Lymphoma is a type of cancer that originates in lymphocytes of the immune system. They often originate in lymph nodes, presenting as an enlargement of the node (a tumor). Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but do not form tumors.[1] There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms.

Thomas Hodgkin published in 1832 the first description of lymphoma, specifically of the form named after him, Hodgkin’s lymphoma. Since, many other forms of lymphoma have been described and many classifications proposed. The 1982 Working formulation classification became very popular. It introduced the category non-Hodgkin lymphoma (NHL), itself divided into 16 different diseases. However, since these different lymphomas have little in common with each other, the NHL label is of limited usefulness for doctors or patients and is slowly being abandoned. The latest classification by the WHO (2001) lists 43 different forms of lymphoma divided in four broad groups.

Some forms of lymphoma are indolent (e.g. small lymphocytic lymphoma), compatible with a long life even without treatment, whereas other forms are aggressive (e.g. Burkitt’s lymphoma), causing rapid deterioration and death. The prognosis therefore depends on the correct classification of the disease, established by a pathologist after examination of a biopsy.

Although older classifications referred to histiocytic lymphomas, these are recognized in newer classifications as of B, T or NK cell lineage. True histiocytic malignancies are rare and are classified as sarcomas.[2]

According to the U.S. National Institutes of Health, lymphomas account for about five percent of all cases of cancer in the United States, and Hodgkin’s lymphoma in particular accounts for less than one percent of all cases of cancer in the United States.

Because the whole system is part of the body’s immune system, patients with a weakened immune system, such as from HIV infection or from certain drugs or medication, also have a higher incidence of lymphoma.

In the 1990s, the Revised European-American Lymphoma (REAL) Classification attempted to apply immunophenotypic and genetic features in identifying distinct clinicopathologic NHL entities. [3]

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Lymphangioleiomyomatosis (LAM) is a rare lung disease that results in disorderly smooth muscle proliferation throughout the bronchioles, alveolar septa, perivascular spaces, and lymphatics, resulting in the obstruction of small airways (leading to pulmonary cyst formation and pneumothorax) and lymphatics (leading to chylous pleural effusion). LAM occurs in a sporadic form, which only affects females, who are usually of childbearing age. LAM also occurs in patients who have tuberous sclerosis.

Sporadic LAM only affects women.

The proliferating smooth muscle that occurs in the type of LAM seen in patients with tuberous sclerosis (TSC-LAM) has been shown to represent clones of the smooth muscle in those patients’ renal angiomyolipomas. Thus it is believed to represent metastases of this “benign” tumor. There is a female preponderance to TSC-LAM.[1]

With LAM, there is diffuse replacement of the pulmonary parenchyma by thin-walled cysts measuring 2-20 mm in diameter, with equal involvement of upper and lower lung zones. On chest X-rays, superimposition of the cysts gives a reticulonodular pattern of interstitial lung disease. High-resolution CT of the chest is both more specific for the diagnosis, as well as better able to assess the degree of pulmonary involvement.

Exact data on survival rates are difficult to collect because LAM is often misdiagnosed as asthma or other more common diseases, and may not be correctly identified until it is in an advanced condition. A comprehensive study of all known British LAM patients found that out of 21 patients that had been observed for 15 years or more since diagnosis, 18 were still alive; and 11 of 12 patients that had been observed for 20 years or more were alive, however, no data is available on respiratory disability.[2]

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Lyme disease, or borreliosis, is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia.[1] Borrelia burgdorferi is the predominant cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii are implicated in most European cases.

Lyme disease is the most common tick-borne disease in the Northern Hemisphere. Borrelia is transmitted to humans by the bite of infected ticks belonging to certain species of the genus Ixodes (the hard-bodied ‘hard ticks’).[2] Early manifestations of infection may include fever, headache, fatigue, depression, and a characteristic skin rash called erythema migrans. Left untreated, late manifestations involving the joints, heart, and nervous system can occur. In most cases, the infection and its symptoms are eliminated with antibiotics, especially if diagnosis and treatment occur early in the course of illness. Late, delayed, or inadequate treatment can lead to late manifestations of Lyme disease which can be disabling and difficult to treat.[3]

