Dentition, diet, tobacco, and alcohol in the epidemiology of oral cancer

Interview and dental examination data were gathered on 584 males with cancer of the oral cavity and on 1,222 control patients with nonneoplastic diseases at Roswell Park Memorial Institute, Buffalo, New York. No dietary characteristics distinguished cancer patients from controls. However, a higher risk of developing oral cancer was associated with heavy smoking, heavy drinking, and poor dentition. When controlled for the other factors, each factor carried a higher risk. Moreover, heavy smokers and heavy drinkers with poor dentition and males with all three traits had a substantially higher risk than would have been expected, if the traits were considered additively. The risk for males with all three traits was 7.7 times that of men with none of these traits.     

Aetiology of haemospermia

There are several unknown factors which cause haemospermia. An earlier developed diagnostic scheme has been expended by novel imaging techniques and biopsy methods. A detailed case history, physical examination and microscopic analysis of the ejaculate is required. In haemo-pyospermia a complete microbiological analysis must be escalated. Noninvasive imaging techniques (ultrasound, computer tomography and magnetic resonance imaging) help in detecting calculous and malignant diseases. So far, as a precise diagnosis has not been available, urethroscopy has been performed. Malignancies (prostate, seminal vesicles) must be histologically verified by biopsies. In contempt of our efforts the practice shows a part of haemospermia remaining essential. Analysing two time periods we found prostatic calculi, chronic prostatitis and carcinoma of the prostate unequivocally as most frequent causes. Considering the rare genital malignancies we find more than 10% frequency. Notably, in our study only 2.4% of the malignancies occurred in patients under 40 years of age. Hence a detailed diagnosis is advocated in haemospermia patients over 40 years. Finally, we may state that in contempt of the applied modern imaging techniques 15% of patients with haemospermia had unknown aetiology.     

Aetiology of keratoconus

Keratoconus has a common association with atopic conditions. Most keratoconus patients rub their eyes excessively. Eye-rubbing is considered the dominant aetiological factor in two-thirds of patients with keratoconus who progress to contact lens wear. A classification of keratoconus based on the dominant aetiological factors is proposed. No significant psychoneurotic factor was found in the keratoconus patients compared with patients in the control group.     

Pancreatic cancer and alcohol

The aetiology of pancreatic cancer remains unknown, as for other cancers, despite continued and exhaustive clinical and laboratory research. Further studies are needed to elucidate the pathogenesis of pancreatic cancer. Due to is anatomical location, detection of carcinoma of the pancreas is difficult in its operable stage. Of the various radiological modalities, real time ultrasonography seems to be most useful and will constitute the major diagnostic approach in the near future.     

Aetiology of assault with respect to alcohol, unemployment and social deprivation: a Scottish accident and emergency department case-control study

In a study to investigate the association between alcohol consumption, unemployment and social deprivation and assault in individuals, 70 victims of assault attending a Scottish accident and emergency department were identified and matched with 70 paired age, sex and time of attendance controls. Seventy per cent were male and 30 per cent female. Cases were more likely to have been drinking (p < 0.001) and to admit to previous assault (p < 0.001), as reported in other studies. Despite living in the same geographical area (p = 0.353), the cases were more likely to be unemployed (p = 0.011) and had a higher mean deprivation score (p = 0.043). These results indicate that violence is associated with unemployment and socio-economic status of the individual and they compliement studies based on population data which have linked rates of violence with low income and social deprivation.     

Venous leg ulcers. Part 1: Aetiology

Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18+/-5 mmHg in the CPAP group and 25+/-8 mmHg in the oxygen group (p<0.05). The PaO2/FiO2 ratio increased in the intubation group (168+/-69 to 240+/-57, p<0.05) and the CPAP group (137+/-17 to 253+/-67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction.     

Correlation between the combination of alcohol consumption and smoking in oral cancer (screening of the population at risk)

The mortality from tumours of all kinds doubled in Hungary between 1960 and 1993, whereas the mortality from tumorous diseases of the oral cavity in the same period increased 5-fold. The results of stomato-oncological screening studies on volunteers from the general population do not reflect this alarming rise. However, the risk of tumorous diseases of the oral cavity may be expected to be much higher among those who smoke and drink heavily. Accordingly, a screening study was carried out among such and endangered population: 300 (230 men and 70 women) subjects who were either homeless or participating in alcohol withdrawal treatment. The results of this screening confirmed the expectation: precancerous lesions were found in or around the oral cavity in 14% of this population, benign tumours in 2.33%, and malignancies in 2.66%.     

