Burkitt lymphoma (or “Burkitt’s tumor”, or “Malignant lymphoma, Burkitt’s type”) is a cancer of the lymphatic system (in particular, B lymphocytes). It is named after Denis Parsons Burkitt, a surgeon who first described the disease in 1956 while working in equatorial Africa.[1][2]

Almost by definition, Burkitt’s lymphoma is associated with c-myc gene translocation. This gene is found at 8q24.

Currently Burkitt’s lymphoma can be divided into three main clinical variants: the endemic, the sporadic and the immunodeficiency-associated variants.[5]

By morphology (i.e. microscopic appearance) or immunophenotype, it is almost impossible to differentiate these three clinical variants. Immunodeficiency-associated Burkitt lymphoma may demonstrate more plasmacytic appearance or more pleomorphism, but these features are not specific.

Consists of sheets of monotonous (i.e. similar in size and morphology) population of medium size lymphoid cells with high proliferative activity and apoptotic activity. The “starry sky” appearance seen[7] under low power is due to scattered tingible-bodies laden macrophages (macrophages containing dead body of apoptotic tumor cells). The old descriptive term of “small non-cleaved cell” is misleading. The tumor cells are mostly medium in size (i.e. tumor nuclei size similar to that of histiocytes or endothelial cells). “Small non-cleaved cells” are compared to “large non-cleaved cells” of normal germinal center lymphocytes. Tumor cells possess small amount of basophilic cytoplasm. The cellular outline usually appears squared off.

Normal B cells possess rearranged immunoglobulin heavy and light chain genes, unlike most T-cells and other cells of the body in which the genes are germline. Each isolated B-cell possesses a unique IgH gene rearrangement, reminiscent of the fingerprint of a person. Since Burkitt lymphoma and other B-cell lymphomas are a clonal proliferative process, all tumor cells from one patient are supposed to possess identical IgH genes. When the DNA of tumor cells is analyzed using electrophoresis, a clonal band can be demonstrated since identical IgH genes will move to the same position. On the contrary, when a normal or reactive lymph node is analyzed using the same technique, a smear rather than a distinct band will be seen. This technique is useful since sometimes benign reactive processes (e.g. infectious mononucleosis) and malignant lymphoma can be difficult to distinguish.

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A bunion is a structural deformity of the bones and the joint between the foot and big toe, and may be painful.[1]

A bunion is an enlargement of bone or tissue around the joint at the base of the big toe (metatarsophalangeal joint).The big toe may turn in toward the second toe (angulation), and the tissues surrounding the joint may be swollen and tender.

Today the term usually is used to refer to the pathological bump on the side of the great toe joint. The bump is the swollen bursal sac and/or an osseous (bony) deformity that has grown on the mesophalangeal joint (where the first metatarsal bone and hallux meet).

The term “hallux valgus” or “hallux abducto valgus” are the most commonly-used medical terms associated with a bunion deformity, where “hallux” refers to the great toe, “valgus” refers to the abnormal angulation of the great toe commonly associated with bunion deformities, and “abducto” refers to the abnormal drifting or inward leaning of the great toe towards the second toe, which is also commonly associated with bunion disorders.

The symptoms of bunions include irritated skin around the bunion, pain when walking, joint redness and pain, and possible shift of the big toe toward the other toes.

Bunions are caused by a biomechanical abnormality, where certain tendons, ligaments, and supportive structures of the first metatarsal are no longer functioning correctly. This biomechanical abnormality may be caused by a variety of conditions intrinsic to the structure of the foot–such as flat feet, excessive ligamentous flexibility, abnormal bone structure, and certain neurological conditions. These factors are often considered genetic. Although some experts are convinced that poor fitting footwear is the main cause of bunion formation,[2] other sources concede only that footwear exacerbates the problem caused by the original genetic deformity.[3]

Bunions are commonly associated with a deviated position of the big toe toward the second toe, and the deviation in the angle between the first and second metatarsal bones of the foot. The small sesamoid bones found beneath the first metatarsal (which help the flexor tendon bend the big toe downwards) may also become deviated over time as the first metatarsal bone drifts away from its normal position. Arthritis of the great toe joint, diminished and/or altered range of motion, and discomfort with pressure applied to the bump or with motion of the joint, may all accompany bunion development.

