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By: John E. Bennett, MD, MACP

  • Adjunct Professor of Medicine, Uniformed Services University of the Health Sciences, F. Edward Hebert School of Medicine
  • Director, Infectious Diseases Training Program, NIH Office of Clinical Research Training and Medical Education, Bethesda, Maryland

https://www.niaid.nih.gov/research/john-e-bennett-md

Tillinghast-Towers Perrin provides actuarial services to virus affecting children buy trimethoprim 960 mg low cost a large number of clients regarding their asbestos liabilities antibiotic resistance mechanisms review purchase trimethoprim 960 mg on line. Third antimicrobial mouthwash purchase trimethoprim without a prescription, a research corporation with extensive experience in asbestos analysis had conducted a similar analysis to antibiotic xi purchase 480mg trimethoprim estimate the average total amount spent for each type of claim in 1998 and 1999. It had worked with a substantial number of defendants to estimate the share of the total value of each type of claim that each of those defendants typically paid and, consequently, the total value of each type of claim. Because our estimates were similar to those obtained by Tillinghast-Towers Perrin, and because Tillinghast had access to a greater amount of data than we did, we did not perform a third analysis using our estimates. Costs and Compensation 91 We then estimated what total spending on a claim of each type would have been, on average, in each year, if all the defendants named on the claim had settled in that year. We then estimated the corresponding average spending per claim by all defendants and insurers combined in either 2000 (when using the Tillinghast estimates) or 1998­1999 (when using the research corporation estimates) by type of claim. We computed the average annual rate of increase in total spending per claim for each type of claim over the 1981­2000 (Tillinghast) or 1998­1999 (research corporation) period. We assumed that the total amount spent per claim, by type of claim, grew at this annual average rate from 1981 through either 2000 or 1998­1999 and computed the resulting average amount spent per claim by type of claim and year. We have no reason to believe that the average total amount spent on each type of claim grew smoothly over that period. Average total spending per claim undoubtedly grew more rapidly in some years than in others. However, the average of the estimates of spending by year we developed by smooth exponential interpolation between 1981 and 2000 or 1998­1999 should be close to the average of the true values over that period. We extrapolated the 1982­2000, or 1982 through 1998­1999, trends in total spending per claim by type of claim to 2001 and 2002. A substantial number of major defendants filed for bankruptcy between 2000 and the summer of 2002. Plaintiff attorneys whom we interviewed told us that they attempt to make up for their inability to obtain compensation from these defendants by demanding larger amounts in compensation from the surviving defendants and by bringing new defendants into the litigation (see Chapter Three). While these actions may have closed some of the gaps opened by the disappearance of the major defendants who petitioned to file for reorganization under Chapter 11, it is quite possible that compensation by type of claim did not grow as rapidly in 2001 and 2002 than it had in other years. If so, our estimate of the amounts spent per claim in 2001 and 2002 will overstate the true amounts. We multiplied our estimate of the number of claims, by type of claim, filed in each year over the period 1982­2002 by the corresponding estimates of the distribution of time-to-disposition and each of the estimates of average spending per claim by type and year. The results are estimates of the total amount paid out by defendants and insurers on each type of claim in each year over the period 1983­2002. We used the Tillinghast-Towers Perrin estimates of the average total amount spent on a claim of each type in 2000 in calculating the estimates presented in Table 5. We used the corresponding estimates of the average total amount spent on a claim of each type in 1998­1999 by the research corporation in calculating the estimates presented in Table 5. They each imply that approximately $70 billion has been spent on asbestos litigation through 2002. Milliman provides actuarial services to a substantial number of defendants and insurers who are involved in asbestos litigation. In the course of their work, Milliman analysts have access to a large volume of data on asbestos payments to date. Using these data, Milliman estimated that about $50 billion was spent on asbestos claims through 2000 (Bhagavatula, 2002). Each of our sets of estimates of total spending on asbestos claims through 2000 implies that the total spending was about $54 billion. Thus, our estimate is similar to that of a well-respected organization with extensive access to data and substantial experience in analyzing asbestos litigation. We also discussed our estimate of total spending on asbestos claims with representatives of several major insurance and reinsurance companies. Milliman estimates that foreign insurers have spent $8 billion on asbestos litigation to date (Bhagavatula, 2002). Foreign insurers accounted for 15 to 22 percent of the expenditures on asbestos