Malignant fibrous histiocytoma in the area of the head and neck]

Although malignant fibrous histiocytoma (MFH) is the most common soft tissue sarcoma of adult life, it is fairly rare in the head and neck region (3-6%). Between 1983 and 1991 8 patients with MFH in the head and neck region have been observed and treated at the ENT-department of the University of Tübingen. 5 patients have been operated (laryngopharyngeal localization), 2 patients underwent irradiation (unresectable fast growing T4-tumors of the pharynx and thyroid) and one female patient refused further therapy after two resections elsewhere. Operated patients showed no evidence of disease 2-8 years after resection (all margins have been controlled histologically). Both irradiated patients died 4 respectively 2 months after full (70 Gy) and incomplete (17 Gy) radiotherapy without visible positive effects. Both patients developed pulmonary metastasis. Since MFH can grow in thin layers along musculaoponeurotic structures the exact size is not always demonstrable by ultrasound, CT or MR scans. Metastasis occur in up to 40%, preferentially in regionary lymph nodes, in lung, liver and skeletal system. These phenomenon requires a full pretherapeutic staging. Histologically MFH is sometimes hard to distinguish from other tumors as for example various sarcomas and pleomorphic carcinoma. Therefore, immunohistochemical (mesenchymal markers) and electron microscopical investigations are advised. Resection with exact histological controll of all margins is the therapy of choice. We experienced that laryngeal MFH (n = 3) can be resected without laryngectomy under certain circumstances. Although unsuccessfull in our two cases, according to the literature, radiotherapy should be administered in unresectable cases. Depending on localization and size of MFH long survival, in single cases healing, of this disease is possible by surgical treatment.     

Histology as a prognostic factor in early gastric cancer.

Of 431 patients with gastric cancer observed in our institution, 23 (5.3%) had early gastric cancer (EGC). Macroscopic presentation, histology, depth of invasion, and lymph node involvement were evaluated in all the cases. All patients underwent surgery and an intensive follow-up was performed. Five of the 23 patients progressed, and the risk factors were examined. Histology seemed to be the main prognostic factor in our study, since intestinal type of EGC was associated to a significantly better prognosis. Total gastrectomy is indicated in the proximal localization of EGC, and should perhaps be performed also in cases presenting undifferentiated histology.     

Treatment options in multiple chemical sensitivity.

The essential features of treatment for chemical sensitivity are: 1) Encouraging the provision of clean air, food, water, and surroundings. 2) Identifying substances to which the patient is sensitive, with subsequent a) enhanced avoidance, or b) specific immunotherapy to reduce the patient's reactivity to those substances. 3) Assessing and enhancing the patient's nutritional status to maximize the body's ability to detoxify and to minimize the free-radical production and oxidative stress of xenobiotics. 4) Addressing concurrent problems such as infections, immunosuppression, and other medical conditions in an appropriate fashion. 5) Evaluating the patient's psychologic status and addressing any social and emotional problems in a compassionate manner. The author believes that multiple chemical sensitivity is a real condition with documented physiologic abnormalities. It is not a functional or psychologic illness or a belief system of the patient. Second, this condition is diagnosable and treatable by various means. These treatment options not only make common sense but usually result in significant improvement for these unfortunate patients, who deserve the very best efforts of their health care providers.     

The relation of the accumulation of cadmium in human placenta to the intake of high-fibre grains and maternal iron status.

Exposure to cadmium via the diet is known to depend to a large extent on the intake of cereal grains, particularly the high-fibre fractions of wheat. Subjects with low iron status absorb more cadmium than those with better iron status. The purpose of the present study was to determine to what extent cadmium accumulation in human placenta is affected by the intake of grain fibre and maternal iron status during pregnancy. Thirty-nine pregnant women participated in the study. In each trimester the women were requested to complete a dietary history and to allow blood samples to be taken for haemoglobin, serum ferritin and serum thiocyanate determinations, the latter as a marker for smoking. At delivery the whole placenta was taken for the determination of the cadmium concentration. The 32 women who had serum thiocyanate levels less than 70 mumol/l, who had completed at least one dietary history and from whom a blood sample was obtained in the third trimester, were included in the final statistical analyses. In the group of women who consumed less than the median intake of grain fibre and had more than 15 micrograms ferritin/l serum in the third trimester, the placenta cadmium concentration was nearly half that in the placentae of women who had consumed more grain fibre or had lower iron status in late pregnancy.     

Formation of mitochondrial phospholipid adducts by nephrotoxic cysteine conjugate metabolites.