Some Lyme disease patients who have completed a course of antibiotic treatment continue to have symptoms such as severe fatigue, sleep disturbance, and cognitive difficulties. Some groups have argued that “chronic” Lyme disease is responsible for a range of medically unexplained symptoms beyond the objectively recognized manifestations of late Lyme disease, and that additional, long-term antibiotic treatment is warranted in such cases.[4] Of four randomized controlled trials of long-term antibiotic courses in patients with ongoing symptoms, two found no benefit[5][6], and two found inconsistent benefits and significant side effects and risks from further antibiotic treatment.[7][8][9] Most expert groups including the Infectious Diseases Society of America and the American Academy of Neurology have found that existing scientific evidence does not support a role for Borrelia nor ongoing antibiotic treatment in such cases.[10][11]

Lyme disease can affect multiple body systems, producing a range of potential symptoms. Not all patients with Lyme disease will have all symptoms, and many of the symptoms are not specific to Lyme disease but can occur in other diseases as well. The incubation period from infection to the onset of symptoms is usually 1–2 weeks, but can be much shorter (days), or much longer (months to years). Symptoms most often occur from May through September because the nymphal stage of the tick is responsible for most cases.[12] Asymptomatic infection exists but is found in less than 7% of infected individuals in the United States.[13] Asymptomatic infection may be much more common among those infected in Europe.[14]

The classic sign of early local infection is a circular, outwardly expanding rash called erythema chronicum migrans (also erythema migrans or EM), which occurs at the site of the tick bite 3 to 32 days after being bitten.[15] The rash is red, and may be warm, but is generally painless. Classically, the innermost portion remains dark red and becomes indurated; the outer edge remains red; and the portion in between clears – giving the appearance of a bullseye. However, the partial clearing is uncommon, and thus a true bullseye occurs in as few as 9% of cases.[16]

Erythema migrans is thought to occur in about 80% of infected patients.[15] Patients can also experience flu-like symptoms such as headache, muscle soreness, fever, and malaise.[17]

Lyme disease can progress to later stages even in patients who do not develop a rash.[18]

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Lung cancer is a disease of uncontrolled cell growth in tissues of the lung. This growth may lead to metastasis, which is invasion of adjacent tissue and infiltration beyond the lungs. The vast majority of primary lung cancers are carcinomas of the lung, derived from epithelial cells. Lung cancer, the most common cause of cancer-related death in men and the second most common in women (after breast cancer),[1] is responsible for 1.3 million deaths worldwide annually.[2] The most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss.[3]

The main types of lung cancer are small cell lung carcinoma and non-small cell lung carcinoma. This distinction is important, because the treatment varies; non-small cell lung carcinoma (NSCLC) is sometimes treated with surgery, while small cell lung carcinoma (SCLC) usually responds better to chemotherapy and radiation.[4] The most common cause of lung cancer is long-term exposure to tobacco smoke.[5] The occurrence of lung cancer in nonsmokers, who account for as many as 15% of cases [6], is often attributed to a combination of genetic factors,[7][8] radon gas,[9] asbestos,[10] and air pollution,[11][12][13] including secondhand smoke.[14][15]

Lung cancer may be seen on chest x-ray and computed tomography (CT scan). The diagnosis is confirmed with a biopsy. This is usually performed via bronchoscopy or CT-guided biopsy. Treatment and prognosis depend upon the histological type of cancer, the stage (degree of spread), and the patient’s performance status. Possible treatments include surgery, chemotherapy, and radiotherapy. With treatment, the five-year survival rate is 14%.[3]

The vast majority of lung cancers are carcinomas—malignancies that arise from epithelial cells. There are two main types of lung carcinoma, categorized by the size and appearance of the malignant cells seen by a histopathologist under a microscope: non-small cell (80.4%) and small-cell (16.8%) lung carcinoma.[16] This classification, based on histological criteria, has important implications for clinical management and prognosis of the disease.

The non-small cell lung carcinomas are grouped together because their prognosis and management are similar. There are three main sub-types: squamous cell lung carcinoma, adenocarcinoma, and large cell lung carcinoma.