litigation through 2000. Nontraditional Defendants Now Account for More Than Half of Asbestos Expenditures. As we noted in Chapter Four, asbestos litigation has spread beyond the asbestos-related manufacturing and installation industries where it first began. Nontraditional defendants and their insurers are also paying an increasing share of the costs to resolve asbestos injury claims. A confidential study of asbestos costs that was shared with us reports that in the early 1980s traditional defendants accounted for about three-quarters of expenditures. In contrast, according to this report, by the late 1990s nontraditional defendants accounted for about 60 percent of asbestos expenditures. This study was performed for a private client by a respected analyst who has had extensive experience in the asbestos litigation area and whose work was cited to us by both plaintiff and defense attorneys. When we sought these data, defendants were generally able to provide these data through 2001. Because the data comprised annual average indemnity payments and defense costs, we had to assume the ratio of defense transaction costs to indemnity did not vary by type of claim. However, the widespread practice of settling claims in blocks, which frequently include different types of claims (see Chapter Three), effectively eliminates differences in the ratio of defense transaction costs to indemnity by type of claim. Accordingly, we used the observations we had for any given year to compute the weighted average ratio of defense transaction costs to total spending for those observations for that year. We then multiplied the ratio for each year and the corresponding estimates of total spending by type of claim to estimate defense transaction costs by year for each type of claim. It also shows the mean and standard deviations of the observations we had for each year through 2001. We assume that defense transaction costs accounted for the same share of total spending in 2002 as they had in 2001. We multiplied our estimates of the share of total spending consumed by defense legal fees and expenses in each year by each of our estimates of total spending in each year from Tables 5. Each of our sets of estimates implies that defense legal fees and expenses consumed more than $21 billion, about 31 percent of the funds spent by defendants and insurers on asbestos personal injury claims through 2002. The defense transaction costs associated with asbestos litigation generally accounted for well over 40 percent of total spending in the 1980s and early 1990s. Defense transaction costs averaged about 44 percent of total asbestos spending in the 1980s and early 1990s. Many of these issues were essentially worked out in the late 1980s and early 1990s in the form of formal judicial decisions, agreements among defendants and insurers regarding joint defense efforts and coverage issues, and agreements between some plaintiff attorneys and defendants to settle claims according to a schedule of payments by claim type. Defense transaction costs averaged about 25 percent of total asbestos spending from the mid-1990s through the early 2000s. Virtually all of our interview respondents discussed what they saw as new instabilities in asbestos litigation after the failure of the Amchem settlement (see Chapter Three). In particular, as an increasing number of major defendants have filed for bankruptcy and ceased paying asbestos claims pending their reorganization, plaintiff attorneys are seeking greater compensation from the defendants who remain in the litigation. Many of those defendants, in turn, are reluctant to pay greater compensation for a given type of claim than they had been paying in the past. Also, we have been told that many defendants are moving away from block settlements of large groups of claims and looking in more detail at individual claims. And a number of those we interviewed believe that as the litigation expands to defendants who had not been involved in the litigation before, there will be new insurance coverage battles. No one we interviewed offered us qualitative or quantitative information about changes in transaction costs resulting from these new sources of instability. But all of these factors have significant potential to influence defense transaction costs, and it seems likely that those costs will increase, at least temporarily, as a result. Because some of these issues may take several years to resolve, such a period of higher costs could be relatively long. Once a bankrupt corporation is reorganized and a trust is established to assume its liabilities, claims processing procedures are largely administrative rather than adversarial. This should lead to dramatically lower transaction costs, as was the case of the Manville Trust. From 1994 to 2000, the Manville Trust reported annual average operating expenses (not including special expenses associated with tobacco litigation) of about $10 million, about 5 percent of the total dollars it paid out to asbestos claimants plus expenses during this period. The Manville Trust also requires that attorneys representing claimants who file claims against it charge a fee of no more than 25 percent of the amount paid to the asbestos claimant. Assuming that these expense ratios are correct, people who file claims against the Manville Trust receive about 70 percent of the total dollars spent by the Trust.