Uracil-ftorafur: an oral fluoropyrimidine active in colorectal cancer

PURPOSE AND DESIGN:This review describes the early clinical development of uracil-ftorafur (UFT), an oral fluoropyrimidine, designed in 1978 by adding uracil to ftorafur. The review focuses on the treatment of colorectal cancer and summarizes the Japanese experience and the phase I and II trials performed in the United States and Europe. RESULTS: Clinical trials of UFT published in the Western world have included 581 patients with colorectal cancer. UFT has been administered in these trials as a single agent or biomodulated by leucovorin (LV). UFT was administered daily in split doses for periods that ranged from 14 to 28 days. The activity of oral UFT in large-bowel cancer when administered with oral LV (approximately 50 mg/dose) has resulted in objective response rates of approximately 40%. Response rates of approximately 25% (range, 17% to 39%) were reported when UFT was administered as a single agent or with lower doses of LV. The highest dose-intensities of UFT are achieved with 28-day schedules of administration. The maximum-tolerated dose (MTD) of UFT with this schedule, when administered concomitantly with oral LV 150 mg daily, is 300 mg/m2 daily. The dose-limiting toxicity (DLT) of UFT has generally been diarrhea. Other commonly described toxicities include nausea and vomiting, fatigue, and stomatitis. Myelosuppression occurs infrequently. Typically, hand-foot syndrome and neurologic toxicity are lacking. CONCLUSION: UFT is a fluoropyrimidine active in colorectal cancer. The oral route of administration and improved safety profile represent important advantages over both conventional and infusional fluorouracil (5-FU) regimens.     

Head and neck cancer: oral care during radiotherapy

For patients with head and neck cancer who are compromised by the side-effects of radiotherapy, effective mouth care is essential. This article describes the detrimental effects of radiotherapy to the oral cavity and provides a practical guide to oral cleansing.     

Metabolic mapping of the effects of oral alcohol self-administration in rats

A method for the quantitation of protein carbonyls, which have been widely employed as markers of protein oxidative damage, is described. Protein carbonyls were derivatized with tritiated sodium borohydride and the tritiated proteins were separated on SDS-PAGE. Protein bands, visualized by Coomassie blue staining, were then excised and incubated in 30% H2O2 at 60 degrees C for 48 h. Tritium, incorporated into the proteins, was quantitated by liquid scintillation counting after gel solubilization by H2O2. This method can be applied to the measurement of carbonylation of specific proteins as it employs SDS-PAGE and has the advantage that unreacted NaB3H4 in the labeling reaction mixture need not be removed. The present method, when combined with immunochemical detection of protein carbonyls, should be very useful in the quantitation of oxidative damage to individual proteins.     

Aetiology of skeletal muscle ''cramps'' during exercise: a novel hypothesis

Secretions of the tick salivary glands are essential to the successful completion of the prolonged feeding of these ectoparasites as well as the conduit by which most tick-borne pathogens are transmitted to the host. In ixodid ticks the salivary glands are the organs of osmoregulation, and excess water from the bloodmeal is returned via saliva into the host. Host blood must continue to flow into the feeding lesion as well as remain fluid in the tick mouthparts and gut. The host's haemostatic mechanisms are thwarted by various anti-platelet aggregatory, anticoagulatory and anti-vasoconstrictory factors in tick saliva. Saliva components suppress the immune and inflammatory response of the host permitting the ticks to remain on the host for an extended period of time and, adventitiously, enhancing the transmission and establishment of tick-borne pathogens. Over the years much work has been done on the numerous enzyme and pharmacological activities found in the tick saliva. The present article reviews the most recent work on salivary gland secretions with special emphasis on how they favour pathogen transmission.     