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In medicine (gastroenterology and hepatology), Budd-Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein or inferior vena cava. It presents with the classical triad of abdominal pain, ascites and hepatomegaly. Examples of occlusion include thrombosis of hepatic veins and membranous webs in the inferior vena cava. The syndrome can be fulminant, acute, chronic, or asymptomatic. It occurs in 1 out of 100,000 individuals and is more common in females. Some 10-20% also have obstruction of the portal vein.

The acute syndrome presents with rapidly progressive: severe upper abdominal pain, jaundice, hepatomegaly (enlarged liver), ascites, elevated liver enzymes, and eventual encephalopathy. The fulminant syndrome presents early with encephalopathy and ascites. Severe hepatic necrosis and lactic acidosis may be present as well. Caudate lobe hypertrophy is often present. The majority of patients have a slower-onset form of Budd-Chiari syndrome. This can be painless. A system of venous collaterals may form around the occlusion which may be seen on imaging as a “spider’s web.” Patients may progress to cirrhosis and show the signs of liver failure.

An asymptomatic form may be totally silent and discovered only incidentally. It is generally not concerning.

Often, the patient is known to have a tendency towards thrombosis, although Budd-Chiari syndrome can also be the first symptom of such a tendency. Examples of genetic tendencies include Protein C deficiency, Protein S deficiency, the Factor V Leiden mutation, and Prothrombin Mutation G20210A [1]. An important non-genetic risk factor is the use of estrogen-containing (combined) forms of hormonal contraception. Other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet’s disease, dacarbazine, pregnancy, and trauma.

Many patients have Budd-Chiari syndrome as a complication of polycythemia vera (myeloproliferative disease of red blood cells). [2] Patients suffering from paroxysmal nocturnal hemoglobinuria (PNH) appear to be especially at risk for Budd-Chiari syndrome, more than other forms of thrombophilia: up to 39% develop venous thromboses [3] and 12% may acquire Budd-Chiari. [4]

A related condition is veno-occlusive disease, which occurs in recipients of bone marrow transplants as a complication of their medication. Although its mechanism is similar, it is not considered a form of Budd-Chiari syndrome.

Any obstruction of the venous vasculature of the liver is referred to as Budd-Chiari syndrome, from the venules to the right atrium. This leads to increased portal vein and hepatic sinusoid pressures as the blood flow stagnates. The increased portal pressure causes: 1) increased filtration of vascular fluid with the formation of protein-rich ascites in the abdomen; and 2) collateral venous flow through alternative veins leading to gastric varices and hemorrhoids. Obstruction also causes hepatic necrosis and eventual centrilobular fibrosis due to ischemia. Renal failure may occur, perhaps due to the body sensing an “underfill” state and subsequent activation of the renin-angiotensin pathways and excess sodium retention.

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Bubonic plague is the best-known manifestation of the bacterial disease plague, caused by the bacterium Yersinia pestis (formerly known as Pasteurella pestis). Bubonic plague is often used synonymously for plague, but it does in fact refer specifically to an infection that enters through the skin and travels through the lymphatics, as is often seen in flea-borne infections. Bubonic Plague kills about 50% of infected patients in 4-7 days without treatment. The Bubonic plague is believed by many to be the Black Death that swept through Europe in the 1340s.

The bubonic plague is an infection of the lymphatic system, usually resulting from the bite of an infected flea. The fleas are often found on rodents, such as rats, and seek out other prey when their rodent hosts die. Once established, bacteria rapidly spread to the lymph nodes and multiply. Yersinia pestis can resist phagocytosis and even reproduce inside phagocytes and kill them. As the disease progresses, the lymph nodes can hemorrhage and become necrotic. Bubonic plague can progress to lethal septicemic plague in some cases.

The most famous symptom of bubonic plague is swollen lymph glands, called buboes. These are commonly found in the armpits, groin or neck. The bubonic plague was the first step of the ongoing plague. Two other forms of the plague, pneumonic and septicemic, resulted after a patient with the bubonic plague developed pneumonia or blood poisoning.

Other symptoms include spots on the skin that are red at first and then turn black, heavy breathing, continuous blood vomiting, aching limbs and terrible pain. The pain is usually caused by the actual decaying, or decomposing of the skin while the infected person is still alive. When death begins the person will get spasms.