The range of microscopical appearances was similar to antibiotics for acne australia discount trimethoprim 480mg with amex that seen in the major glands antibiotics for acne brands generic trimethoprim 480mg line. Myoepithelial carcinoma this is a rare salivary gland tumour and 26% of cases in a review of the literature (9 cases) involved the oral cavity or oropharynx 668 and only isolated cases have been published since this review 1827 virus 43215 purchase trimethoprim 480 mg overnight delivery. The clinical signs and symptoms are non-specific and the microscopical features are considered in Chapter 5 virus komputer buy trimethoprim on line amex. Carcinoma ex pleomorphic adenoma Lesions involving the oral and oropharyngeal minor glands formed 17. They usually form a painless mass of long duration and there may be a history of recent rapid growth, often with ulceration. Tumour presenting as a firm swelling on the lateral aspect of the junction between the hard and soft palate. B Plasmacytoid, or hyaline myoepithelial cells are often a conspicuous feature of pleomorphic adenomas of minor glands. C Tumors may have an abundant lipomatous component that is occasionally misinterpreted as invasion. Both basal cell adenoma and canalicular adenoma can show multifocal tumours and evidence of duct transformation within salivary gland lobules. Mucinous adenocarcinoma is very rare while clear cell carcinoma is a controversial entity; both are discussed in Chapter 5. Oral pleomorphic adenomas are similar microscopically to tumours elsewhere but frequently lack encapsulation, especially in the palate. Some tumours have a strikingly lipomatous stroma and this should not be misinterpreted as tumour invading fat. Cases of intraoral pleomorphic adenoma with florid pseudoepitheliomatous hyperplasia of the overlying mucosa have been reported following incisional biopsy 2541. Basal cell adenoma About 20% of basal cell adenomas involve the oral cavity and the upper lip and buccal mucosa are the most common sites 669. Cystadenoma these lesions are uncommon and form 7% of benign minor gland tumours 668. Of these, 30% arose in the lips, 23% in the cheek, 20% in the palate and 26% in other oral and oropharyngeal sites. Canalicular adenoma and duct papillomas arise almost exclusively in the minor salivary glands and are discussed in detail in Chapter 5. Pleomorphic adenoma these amount to 40-70% of minor gland tumours, the large majority of cases being located in the palate, lips and buccal mucosa 2711. They usually present as painless, slow-growing, submucosal masses, but occasionally they are traumatised and bleed or ulcerate. They rarely exceed 3 sphere cm in diam- Myoepithelioma the minor glands are the common site for and myoepitheliomas account for about 42% of all of these tumours. They show the same range of morphological variation described in Chapter 5, but predominantly plasmacytoid tumours have a predilection for the palate of younger individuals 546. During the course of the disease or initially, mucosal membranes such as oral mucosa, lymph nodes and visceral organs may be affected, sometimes without skin involvement. They are particularly frequent in distal extremities and may be accompanied by lymphoedema. The disease is usually indolent, lymph node and visceral involvement occurs infrequently. A variant of endemic disease, a lymphadenopathic form in African children is rapidly progressive and highly lethal. It develops in a few months to several years after the transplantation of solid organs or immunosuppressive treatment for a vari- Table 4. The disease may resolve entirely upon withdrawal of immunosuppressive treatment although immunosuppressive treatment although its course is somewhat unpredictable. Early lesions of the skin or the mucosa are uncharacteristic and present with subtle vascular proliferation 2216. In the patch stage, vascular spaces are increased in number, of irregular shape, and may dissect collagen fibres in the superficial corium. Endothelial cells lining the spaces are flattened or more oval, with little atypia. Admixed are sparse lymphocytes and plasma cells; frequently, extravasated erythrocytes and deposits of hemosiderin surround the vas- cular structures. Slits lined by attenuated endothelial cells between collagen bundles are also seen. In some cases, there is a proliferation of spindle or oval endothelial cells around pre-existing blood vessels in the dermis or submucosa. Slit-like spaces, lymphocyte and plasma cell infiltration and extravasated erythrocytes are also observed. There is more extensive angio-proliferation with vascular spaces showing jagged outlines. Inflammatory infiltrate is denser and extravascular red cells and siderophages are numerous. Hyaline globules (likely representing destroyed red blood cells) are frequently found. Nodular stage is characterized by welldefined nodules of intersecting fascicles of spindle cells with only mild atypia and numerous slit-like spaces containing red cells. The lumina may be either empty or contain proteinaceous fluid, lymphocytes and sometimes a few erythrocytes. Epidemiology Lymphangiomas are common paediatric lesions, which most often present at birth or during the first years of life. Lymphangiomas appear mostly in the head and neck area but may be found in any other part of the body. Etiology Early or even congenital appearance in life and lesional architecture are in favour of a developmental malformation, with genetic abnormalities playing an additional role