tolerance. We selected fifty patients of hirsutism from the department of dermatology for the study. A thorough physical examination with specific emphasis on signs of virilization (including frontal baldness, loss of female body contours, increased muscularity, acne, clitoromegaly, and atrophy of breast) was done in all the patients.

Copyright of Advances in Hygiene & Experimental Medicine / Postepy Higieny i Medycyny Doswiadczalnej is the property of Sciendo and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Congenital adrenal hyperplasia (CAH) is an autosomal recessive defect in steroidogenesis, mostly affecting 21-hydroxylase enzyme deficiency. The other seldom cortisol synthesis abnormalities include deficiencies of: 11beta-hydroxylase, 3beta-hydroxysteroid dehydrogenase, 17beta-hydroxylase, 17,20-lase and 11 beta-hydroxysteroid dwehydrogenase type 1. There are three main types, depending on the clinical level of 21-hydroxylase deficiency: (1) classical form--salt-wasting CAH (2) the classical form non- salt-wasting (3) non-classical form. CAH incidence is estimated at 1/14 000-1/10 000, of which about 70% is the classic salt-wasting form. The clinical picture varies considerably depending on the form. In the classic salt-wasting CAH may develop into the a shock. In classic CAH without loss of salt dominates virilization in girls and precocious puberty in boys. A non-classical forms usually presents as hyperandrogenisation and fertility. CAH treatment is mainly based on the use of glucocorticoid therapy, and if necessary supplemented mineralocorticoids. There is also potential to consider prenatal treatment (female fetuses diagnosed as CAH) with the use of dexamethason. However this kind of treatment is related to some medical and ethical controversies.

Hypogonadism in men is defined as a complex of signs and symptoms due to testosterone deficiency or inappropriate production, which occurs in about 1-2%. Symptoms of hypogonadism depend primarily on the age of the male patients at the time of development of the hypogonadism (pre- or postpubertal). The dominant findings are: impaired puberty, decrease of virilization, infertility or decrease of spermatogenesis, impotence and gynecomastia. Classically hipogonadism is divided into primary (hypergonadotropic) and secondary (hypogonadotropic). The most common causes of primary hypogonadism is Klinefelter's syndrome, while secondary--pituitary tumors. "Peripheral" hypogonadism results from androgen receptor polymorphism. The role of therapy of hypogonadism is to restore or maintain proper spermatogenesis as well as testosterone replacement therapy. Gonadotropin and testosterone therapy is available in treatment of hypogonadism in men. The treatment strategy depends on the age of patient and the goals of therapy (restore of fertility and/or produce and maintain of virilization). The gonadototropins and GnRH are useful in spermetogenesis stimulation. The testosterone replacement therapy is efficacious and safe. Testosterone esters and gels are widely applied.

The authors describe a case of an adult woman with congenital adrenal hyperplasia caused by 11beta-hydroxylase deficiency. The patient presented not only typical features of this disease such as virilization and hypokaliemic hypertension but also rare pathologies, such as ectopic adrenal tissues, salt loss during infancy, and functional adrenomedullary hyperactivity. In spite of the severe disease and delays in its diagnosis and adequate treatment, significant improvement in appearance and normalization of blood pressure as well as the birth of a healthy child were achieved. The paper also discusses current opinions concerning the pathogenesis and treatment in CAH with 11beta-hydroxylase deficiency as well as difficulties in diagnostic and therapeutic management.

Adrenocortical carcinoma is a rare neoplasm occurring with a frequency of 1-2 cases per million. It is characterized by significant malignancy with mean survival of about 28 months, and in the presence of documented metastases survival is shorter up to 8 months. This type of a tumor is slightly more frequent in women (58.6%) than in men (41.4%). Etiology of adrenocortical carcinoma is still unclear, but a role of genetic and environmental factors has been largely considered. Most of the carcinomas (60%) are functional and usually the first manifestation is Cushing's syndrome with virilization. The tumor size is still the best single predictor of prognosis. Histopathology specimen from biopsy or obtained during operation should be stained for Melan A, which can confirm the adrenal origin of the tumor. The only method of treatment is a complete surgical excision of the carcinoma. However, because of its dynamics, metastases cannot be reliably excluded. We presented the case of functioning adrenocortical cancer in 37-year-old patient who at time of diagnosis had 12 cm in diameter tumor of the left adrenal gland and metastases to the liver and lung. In the article the symptoms associated with hormones produced by the carcinoma, diagnostics and treatment with regard to the progression of the disease have also been discussed.

The aim of the study was analysis of preoperative diagnostics of patients who underwent laparoscopic adrenalectomy. In the preoperative diagnostics in 10 patients (22.2%) pheochromocytoma was found, in 8 (17.8%) Conn's syndrome, in 4 (8.9%) Cushing's syndrome and in 1 (2.2%) adrenal virilization. Full accordance between histopathological findings and preoperative diagnosis was achieved in 91% of cases. Four cases of discrepancy were: 1 false positive preoperative diagnosis of aldosteronoma, 1 false positive and 2 false negative diagnosis of pheochromocytoma.

