A patient with primary malignant melanoma localized to the right gluteal region is described. Four years later and after intercurrent influenza, disseminated metastases of malignant melanoma to the skin occurred. After a further 6 months melanodermia developed and lasted until the death of the patient (6 months later). Autopsy revealed melanosis of the visceral organs. Histology taken from internal organs using S-100 protein and HMB-45 melanoma methods confirmed metastases of malignant melanoma to the skin, oral cavity, palatal tonsils, nasal and nasopharyngeal mucosae, lungs, myocardium and brain. The authors discuss the mechanism of melanosis--a rare sign in patients with metastasizing malignant melanoma.

From the archive of BB Biocyt company, 32 urinary bladder carcinomas (urothelium carcinomas, UC) and 7 cases of chronic cystitis were selected and examined in semiserial sections for the following antigens: 1) cell proliferation marker Ki-67 (expressed in the nuclei), 2) cell cycle regulator p16/INK4a polypeptide (expressed in the cytoplasm and nuclei), 3) urothelium marker p63 (expressed in the nuclei), 4) cytokeratin 7 (CK7). 5) cytokeratin 20 (CK20) and 6) high molecular weight cytokeratin (HMWCK). Invasive urothelium carcinomas showing a high grade dysplasia (invasive HG UC) comprised over the half (20 out of 32) of the investigated tumours. Microinvasion to lamina propria (seen in three HG papillary carcinomas) was regarded as an early infi ltration even when the position of muscular layer could not be determined. Classical invasion across the urinary bladder wall and/or to surrounding tissues was found in 17 cases of low-differentiated HG UCs. The rest (9 out of 32 neoplasms) were either non-invasive papillary carcinomas of high (non-invasive HG UC, 5 cases) or low malignant potential (noninvasive LG UC, 4 cases). Finally, 3 cases were papillary urothelium neoplasms of low malignant potential (PUNLMP). HMWCK was present in all invasive tumours, whereas the frequency of other urothelium markers ranged from 65 to 88 %. Nevertheless, at least two markers were expressed in each invasive tumour. Staining for Ki-67 antigen was positive in over 50 % of the nuclei of HG UCs, while in the LG UCs, the frequency of positive Ki-67 staining did not exceed 25 %. In PUNLMP, the positive rate of Ki-67 stained dysplastic cells was below 10 %. The staining for p16 antigen did not correlate with the degree of dysplasia within urothelium tumours. For routine diagnostic, we recommend to combine the Ki-67 staining with detection of HMWCK. In cases of chronic cystitis, which developed urothelial hyperplasia and/or squamous metaplasia, the presence of p63 antigen was a relevant marker confi rming the urothelial origin of the altered transitional cells (Tab. 6, Fig. 4, Ref. 69)

The anti-apoptotic protein survivin was detected in a panel of 27 dysplastic nevi. From each representative paraffin block 4 mm sections were cut and stained with anti-survivin antibody (DAKO, Clone 12C4). In each section, the labeling intensity, the subcellular location of survivin antigen, the percentage of labeled cells and the degree of dysplasia were assessed. Survivin was present in 23 out of 27 cases (85.2%), but absent in 4/27 cases (14.8%). Positive staining was confined to the cytoplasm (C) of nevus cells only in 18 cases (66.7%), while cytoplasmic as well as nuclear positivity (NC) was found in 5 cases (18.5%). In no case solely nuclear staining could be seen. Furthermore, in 4 out of 5 cases (80%) with NC staining, severe dysplasia was found. Our data point at usefulness of survivin staining, otherwise rarely performed in dysplastic nevi. We confirm the importance of nuclear location of the survivin antigen, which may be helpful for assessing the possible progression to melanoma.

Abstract:We examined the expression of potential tumor marker survivin by immunohistochemical staining using antisurvivin antibody (DAKO, Clone 12C4) in a panel of 25 malignant melanomas. In each section, we assessed the percentage of positively stained tumor cells, the intensity of staining and its subcellular localization. Survivin was present in 23 out of 25 cases (92%). Nuclear staining was found in 2 of these 23 cases (8.7%) only, while cytoplasmic staining only was seen in 3 of them (13%). The combined nuclear as well as cytoplasmic localization of survivin was demonstrated in 18 out of 23 cases (78.3%). In 2 cases revealing nuclear staining only, the worse histological features were more pronounced than in 3 cases with cytoplasmic staining only. Our results suggest that nuclear positivity of survivin may correlate with the degree of malignancy. In addition, we conclude that overexpression of survivin involved in the pathogenesis of melanoma represents an important diagnostic marker.

The first case of VATER syndrome was described by Quan and Smith in 1973. 1 The syndrome represents a complex anomaly of skeletal structures and internal organs, an association of vertebral defects with anal atresia, tracheoesophageal fistula (TEF), and radial limb dysplasia.2 Generally, TEF may occur with or without esophageal atresia. In 85% of the VATER syndrome cases, TEF results from a fistulation of the distal esophagus to the trachea by an atretic proximal blind end of the esophagus. Polyhydramnion and excessive salivation are early clinical manifestations of TEF, followed by choking, coughing and cyanosis after the first feeding. These symptoms can even appear before the first feeding due to a saliva and gastric content aspiration.3 Therefore, surgical repair of this anomaly within the first 24 hours after delivery presents the treatment of choice and may be of vital importance. 4Our case report deals with a rare secondary aortoesophageal fistula (AEF) which developed after continuous nasogastric intubation of a child with VATER syndrome, who was operated on for congenital esophageal atresia associated with TEF. Case ReportA premature male infant was born at 1730 g in the 35th week of gestation by Cesarean section, which was indicated due to a placental abruption and early amniotic fluid escape. The delivery was complicated by severe asphyxia, cyanosis and bradycardia with the Apgar score of 1/6/8. After complete resuscitation normal vital parameters were restored.A series of clinical, laboratory (including genetic) examinations were done and a complex polymalformation was proved. It consisted of hypoplastic left thumb, 3rd and 5th thoracic hemivertebral malformation, presence of thirteen pairs of ribs, stenosis of penile urethra, proximal esophageal atresia with fistulation of the distal esophageal part to the trachea (type IIIb sec Vogt), 4 and stenosis of the penile urethra. To prevent possible stomach content pulmonary aspiration and to open a feeding passage, it was vital to operate on the newborn on the second day of his life. Dorsal mediastinum was reached surgically via the right-side thoracotomy. In addition to atresia, the situation before the reconstruction was complicated by a pathological position of the proximal esophageal part to the left, and the descending aorta to the right side. The division of fistula and reconstruction of the esophagus by means of end-to-end anastomosis on a nasogastric tube were performed. The postoperative location of these structures was crossbreeding, with an intimate neighboring of their walls.After the operation, the newborn was mechanically ventilated, and on the 2nd postoperative day, a punction epicystotomy was done for a bilateral ureterohydro-nephrosis. The postoperative course was further complicated by a persisting thrombocytopenia, as well as the development of bacterial pneumonia. Pneumonia was treated successfully with an appropriate antibiotic therapy which commenced after sensitivity had been micro-biologically verified.On the 48th day of the infant...