in cystic lymphangioma of the neck in association with Turner syndrome 416. Clinical features the lesion presents as a somewhat circumscribed painless swelling, which is soft and fluctuant on palpation. In oral involvement, the tongue is the site of predilection, the majority of lymphangiomas being located on the dorsal surface of the anterior part of the tongue. The size may vary from pinhead dimensions to massive lesions involving the entire tongue and surrounding structures. Electron microscopy the endothelium of thin-walled vessels is not enveloped by a basement membrane and no pericytes are attached to it, thus directly contacting with the interstitium. With increasing calibre the vessels may acquire pericytes and smooth muscle, respectively. Current interest is centred on treating these lesions with sclerosing agents 2117, interferon 1953 or bleomycin 2903A. There is an exceedingly rare case report of a squamous cell carcinoma arising in a lymphangioma of the tongue 203. A staging system of lymphatic malformations of the head and neck based on the anatomic location has shown to be of relevance in predicting prognosis and outcome of surgical intervention 561,991. Macroscopy Lymphangiomas form a multicystic or spongy mass, the cavities of which contain watery to milky fluid. Histopathology Lymphangiomas are characterized by thin-walled, dilated lymphatic vessels of different size, which are lined by a flat- A B Lymphangioma of the tongue 195. Epidemiology In 1995, nineteen cases of the previously undescribed entity were reported. The reported age range varies from 9-78 years; there is no distinct sex predilection. Clinical features Most tumours presented as an otherwise asymptomatic, slow growing solitary nodule in the anterior dorsal tongue. Macroscopy the cut surface has a gelatinous consistency with occasional foci of haemorrhage. Occasionally, muscle fibres and nerve branches may be entrapped within the tumour. It is composed of round, cup-shaped, fusiform, or polygonal cells with uniform small nuclei and moderate amounts of faintly basophilic cytoplasm; some tumours may show nuclear pleomorphism, hyperchroFig. Histogenesis the tumour cells are possibly derived from undifferentiated ectomesenchymal progenitor cells that have migrated from the neural crest 2410. In addition, the presence of myxoglobulosis-like changes has been reported 1169.

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Q: If a family is requesting a serology titer to antibiotic 3 days uti generic 480 mg trimethoprim with visa circumvent the required immunizations and the family has health insurance which covers immunizations but the insurance does not cover serology titers antibiotic resistance fact sheet cheap 480mg trimethoprim otc, whose responsibility is it to antibiotic resistant bacteria in dogs generic 480 mg trimethoprim with amex pay for the serology titers? Once a person has received the complete series of a recommended vaccination antibiotic kill good bacteria order 960 mg trimethoprim fast delivery, he/she is assumed to have produced the needed immunity level to protect them from the disease. A serology test done without a specific public health or medical reason can be difficult to interpret and can sometimes lead to a person receiving extra vaccines. However, a negative or equivocal serology titer might mean that the individual is susceptible to the disease even if he/she completed the full series of vaccines. Please also refer to the question, "Q: Are serology titers acceptable as laboratory evidence of immunity in lieu of completing a vaccination series? The statute stipulates that each violation of any provision of the State Sanitary Code shall constitute a separate offense and shall be punishable by a penalty of not less than $50 nor more than $1000. A: If you receive a foreign immunization record, you can accept it with proper written documentation. Higher Education Regulations Q: What are the immunization requirements for students entering institutions of higher education? Below are the specific vaccination requirements for attendance: Hepatitis B: Students entering a two- or four-year institution and enrolled with a course study of 12 or more credit hours per semester or term shall have received three doses of a hepatitis B containing vaccine, or alternatively any two doses of a hepatitis B vaccine licensed and approved for a two-dose regimen administered to the student between 11 through 15 years of age. Measles, Mumps, Rubella: Two doses of measles vaccine and 1 dose of mumps and rubella vaccine are required. Students attending two-year institutions and students who do not reside in a campus dormitory are exempt from this requirement. All four-year institutions are required to provide information on meningococcal disease to all new students (including those students who are commuters) prior to matriculation. This information will need to include the nature and severity, causes, disease prevention and treatments, and the availability of a meningococcal vaccine to prevent disease. Q: Are students 31 years of age and older subject to the immunization requirements set forth in N. The institution shall keep the records on file in such form and manner as prescribed by the department. However, in certain situations, institutions of higher education may have additional vaccine requirements. Prospective students should review the individual policies of the college or university. For adolescents who receive the first dose at age 13 through 15 