Nephrotoxic cysteine conjugates derived from a variety of halogenated alkenes are enzymatically activated via the beta-lyase pathway to yield reactive sulfur-containing metabolites which bind covalently to cellular macromolecules. Mitochondria contain beta-lyase enzymes and are primary targets for binding and toxicity. Previously, mitochondrial protein and/or DNA have been considered as molecular targets for cysteine conjugate metabolite binding. We now report that metabolites of nephrotoxic cysteine conjugates form covalent adducts with rat kidney mitochondrial phospholipids. Rat kidney mitochondria were incubated with the 35S-labeled conjugates S-(1,1,2,2-tetrafluoroethyl)-L-cysteine (TFEC), S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine (CTFC), S-(1,2-dichlorovinyl)-L-cysteine, and S-(1,2,3,4,4-pentachlorobutadienyl)-L-cysteine. Quantitation of metabolite binding to whole mitochondria and to mitochondrial protein and lipid fractions revealed that as much as 42% of the 35S-label associated with the mitochondria was found in the lipid fraction. Total lipids were also extracted from 35S-treated mitochondria and separated by thin-layer chromatography. 35S-Containing metabolites were found in the lipid fractions from mitochondria treated with each of the conjugates. Lipids from both [35S]CTFC- and [35S]-TFEC-treated mitochondria contained major 35S-labeled lipid adducts which had similar mobility by thin-layer chromatography. Fatty acid analysis, 19F and 31P NMR spectroscopy, and mass spectrometric analyses confirmed that the major TFEC and CTFC adducts are thioamides of phosphatidylethanolamine.     

Two-color analysis of lymphocyte subpopulations in patients with nephrotic syndrome due to membranous nephropathy.

Two-color flow cytometry was carried out to determine the correlation between cell-mediated immunity and the levels of proteinuria in 30 patients with membranous nephropathy. Lymphocyte subpopulations were measured by two-color flow cytometry using various monoclonal antibodies of the Leu series. Clinically, the patients were divided into four stages as follows: 1. untreated nephrotic stage, 2. prednisolone (PSL) treated nephrotic stage, 3. persistent proteinuric stage (incomplete remission, ICR) and 4. complete remission (CR). Two-color flow cytometry showed a significant decrease in Leu 2a+15+ (suppressor T) cells and relative increase in Leu 3a+8+ (suppressor inducer T) cells in the untreated nephrotic stage. The mean Leu 3a+8-/Leu 2a+15+ (helper/suppressor) cell ratio was normalized in the persistent proteinuric stage or complete remission after treatment with PSL. Patients with membranous nephropathy showed a significant elevation of Leu 2a+DR+ cells after treatment with PSL. The abnormalities of suppressor T cells and suppressor inducer T cells in the peripheral blood appear to reflect the levels of proteinuria in patients with membranous nephropathy. It was concluded that PSL might stimulate Leu 2a positive cells and then increase the number of Leu 2a+15+ cells in the peripheral blood of patients with membranous nephropathy.     

Premalignant lesions and nonsquamous malignancy of the penis and carcinoma of the scrotum.

Premalignant lesions of the penis include cutaneous horn, balanitis xerotica obliterans, and leukoplakia. The true incidence of progression of each of these to squamous-cell carcinoma is unknown. Bowenoid papulosis, erythroplasia of Queyrat, and Bowen's disease are histologically identical to in situ carcinoma. Although the first is consistently benign, the latter two regularly evolve into invasive cancer. Malignant scrotal lesions include squamous-cell carcinoma, liposarcoma, leiomyosarcoma, basal-cell carcinoma, extramammary Paget's disease, erythroplasia of Queyrat, malignant melanoma, and metastases. Hemangioma can be confused with carcinoma.     

Aluminium speciation in cerebrospinal fluid of acutely aluminium-intoxicated dialysis patients before and after desferrioxamine treatment; a step in the understanding of the element's neurotoxicity

Background: The association between aluminium and dialysis encephalopathy and deterioration of the neurological state during desferrioxamine treatment of dialysis patients is well established. At present little is known about the speciation and the mechanisms underlying the element's neurotoxicity. Methods. Aluminium speciation was performed in cerebrospinal fluid samples of acutely aluminium-intoxicated dialysis patients using a recently developed high-performance liquid chromatographic/electro-thermal atomic absorption spectrometric hybrid method. Results: Baseline cerebrospinal fluid aluminium levels of samples taken shortly after the intoxication were low but elevated (5.0±2.0 &mgr;g/l, n=3) as compared to subjects with normal renal function (<1 &mgr;g/l). In contrast to the situation noted in serum and to the iron speciation in cerebrospinal fluid, aluminium was not bound to transferrin but appeared as two distinct compounds, the main fraction eluting at the elution volume of aluminium citrate/silicate. The second compound was not identified. Forty-four hours after desferrioxamine administration the cerebrospinal fluid aluminium levels had increased up to a concentration of 10.3±2.5 &mgr;g/l (n=3). This was accompanied by a change in the speciation profile with aluminium appearing at the elution volume of aluminoxamine. Conclusion: Our findings may contribute to a better understanding of the neurotoxic effects of aluminium and its desferrioxamine chelate in dialysis patients.