Aetiology and pathogenesis of alcoholic liver disease

Until the 1960s, liver disease of the alcoholic patient was attributed exclusively to dietary deficiencies. Since then, however, our understanding of the impact of alcoholism on nutritional status has undergone a progressive evolution. Alcohol, because of its high energy content, was at first perceived to act exclusively as 'empty calories' displacing other nutrients in the diet, and causing primary malnutrition through decreased intake of essential nutrients. With improvement in the overall nutrition of the population, the role of primary malnutrition waned and secondary malnutrition was emphasized as a result of a better understanding of maldigestion and malabsorption caused by chronic alcohol consumption and various diseases associated with chronic alcoholism. At the same time, the concept of the direct toxicity of alcohol came to the forefront as an explanation for the widespread cellular injury. Some of the hepatotoxicity was found to result from the metabolic disturbances associated with the oxidation of ethanol via the liver alcohol dehydrogenase (ADH) pathway and the redox changes produced by the generated NADH, which in turn affects the metabolism of lipids, carbohydrates, proteins and purines. Exaggeration of the redox change by the relative hypoxia which prevails physiologically in the perivenular zone contributes to the exacerbation of the ethanol-induced lesions in zone 3. In addition to ADH, ethanol can be oxidized by liver microsomes: studies over the last twenty years have culminated in the molecular elucidation of the ethanol-inducible cytochrome P450IIE1 (CYP2E1) which contributes not only to ethanol metabolism and tolerance, but also to the selective hepatic perivenular toxicity of various xenobiotics. Their activation by CYP2E1 now provides an understanding for the increased susceptibility of the heavy drinker to the toxicity of industrial solvents, anaesthetic agents, commonly prescribed drugs, 'over the counter' analgesics, chemical carcinogens and even nutritional factors such as vitamin A. Ethanol causes not only vitamin A depletion but it also enhances its hepatotoxicity. Furthermore, induction of the microsomal pathway contributes to increased acetaldehyde generation, with formation of protein adducts, resulting in antibody production, enzyme inactivation and decreased DNA repair; it is also associated with a striking impairment of the capacity of the liver to utilize oxygen. Moreover, acetaldehyde promotes glutathione depletion, free-radical mediated toxicity and lipid peroxidation. In addition, acetaldehyde affects hepatic collagen synthesis: both in vivo and in vitro (in cultured myofibroblasts and lipocytes), ethanol and its metabolite acetaldehyde were found to increase collagen accumulation and mRNA levels for collagen. This new understanding of the pathogenesis of alcoholic liver disease may eventually improve therapy with drugs and nutrients.     

Diagnosis and patient management of oral cancer

With an average age of 60 at diagnosis, oral cancer is largely a disease of older adults. This article reviews the incidence, risk factors, early detection and diagnosis of oral cancer, as well as the principles of multidisciplinary management. Considerations for dental treatment planning prior to radiation therapy and surgery for oral cancer are included.     

Management of "localized" oral cancer

We have outlined the clinical manifestations of "localized" malignant lesions of the intraoral cavity, their clinical behavior after intraoral excision, and their control rate employing intraoral excision as primary therapy. We must keep in mind that these small "localized" cancers are potential "killers" and the five year mortality from disease in our series was 25 per cent. This mortality may decrease with (1) more careful selection when patients are included in the "localized" lesion group and (2) earlier use of composite procedures in questionable cases.     

Clinical study day on oral cancer

An H-shaped device was invented to facilitate placement of the distal interlocking screws during closed femoral nailing. Eleven sound cadaveric femurs were experimentally nailed before the application of the device in 15 patients with a femoral shaft fracture. In all experimental cases the insertion of the distal screws proved to be easy. In 11 of 15 patients with a femoral fracture, distal locking was achieved using the H-device. These primary results should stimulate further clinical application of the device.     

A childhood cancer sibling''s oral history

Ferric nitrilotriacetate (Fe-NTA) is a potent nephrotoxic agent. In this communication, we show the modulatory effect of DL-alpha-tocopherol (Vitamin-E) on ferric nitrilotriacetate (Fe-NTA)-induced renal oxidative stress, toxicity and hyperproliferative response in rats. Fe-NTA-treatment enhances the susceptibility of renal microsomal membrane for iron-ascorbate-induced lipid peroxidation and hydrogen peroxide generation which are accompanied by a decrease in the activities of renal antioxidant enzymes, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and depletion in the level of renal glutathione. Parallel to these changes, a sharp increase in blood urea nitrogen and serum creatinine has been observed. In addition, Fe-NTA-treatment also enhances renal ornithine decarboxylase activity (ODC) and increases [3H]thymidine incorporation in renal DNA. Prophylactic treatment of animals with Vit.E daily for 1 week prior to the administration of Fe-NTA resulted in the diminution of Fe-NTA-mediated damage. Enhanced susceptibility of renal microsomal membrane for lipid peroxidation induced by iron-ascorbate and hydrogen peroxide generation were significantly reduced (P < 0.05). In addition, the depleted level of glutathione and inhibited activities of antioxidant enzymes recovered to significant levels (P < 0.05). Similarly, the enhanced blood urea nitrogen and serum creatinine levels which are indicative of renal injury showed a reduction of about 50% at a higher dose of Vit.E. The pretreatment of rats with Vit.E reduced the Fe-NTA-mediated induction in ODC activity and enhancement in [3H]thymidine incorporation in DNA. The protective effect of Vit.E was dose dependent. In summary, our data suggest that Vit.E is an effective chemopreventive agent in kidney and may suppress Fe-NTA-induced renal toxicity.