years, a one-time booster dose should be administered, preferably at age 16 through 18 years, before the peak in increased risk. Routine vaccination of healthy persons who are not at increased risk for exposure to N. A serogroup B meningococcal vaccine series may be administered to adolescents and young adults 16 through 23 years of age to provide short term protection against most strains of serogroup B meningococcal disease. This recommendation is labeled as "Category B" meaning that individual clinical decision making is recommended. You should discuss with your healthcare provider whether you are a candidate for the serogroup B vaccine. A: There are currently statutes and regulations requiring distribution of meningococcal educational materials. Educational material provided to students should include information about serogroup B meningococcal disease and the serogroup B vaccine. A: Most school nurses have read-only access, which does not allow you to enter vaccine doses. If school nurses would like to add history or previous vaccine doses, they should contact the regional trainer for their county available at the following link, njiis. A: Yes, vaccine doses entered as history will be added to the official immunization record. Clinician Resources Q: Where can I obtain the Vaccine Declination ("Refusal to Vaccinate") form? A: Clinicians may refer to the American Academy of Pediatrics website 2. However, healthcare institutions and facilities may have their own policies and procedures which may require a signature as a form of consent prior to the administration of vaccine. For further questions pertaining to school immunization requirements, please send an email to immschoolquestions@doh. Please include all your contact information, including your phone number, so your inquiry can be addressed in a timely manner. Additionally, this section contains Missouri specific resources such as the required vaccination schedule and meningitis case reporting form. Raise awareness of meningitis B vaccination amongst student health providers and other providers that treat college-aged students 2. Inform providers about Missouri specific legislation and provide them with resources on Men B. Deliver copies of the parent talking points to parents of students and patients who are thinking about getting vaccinated. Provide young adults who are getting vaccinated with the resources they need to track their immunizations. Post or provide copies of "What you need to know" or "Frequently Asked Questions" so that providers, parents and young adults to inform them about the dangers of Meningits B and encourage vaccination. Adolescents and young adults have an increased risk of contracting meningococcal disease, also known as meningitis, which is a bacterial infection that can lead to lifelong complications and even death. Living in communal living spaces, using shared locker rooms and bathrooms, sharing drinks, and kissing are all things that your child may do in college. As meningitis is spread by saliva, these activities will put your child at increased risk for getting meningitis. As of 2016, Missouri requires that all students living in on-campus housing be vaccinated unless the student has a medical or religious exemption. While the vaccine for MenB is not required for students living offcampus, I recommend it for all individuals age 16 -23 years and for any person working in close contact with students. It is recommended that adolescents are vaccinated at ages 11 to 12 years, with a booster dose at 16 years. Adolescents and young adults have an increased risk of contracting meningitis, which is a bacterial infection that can lead to lifelong complications and even death. Living in dorms, using shared locker rooms and bathrooms, sharing drinks, and kissing are all things that will put *you* at risk of getting this illness. If *you* get a fever, headache, stiff neck, nausea, vomiting, and/or a rash please make an appointment at the student health center right away. Meningococcal disease is any illness that is caused by Neisseria meningitids, a type of bacteria, also called meningococcus. These illnesses can be severe including infections of the lining of the brain and spinal cord (meningitis) and bloodstream infections (bacteremia or septicemia)1. Three different types (or serogroups) of the bacteria, serogroups B, C, and Y, are the most prevalent in the United States 2. In the first 6 months of 2017, there were 6 cases in Missouri, an increase by 3 cases from the previous year. Early symptoms of meningitis are often mistaken for flu or less serious illnesses, which can cause a delay in diagnosis and treatment. Symptoms progress very quickly and may include: stiff neck, high fever, headache, nausea, vomiting, purplish rash, and exhaustion. Students who experience these symptoms, especially if they are sudden, progressive or severe, should be seen by a medical profession as soon as possible. Respiratory and throat secretions, such as saliva or spit, can spread the bacteria during close contact, such as kissing or sharing drinks 2. Living in dorms or using shared locker rooms and bathrooms increases exposure to the bacteria. MenB protects against serogroup B, the most common meningococcal disease serogroup in the United States. Vaccination is recommended for anyone age 16 to 23 years, with a preferential recommendation for those 16 to 18 years1,2. Private insurance also covers serogroup B vaccines; however, it is important to check with individual payers.