Accounting for 31.2% of lung cancers,[16] squamous cell lung carcinoma usually starts near a central bronchus. Cavitation and necrosis within the center of the cancer is a common finding. Well-differentiated squamous cell lung cancers often grow more slowly than other cancer types.[4]

Adenocarcinoma accounts for 29.4% of lung cancers.[16] It usually originates in peripheral lung tissue. Most cases of adenocarcinoma are associated with smoking; however, among people who have never smoked (“never-smokers”), adenocarcinoma is the most common form of lung cancer.[20] A subtype of adenocarcinoma, the bronchioloalveolar carcinoma, is more common in female never-smokers, and may have different responses to treatment.[21]

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The long QT syndrome (LQTS) is a rare congenital heart condition with delayed repolarization following depolarization (excitation) of the heart, associated with syncope (fainting) due to ventricular arrhythmias, possibly of type torsade de pointes, which can deteriorate into ventricular fibrillation and ultimately sudden death. Arrhythmia in individuals with LQTS are often associated with exercise or excitement.

Individuals with LQTS have a prolongation of the QT interval on the ECG. The QRS complex corresponds to ventricular depolarization while the T wave corresponds to ventricular repolarization. The QT interval is measured from the Q point to the end of the T wave. While many individuals with LQTS have persistent prolongation of the QT interval, some individuals do not always show the QT prolongation; in these individuals, the QT interval may prolong with the administration of certain medications.

The first documented case of Long QT syndrome was described in Leipzig by Meissner in 1856, where a deafmute girl died after her teacher yelled at her. When the parents were told about her death, they told that her older brother who also was deafmute died after a terible fright[1]. This was before the ECG was invented but is likely the first described case of Jervell and Lange-Nielsen syndrome. In 1957 the first case documented by ECG was described bý Anton Jervell and Fred Lange-Nielsen. Romano, in 1963, and Ward, in 1964, separately described the more common variant of Long QT syndrome with normal hearing, later called Romano-Ward syndrome.

Genetic LQTS can arise from mutation to one of several genes. These mutations tend to prolong the duration of the ventricular action potential (APD), thus lengthening the QT interval. LQTS can be inherited in an autosomal dominant or an autosomal recessive fashion. The autosomal recessive forms of LQTS tend to have a more severe phenotype, with some variants having associated syndactyly (LQT8) or congenital neural deafness (LQT1). A number of specific genes loci have been identified that are associated with LQTS. Genetic testing for LQTS is clinically available and may help to direct appropriate therapies (Overview of LQTS Genetic Testing). The most common causes of LQTS are mutations in the genes KCNQ1 (LQT1), KCNH2 (LQT2), and SCN5A (LQT3); the following is a list of all genes associated with LQTS:

Drug induced LQT is usually a result of treatment by anti-arrhythmic drugs such as amiodarone or a number of other drugs that have been reported to cause this problem (e.g. cisapride). Some anti-psychotic drugs, such as Haloperidol and Ziprasidone, have a prolonged QT interval as a rare side effect. Genetic mutations may make one more susceptible to drug induced LQT.

LQT1 is the most common type of long QT syndrome, making up about 30 to 35 percent of all cases. The LQT1 gene is KCNQ1 which has been isolated to chromosome 11p15.5. KCNQ1 codes for the voltage-gated potassium channel KvLQT1 that is highly expressed in the heart. It is believed that the product of the KCNQ1 gene produces an alpha subunit that interacts with other proteins (particularly the minK beta subunit) to create the IKs ion channel, which is responsible for the delayed potassium rectifier current of the cardiac action potential.

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Locked-In syndrome is a condition in which a patient is aware and awake, but cannot move or communicate due to complete paralysis of nearly all voluntary muscles in the body. It is the result of a brain stem lesion in which the ventral part of the pons is damaged. The condition has been described as “the closest thing to being buried alive”. In French, the common term is “maladie de l’emmuré vivant”, literally translated as walled-in alive disease; in German it is sometimes called “Eingeschlossensein”. [1]

Locked-in syndrome is also known as Cerebromedullospinal Disconnection,[2] De-Efferented State, Pseudocoma,[3] and ventral pontine syndrome.

The term for this disorder was coined by Plum and Posner in 1966.[4][5]

Locked-in syndrome is usually the result of quadriplegia and inability to speak in otherwise cognitively-intact individuals. Those with locked-in syndrome may be able to communicate with others by coding messages by blinking or moving their eyes, which are often not affected by the paralysis.

Patients who have locked-in syndrome are conscious and aware with no loss of cognitive function. They can sometimes retain proprioception and sensation throughout their body. Some patients may have the ability to move certain facial muscles, most often some or all of the extraocular eye muscles.