The deadly disease has claimed nearly 200 million lives (although there is some debate as to whether all of the plagues attributed to it are in fact the same disease). The first recorded epidemic ravaged the Byzantine Empire during the sixth century, and was named the Plague of Justinian after the emperor, who was infected but survived. The most infamous and devastating instance of the plague was the Black Death, which killed a third of the population of Europe. The Black Death is thought to have originated in the Gobi Desert. Carried by the fleas on rats, it spread along trade routes and reached the Crimea in 1346. In 1347 it spread to Constantinople and then Alexandria, killing thousands every day, and soon arrived in Western Europe.

The next few centuries were marked by several local outbreaks of lesser severity. The Great Plague of London, 1665–1666, was the last major outbreak of the bubonic plague in Europe. The plague resurfaced in the mid-18th century; like the Black Death, the Third Pandemic began in Central Asia. It spread worldwide, killing millions, into the early 20th century.

During the second sino-japanese war, plague was used as a bacteriological weapon by the Imperial Japanese Army. These weapons were provided by Shiro Ishii’s units and used in experiments on humans before being used on the field. For example, in 1940, the Imperial Japanese Army Air Service bombed Ningbo with fleas carrying the bubonic plague.[1] During the Khabarovsk War Crime Trials the accused, such as Major General Kiyashi Kawashima, testified that, in 1941, some 40 members of Unit 731 air-dropped plague-contaminated fleas on Changde. These operations caused epidemic plague outbreaks.[2]

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The Brugada syndrome is a genetic disease that is characterised by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death. It is also known as Sudden Unexpected Death Syndrome[1] (SUDS), and is the most common cause of sudden death in young men without known underlying cardiac disease in Thailand and Laos[2].

Although the ECG findings of Brugada syndrome were first reported[3] among survivors of cardiac arrest in 1989, it was only in 1992 that the Brugada brothers[4] recognised it as a distinct clinical entity, causing sudden death by causing ventricular fibrillation (a lethal arrhythmia) in the heart.

Approximately 20% of the cases of Brugada syndrome have been shown to be associated with mutation(s) in the gene that encodes for the sodium ion channel in the cell membranes of the muscle cells of the heart (the myocytes). The gene, named SCN5A, is located on the short arm of the third chromosome (3p21). Loss-of-function mutations in this gene lead to a loss of the action potential dome of some epicardial areas of the right ventricle. This results in transmural and epicardial dispersion of repolarization. The transmural dispersion underlies ST-segment elevation and the development of a vulnerable window across the ventricular wall, whereas the epicardial dispersion of repolarization facilitates the development of phase 2 reentry, which generates a phase 2 reentrant extrasystole that captures the vulnerable window to precipitate ventricular tachycardia and/or fibrillation that often results in sudden cardiac death. At present time however, all the reported patients died because of the disease and submitted to detailed necropsy study, have shown a structural right ventricular pathology underlying the syndrome.

Over 160 mutations in the SCN5A gene have been discovered to date, each having varying mechanisms and effects on function, thereby explaining the varying degrees of penetration and expression of this disorder. [7]

An example of one of the mechanisms in which a loss of function of the sodium channel occurs is a mutation in the gene that disrupts the sodium channel’s ability to bind properly to ankyrin-G, an important protein mediating interaction between ion channels and cytoskeletal elements. Very recently a mutation in a second gene, Glycerol-3-phosphate dehydrogenase 1-like gene (GPD1L) has been shown to result in Brugada Syndrome in a large multigenerational family (London, 2006). This gene acts as an ion channel modulator in the heart, although the exact mechanism is not yet understood.

Recently Antzelevitch has identified mutations in the L-type calcium channel subunits (CACNA1C (A39V and G490R) and CACNB2 (S481L)) leading to ST elevation and a relatively short QT interval (below 360 msec).[8]

This condition is inherited in an autosomal dominant pattern and is more common in males. In addition it has a higher prevalence in most Asian populations.

Genetic testing for Brugada syndrome is clinically available and may help confirm a diagnosis in patients suspected of having Brugada syndrome, as well as differentiate between relatives who are at-risk for the disease and those who are not (Overview of Brugada Syndrome Genetic Testing).

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Brucellosis, also called undulant fever, or Malta fever, is a highly contagious zoonosis caused by ingestion of unsterilized milk or meat from infected animals, or close contact with their secretions. Brucella spp. are small, gram-negative, non-motile, non-spore-forming rods, which function as facultative intracellular parasites that cause chronic disease, which usually persists for life. Brucellosis has been recognized in both animals and humans since the 19th century.