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Differential diagnosis In contrast to infection 4 weeks after birth buy trimethoprim 480 mg overnight delivery intraductal papillomas antibiotic prices cheap 960 mg trimethoprim amex, papillary cystadenomas are morphologically multicystic with numerous small to antibiotic 5 day order trimethoprim 480 mg online medium-sized cystic spaces antibiotic ointment for dogs cheap trimethoprim 480 mg free shipping. Localization the vast majority of cases have occurred in the minor salivary glands. Major salivary gland involvement is very rare with the parotid gland being the most frequently involved. Extending into the lumen of the cystic space are fronds of columnar epithelium supported by a central fibrovasacular core. The lack of encapsulation of the ductal structures can at times give the false impression of an invasive growth pattern. Differential diagnosis the differential diagnosis typically centres around three lesions: squamous papilloma, inverted ductal papilloma, and mucoepidermoid carcinoma. Squamous papilloma is composed entirely of squamous epithelium and lacks the endophytic growth pattern and glandular differentiation of sialadenoma papilliferum. Inverted ductal papilloma in contrast to the sialadenoma papilliferum, lacks the glandular complexity, and is a well-circumscribed tumour with blunted, pushing non-infiltrative margins. The invasive pattern and variable mixture of epidermoid, intermediate, mucous, and clear cells found in mucoepidermoid carcinoma set it apart from sialadenoma papilliferum. Prognosis and predictive factors the recurrence rate for sialadenoma papilliferum is in the 10-15% range based on 20 reported cases with adequate follow-up 264. Therefore, it is characterized by a higher risk of recurrence than the other types of ductal papillomas of the salivary gland. Surface growth is exophytic and papillary to verrucous in nature with clusters of underlying minor salivary gland tissue deep to the surface. A Ductal ectasia of varying caliber with lining cells forming short luminal projections or nodular thickenings. B Ductal structures are lined by cuboidal cells with large, uniform and centrally placed nuclei as well as a tall columnar cell population. Other intraoral sites are the upper lip, the retromolar pad, and the faucial pillar 264. Clinical features the sialadenoma papilliferum typically manifests as a painless, exophytic papillary growth that is often interpreted clinically as a squamous papilloma. Macroscopy Gross findings usually show a welldemarcated papillary or verrucoid, sessile to pedunculated surface morphology. Histopathology the neoplasm consists of a biphasic pat- tern with a glandular component consisting of collections of cysts and duct-like spaces underlying a papillary or verrucous type proliferation of squamous epithelium. These papillary extensions of squamous epithelium are supported by fibrovascular cores and extend above the level of the adjacent mucosa. At or near the base of the fronds there is a transition from squamous epithelium to columnar ductal epithelium, which lines the proliferating ductal elements. These ductal elements consist of small and ectatic ducts, some of which show cystic enlargement. The ducts and their papillary folds are lined by a double row of cells showing a basal layer composed of cuboidal cells and a luminal lining of low columnar cells. Mucocytes can be interspersed throughout the lining of ductal cells as well as in the squamous component. Columnar oncocytic cells may also 272 Tumours of the salivary glands Cystadenoma A. Michal Definition Cystadenoma is a rare benign epithelial tumour characterized by predominantly multicystic growth in which the epithelium demonstrates adenomatous proliferation. There is a female predominance and the average age of patients with cystadenoma is about 57 years (range 12-89). Localization About 45% of all cases of cystadenoma arise in the parotid; the majority of tumours are located in minor salivary glands, particularly in the lips and buccal mucosa 668,2711. Clinical features Cystadenomas of the major glands typically present as slowly enlarging painless masses. In oral mucosa, these tumours produce smooth-surfaced nodules that resemble mucoceles. Macroscopy Cut section reveals