Testicular torsion is a surgical urgency. It may lead to loss of that organ and moreover, as revealed by experimental studies and clinical findings in adults, induces autoimmunological reactions with subsequent male infertility. To elucidate these sequellae the following questions seem to be relevant 1. Are there any antisperm antibodies or shifts in T cell CD4+, CD8+ and NK subpopulations in boys with a history of testicular torsion? 2. Is production of antisperm antibodies initiated and maintained in childhood, and amplified after puberty? 3. Does the age at testicular torsion and duration of exposure to sperm antigens/testicular tissue have an effect on induction and levels of antisperm antibodies? 4. Is hormonal function of testis/testes and gonadotropic activity of the pituitary gland normal in these patients? 5. What conditions (duration, subjective and objective symptoms) are associated with testicular torsion; what kind of intraoperative findings can be expected; what is the influence of testicular torsion on the twisted testis? The study group (GB) consisted of 37 boys and men aged from 8 months to 27 years (mean 12.3 years) recruited from 86 patients seen for testicular torsion at the Department of Pediatric Surgery, Pomeranian Academy of Medicine in Szczecin, between 1967 and 1992. The control group (GK) comprised 42 healthy boys and men aged 3 to 33 years (mean 12.1 years) (Tab. 1). The analysis was based on: 1) clinical files; 2) follow-up results; 3) laboratory findings; 4) statistics. According to clinical data and physical examination, testicular torsion usually appeared during puberty, neonatal period and infancy and the mean duration of torsion was 12.4 days. The best prognosis for salvage of the twisted testis was for torsions lasting no longer than 8 hours. Only 8 of 37 twisted testes could be salvaged (including 4 hypotrophic testes; Tab. 2). There were 21 positive ELISA tests (level of antisperm antibodies exceeding 2 fg/pl) in the study group (mean 4.45 +/- 5.6 fg/pl), including 13 boys with testicular torsion in the prepubertal age and 8 during puberty (Tab. 3). A tendency to higher levels of antibodies with age was observed. In the control group there were 35 negative and 7 positive results (mean 1.05 +/- 1.86 fg/pl) (Tab. 4), significantly less than in the study group (p < 0.001). Trend curves (Fig. 1) and Pearson's correlation coefficients (Fig. 2) for levels of antibodies and age at presentation of testicular torsion were established for both groups. Mean percentages of CD4+, CD8+ and NK cells (indirect immunofluorescence test with monoclonal antibodies) were insignificantly lower in the study group (Fig. 3). Shifts in favor of CD4+ and NK subpopulations found in some patients correlated with high levels of antisperm antibodies (Tab. 5 and Fig. 4). Elevated LH and/or FSH (21 patients) and/or testosterone levels (13 patients) were usually observed during puberty (Tab. 6). The results indicate that antisperm antibodies are detected in more than half of the boys with a history of testicular torsion. This is accompanied in some cases by shifts in CD4+ and NK lymphocyte subpopulations correlating with high antibody levels. Production of antisperm antibodies initiated during prepuberty (in infancy or even in the neonatal period) persists and is amplified after puberty due to increasing amounts of antigen material. Age at testicular torsion (age at potential exposure to spermatic antigens/testicular tissue from the twisted or de-twisted testis with severe haemorrhagic lesions or left in the abdominal cavity) has an effect on the future production and levels of antisperm antibodies. Disturbances in the secretion of LH and/or FSH were observed in 2/3 of the boys/men with a history of testicular torsion. Abnormal secretion of testosterone was found in 1/3 of the patients. These hormonal disorders seem to have no influence on virilization, libido or sexual potency.

We report a case of 24 year old patient with secondary amenorrhea, virilization and elevated serum testosterone concentration, in which cystic-solid tumor in right ovary was found. Surgical treatment was applied--adnexectomy. Histopathologic examination supported suspicion of androblastoma. After treatment regulation of menses and serum testosterone level was obtained.

Androgen insensitivity syndrome (AIS) is caused by mutation in androgen receptor (AR) gene. This phenomenon leads to the defect of the virilization of the external genitalia and is one of the causes of human male pseudohermaphroditism. Molecular diagnosis of AR gene mutations is very complex because of heterogeneity of AR mutations. AIS is X-linked recessive trait and therefore the simple diagnosis of AIS carriers is a very important problem. Detection of AIS carriers by using the analysis of CAG repeating sequence polymorphism of exon 1 or AR gene is reported.

A two year old girl with symptoms of virilization was investigated and an adrenal gland tumor with morphological sings of malignancy was diagnosed. After surgery, irradiation and chemotherapy, a complete recovery was observed. The authors point out the diagnostical difficulties in similar cases. Our observation seems to confirm earlier suggestions, that in cases with predominant androgen activity the better prognosis is expected.

A case of male hermaphroditism is presented. It complied with all traditional criteria of male hermaphroditism due to Leydig's cells hypoplasia (anomaly of the internal genitalia, karyotype 46, XY, presence of the testicular tissue, no response of the hypoplastic Leydig's cells to HCG stimulation with simultaneous dramatic decrease in their number in the interstitial tissue. Emphasis is on the marked difference in incomplete virilization of the external genitalia related to the occurrence of Leydig's cells insufficiency.