The disease now called brucellosis, under the name “Mediterranean fever”, first came to the attention of British medical officers in Malta during the Crimean War in the 1850s. The causal relationship between organism and disease was first established by Dr. David Bruce in 1887.[1][2]

In 1897 Danish veterinarian Bernhard Bang isolated Brucella abortus as the agent and the additional name Bang’s disease was assigned. In modern usage “Bang’s disease” is often shortened to just “bangs” when ranchers discuss the disease or vaccine.

Maltese doctor and archaeologist Sir Temi Zammit identified unpasteurized milk as the major source of the pathogen in 1905, and it has since become known as Malta Fever, or deni rqiq locally. In cattle this disease is also known as contagious abortion and infectious abortion.

The popular name “undulant fever” originates from the characteristic undulance (or “wave-like” nature) of the fever which rises and falls over weeks in untreated patients. In the 20th Century, this name, along with “brucellosis” (after Brucella, named for Dr Bruce), gradually replaced the 19th Century names “Mediterranean fever” and “Malta fever”.

In 1989, Saudi Arabian neurologists discovered neurobrucellosis, a neurological involvement in brucellosis.[3][4]

Species infecting domestic livestock are B. melitensis (goats and sheep), B. suis (pigs, see Swine brucellosis), B. abortus (cattle and bison), B. ovis (sheep), and B. canis (dogs). B. abortus also infects bison and elk in North America and B. suis is endemic in caribou. Brucella species have also been isolated from several marine mammal species (pinnipeds and cetaceans.)

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Brown-Sequard Syndrome or Brown-Séquard syndrome, also known as Brown-Séquard’s hemiplegia and Brown-Séquard’s paralysis, is a loss of motor function (paralysis and ataxia) and sensation caused by the lateral hemisection (cutting) of the spinal cord. Other synonyms are crossed hemiplegia, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis and spinal hemiparaplegia.

The hemisection of the cord results in a lesion of each of the three main neural systems:

As a result of the injury to these three main brain pathways the patient will present with three lesions.

Brown-Séquard syndrome may be caused by a spinal cord tumor, trauma (such as a gunshot wound or puncture wound to the neck or back), ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis.

Brown Sequard syndrome is an incomplete spinal cord lesion characterized by clinical presentation reflecting hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same side as the lesion and deficits in pain and temperature sensation on the opposite side on physical exam. This is called ipsilateral (on the same side as the spinal cord lesion) hemiplegia and contralateral (on the opposite side) pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because these nerve fibers of the spinothalamic tract cross the spinal cord. In its pure form, it is rarely seen. Incomplete forms are also observed. The most common cause is penetrating trauma such as a gunshot wound or stab would to the spinal cord. This may be seen most often in the cervical (neck) or thoracic spine. Other causes are tumors, bleeding episodes, tuberculosis, and multiple sclerosis.

The presentation can be progressive and incomplete. It can advance from a typical Brown Sequard syndrome to complete paralysis. It is not always permanent, and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology which caused it in the first place.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If there syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant. [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14]

Any presentation of spinal injury which is an incomplete lesion can be called a partial Brown Sequard or incomplete Brown Sequard syndrome, so long as it has characterized by features of a motor loss on the same side of the spinal injury and loss of sensation on the opposite side.

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Bronchiectasis is a disease that causes localized, irreversible dilation of part of the bronchial tree. It is classified as an obstructive lung disease, along with bronchitis and cystic fibrosis. Involved bronchi are dilated, inflamed, and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions. Bronchiectasis is associated with a wide range of disorders, but it usually results from necrotizing bacterial infections, such as infections caused by the Staphylococcus or Klebsiella species or Bordetella pertussis.[1]

Rene Theophile Hyacinthe Laënnec, the man who invented the stethoscope, used his creation to first discover bronchiectasis in 1819.[2]. The disease was researched in greater detail by Sir William Osler in the late 1800s; in fact, it is suspected that Osler actually died of complications from undiagnosed bronchiectasis[3].

Dilation of the bronchial walls results in airflow obstruction and impaired clearance of secretions because the dilated areas disrupt normal air pressure in the bronchial tubes, causing sputum to pool inside the dilated areas instead of being pushed upward[4]. The pooled sputum provides an environment conducive to the growth of infectious pathogens, and these areas of the lungs are thus very vulnerable to infection. The more infections that the lungs experience, the more damaged the lung tissue and alveoli become. When this happens, the bronchial tubes become more inelastic and dilated, creating a self-perpetuating cycle of further damage to the lungs.