multiple small cystic spaces or a single large cyst surrounded by lobules of salivary gland or by connective tissue. Histopathology Cystadenomas are often well circumscribed and surrounded by complete or incomplete fibrous capsules. The tumours are composed of cystic spaces, the number and size of which is variable. Most cases are multilocular with individual cystic spaces separated by limited amounts of intervening stroma. The lumens often contain eosinophilic material with scattered epithelial, inflammatory or foamy cells. Rarely, psammoma bodies or crystalloids have been described within the luminal secretion 2389. Oncocytic, mucous, epidermoid and apocrine cells are sometimes present focally or may even predominate. An oncocytic variant of cystadenoma is composed predominantly of oncocytes in unilayered or bilayered papillary structures thus resembling the epithelium of Warthin tumour without lymphoid stroma. An unusual case of oncocytic cystadenoma with apocrine, mucinous, sebaceous and signet ring cell appearance has been described 1715. Cystadenomas of the salivary glands are usually devoid of foci of solid growth, cytologic atypia, fibrosis and apposed lymphoid tissue 790. Papillary cystadenoma is composed of large multilocular or unilocular cysts with multiple papillary projections. Mucinous cystadenoma is composed of multiple cysts lined by mucous tall columnar epithelium with small basally situated nuclei and eosinophilic to clear cytoplasm. The columnar epithelial lining has a uniform thickness with limited papillary growth. Prognosis and predictive factors Cystadenomas are benign tumours, and conservative but complete surgical removal is recommended. The tumours are unlikely to recur but rare cases of mucinous cystadenoma with malignant transformation have been described 1716. C Oncocytic variant of cystadenoma is composed of prevailing oncocytes present in unilayered or bilayered papillary structures thus resembling Warthin tumour without lymphoid stroma. D Oncocytic cystadenoma with apocrine, mucinous, sebaceous and signet ring cell appearance. A Cystic spaces are lined by columnar epithelium with multiple papillary projections. The ratio of benign to malignant mesenchymal tumours varies from series to series, ranging from 18:1-2. Over 85% of soft tissue tumours arise in the parotid gland, over 10% involve the submandibular gland and, rarely, a tumour arises in the sublingual gland. Vascular tumours are the most common benign mesenchymal neoplasm, accounting for almost 40% of the benign tumours 669,2301. Seventy-five to 80% of the vascular neoplasms are haemangiomas, typically the juvenile or cellular variant, with the greatest incidence occurring in the first decade of life 430. Other major salivary gland benign soft tissue neoplasms include neural tumours, most frequently neurofibroma or schwannoma 669 and fibroblastic/myofibroblastic tumours, most frequently nodular fasciitis, and fibromatosis with an infrequent myofibromatosis, fibroma, haemangiopericytoma, solitary fibrous tumour 953,2248 or inflammatory pseudotumour (inflammatory myofibroblastic tumour 775) 2794 being reported. Lipomas, including the pleomorphic variety 934 and miscellaneous other tumours including granular cell tumour 2222, angiomyoma, glomangioma, myxoma, fibrous histiocytoma, giant cell tumour, osteochondroma and rarely a metastatic sarcoma may be also seen. Several cases of lipomas entrapping salivary glandular tissue have been recently described and termed sialolipomas 810,1824, including a congenital case 1129. Salivary gland sarcomas arise in an older population than their benign soft tissue counterparts. Almost any type of sarcoma can arise primarily in the salivary gland 87,669,1583. These are aggressive neoplasms; 40-64% of patients develop recurrences, 38-64% develop metastases (usually haematogenous), and the mortality rate ranges from 36-64% with death occurring frequently within 3 years of diagnosis 87,1583. The most successful treatments are wide surgical excision or surgery combined with radiation. For more specific information about each type of tumour, refer to the other texts 775,2745. B Lowpower view of a palatal tumour showing a mass clearly demarcated from the adjacent salivary gland tissue.

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