There are three types of brochiectasis, varying by level of severity. Fusiform (cylindrical) bronchiectasis (the most common type) refers to mildly inflamed bronchi that fail to taper distally. In varicose bronchiectasis, the bronchial walls appear beaded, because areas of dilation are mixed with areas of constriction. Saccular (cystic) bronchiectasis is characterized by severe and irreversible ballooning of the bronchi peripherally, with or without air-fluid levels.[5] Chronic productive cough is prominent, occurring in up to 90% of patients with bronchiectasis. Sputum is produced on a daily basis in 76% of patients.[6]

Generally, persons suffering from bronchiectasis tend to be infected by Haemophilus influenzae early on in the disease course. Secondary infection is usually due to Staphylococcus aureus; followed by Moraxella catarrhalis and finally Pseudomonas aeruginosa.[7]

There are both congenital and acquired causes of bronchiectasis. Kartagener syndrome, which affects the mobility of cilia in the lungs[8], aids in the development of the disease. Another common genetic cause is cystic fibrosis, in which a small number of patients develop severe localized bronchiectasis[9]. Young’s syndrome, which is clinically similar to cystic fibrosis, is thought to significantly contribute to the development of bronchiectasis. This is due to the occurrence of chronic, sinopulmonary infections.[10] Patients with alpha 1-antitrypsin deficiency have been found to be particularly susceptible to bronchiectasis, for unknown reasons. [11] Other less-common congenital causes include primary immunodeficiencies, due to the weakened or nonexistent immune system response to severe, recurrent infections that commonly affect the lung.[12]

Acquired bronchiectasis occurs more frequently, with one of the biggest causes being tuberculosis. Endobronchial tuberculosis commonly leads to bronchiectasis, either from bronchial stenosis or secondary traction from fibrosis.[13] An especially common cause of the disease in children is acquired immune deficiency syndrome, stemming from the human immunodeficiency virus. This disease predisposes patients to a variety of pulmonary ailments, such as pneumonia and other opportunistic infection.[14]. Bronchiectasis can sometimes be an unusual complication of inflammatory bowel disease, especially ulcerative colitis. It can occur in Crohn’s disease as well, but does so less frequently. Bronchiectasis in this situation usually stems from various allergic responses to inhaled fungus spores.[15] Recent evidence has shown an increased risk of bronchiectasis in patients with rheumatoid arthritis who smoke. One study stated a tenfold increased prevalence of the disease in this cohort[16]. Still, it is unclear as to whether or not cigarette smoke is a specific primary cause of bronchiectasis.

Other acquired causes of bronchiectasis involving environmental exposures include respiratory infections, obstructions, inhalation and aspiration of ammonia and other toxic gases, pulmonary aspiration, alcoholism, heroin (drug use), and various allergies.[17]

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A brain tumor (brain tumour outside the US; see spelling differences) is any intracranial tumor created by abnormal and uncontrolled cell division, normally either in the brain itself (neurons, glial cells (astrocytes, oligodendrocytes, ependymal cells), lymphatic tissue, blood vessels), in the cranial nerves (myelin-producing Schwann cells), in the brain envelopes (meninges), skull, pituitary and pineal gland, or spread from cancers primarily located in other organs (metastatic tumors). Primary (true) brain tumors are commonly located in the posterior cranial fossa in children and in the anterior two-thirds of the cerebral hemispheres in adults, although they can affect any part of the brain. In the United States in the year 2005, it was estimated that there were 43,800 new cases of brain tumors (Central Brain Tumor Registry of the United States, Primary Brain Tumors in the United States, Statistical Report, 2005–2006),[1] which accounted for 1.4 percent of all cancers, 2.4 percent of all cancer deaths,[2] and 20–25 percent of pediatric cancers.[2][3] Ultimately, it is estimated that there are 13,000 deaths per year in the United States alone as a result of brain tumors.[1]

In the US, approximately 2000 children and adolescents younger than 20 years of age are diagnosed with malignant brain tumors each year. Higher incidence rates were reported in 1985–94 than in 1975–84. There is some debate as to possible reasons; one theory is that the trend is the result of improved diagnosis and reporting, since the jump occurred at the same time as MRIs became available widely, and since there was no coincident jump in mortality. The CNS cancer survival rate in children is approximately 60%. The rate varies with the age of onset, with younger patients having higher mortality, and cancer type.[4]

In children under 2, about 70% of brain tumors are medulloblastoma, ependymoma, and low-grade glioma. Less commonly, and seen usually in infants, are teratoma and atypical teratoid rhabdoid tumor.[5] Germ cell tumors, including teratoma, make up just 3% of pediatric primary brain tumors, but the worldwide incidence varies significantly.[6]

Symptoms of brain tumors may depend on two factors: tumor size (volume) and tumor location. The time point of symptom onset in the course of disease correlates in many cases with the nature of the tumor (“benign”, i.e. slow-growing/late symptom onset, or malignant, fast growing/early symptom onset) is a frequent reason for seeking medical attention in brain tumor cases.

Large tumors or tumors with extensive perifocal swelling edema inevitably lead to elevated intracranial pressure (intracranial hypertension), which translates clinically into headaches, vomiting (sometimes without nausea), altered state of consciousness (somnolence, coma), dilatation of the pupil on the side of the lesion (anisocoria), papilledema (prominent optic disc at the funduscopic examination). However, even small tumors obstructing the passage of cerebrospinal fluid (CSF) may cause early signs of increased intracranial pressure. Increased intracranial pressure may result in herniation (i.e. displacement) of certain parts of the brain, such as the cerebellar tonsils or the temporal uncus, resulting in lethal brainstem compression. In young children, elevated intracranial pressure may cause an increase in the diameter of the skull and bulging of the fontanelles.

Depending on the tumor location and the damage it may have caused to surrounding brain structures, either through compression or infiltration, any type of focal neurologic symptoms may occur, such as cognitive and behavioral impairment, personality changes, hemiparesis, hypesthesia, aphasia, ataxia, visual field impairment, facial paralysis, double vision, tremor etc. These symptoms are not specific for brain tumors – they may be caused by a large variety of neurologic conditions (e.g. stroke, traumatic brain injury). What counts, however, is the location of the lesion and the functional systems (e.g. motor, sensory, visual, etc.) it affects.

A bilateral temporal visual field defect (bitemporal hemianopia—due to compression of the optic chiasm), often associated with endocrine disfunction—either hypopituitarism or hyperproduction of pituitary hormones and hyperprolactinemia is suggestive of a pituitary tumor.

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Bowen’s disease (BD) is a neoplastic skin disease, considered either as an early stage or intraepidermal form of squamous cell carcinoma. It was named after Dr John T. Bowen, the doctor who first described it in 1912. Erythroplasia of Queyrat is a form of squamous cell carcinoma in situ possibly induced by HPV.

Causes of BD include solar damage, arsenic, immunosuppression (including AIDS), viral infection (human papillomavirus or HPV) and chronic skin injury and dermatoses.

Bowen’s disease typically presents as a gradually enlarging, well demarcated erythematous plaque with an irregular border and surface crusting or scaling. BD may occur at any age in adults but is rare before the age of 30 years – most patients are aged over 60. Any site may be affected, although involvement of palms or soles is uncommon. BD occurs predominantly in women (70-85% of cases); about three-quarters of patients have lesions on the lower leg (60-85%), usually in previously or presently sun-exposed areas of skin. A persistent progressive non-elevated red scaly or crusted plaque which is due to an intradermal carcinoma and is potentially malignant. Atypical squamous (resembling fish scales) cells proliferate through the whole thickness of the epidermis. The lesions may occur anywhere on the skin surface or on mucosal surfaces. The cause most frequently found is trivalent arsenic compounds. Freezing, cauterization or diathermy coagulation is often effective treatment.

Bowen’s is equivalent to squamous cell carcinoma in situ. The entire tumor is confined to the epidermis and does not invade into the dermis. The cells in Bowen’s are extremely unusual or atypical under the microscope and in many cases look worse under the microscope than the cells of many outright and invading squamous-cell carcinomas. The degree of atypia (strangeness, unusualness) seen under the microscope best tells how cells may behave should they invade another portion of the body.

Photodynamic therapy (PDT), Cryotherapy (freezing) or local chemotherapy (with 5-fluorouracil) are favored by some clinicians over excision. Because the cells of Bowen’s disease have not invaded the dermis, it has a much better prognosis than invasive squamous cell carcinoma. Outstanding result have been noted with the use of imiquimod for Bowen’s disease of the skin, including the penis (erythroplasia of Queyrat). Imiquimod is not FDA approved for the treatment of squamous cell carcinoma.

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