Unlike persistent vegetative state, in which the upper portions of the brain are damaged and the lower portions are spared, locked-in syndrome is caused by damage to specific portions of the lower brain and brainstem with no damage to the upper brain.

Possible causes of locked-in syndrome include:

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Listeriosis is a bacterial infection caused by a gram-positive, motile bacterium, Listeria monocytogenes.[1] Listeriosis is relatively rare and occurs primarily in newborn infants, elderly patients, and patients who are immunocompromised.[2]

In veterinary medicine, however, listeriosis can be a quite common condition in some farm outbreaks. It can also be found in wild animals; see listeriosis in animals.

Listeriosis symptoms include vomiting, nausea, stomach cramps, diarrhea, severe headache, constipation, persistent fever, stiff neck, loss of balance and convulsions.[3]

Incidence in 2004–2005 was 2.5–3 cases per million population a year in the USA, where pregnant women accounted for 30% of all cases.[4] Of all nonperinatal infections, 70% occur in immunocompromised patients. Incidence in the USA has been falling since the 1990s, in contrast to Europe where changes in eating habits have led to an increase during the same time. In Sweden, it has stabilized at around 5 cases per annum per million population, with pregnant women typically accounting for 1–2 of some 40 total yearly cases.[5]

Listeria monocytogenes is ubiquitous in the environment. The main route of acquisition of Listeria is through the ingestion of contaminated food products. Listeria has been isolated from raw meat, dairy products, vegetables, and seafood. Soft cheeses, unpasteurized milk and unpasteurised pâté are potential dangers; however, some outbreaks involving post-pasteurized milk have been reported.[1]

There are four distinct clinical syndromes:

Rarely listeriosis may present as cutaneous listeriosis. This infection occurs after direct exposure to L. monocyogenes by intact skin and is largely confined to veterinarians who are handling diseased animals, most often after a listerial abortion.[6]

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Lhermitte-Duclos disease (dysplastic gangliocytoma of the cerebellum, LDD) is a rare, slowly growing tumor of cerebellum, sometimes considered as hamartoma, characterized by diffuse hypertrophy of the stratum granulosum of the cerebellum. It is often associated with Cowden syndrome and is pathognomonic for this disease[1]. It was described by Jacques Jean Lhermitte and P. Duclos in 1920[2].

Lhermitte-Duclos disease is a rare entity; approximately 220 cases of LDD have been reported in medical literature[3]. It’s most common in 3. and 4. decade of life.

Cowden disease is caused by mutations of PTEN gene.

Main clinical signs are:

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Leukoplakia is adherent white plaques or patches on the mucous membranes of the oral cavity, including the tongue. The clinical appearance is highly variable. Leukoplakia is not a specific disease entity, but is diagnosis of exclusion. It must be distinguished from diseases that may cause similar white lesions, such as candidiasis or lichen planus.

Leukoplakic lesions are found in approximately 3% of the world’s population. Like erythroplakia, leukoplakia is usually found in adults between 40 and 70 years of age, with a 2:1 male predominance.

Leukoplakia has a multifactorial etiology. Most result from the use of tobacco products. It is thought to be formed by chronic irritation in the mouth. Bloodroot, otherwise known as sanguinaria, is also believed to be associated with leukoplakia.[1]

5% to 25% of leukoplakias are premalignant lesions; wherefore, all leukoplakias should be treated as premalignant lesions by dentists and physicians – they require histologic evaluation or biopsy. Hairy leukoplakia, which is associated with HIV infection and other diseases of severe immune deficiency, is not a premalignant lesion.

The treatment of leukoplakia mainly involves avoidance of predisposing factors — tobacco cessation, smoking, quitting betel chewing, abstinence from alcohol — and avoidance of chronic irritants, e.g., the sharp edges of teeth. A biopsy should be done, and the lesion surgically excised if pre-cancerous changes or cancer is detected.

Taking beta-carotene orally seems to induce remission in patients with oral leukoplakia. Further research is needed to confirm these results.[2]

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Leukemia (Greek leukos ?e????, “white”; aima a?µa, “blood”) is a cancer of the blood or bone marrow and is characterized by an abnormal proliferation (production by multiplication) of blood cells, usually white blood cells (leukocytes). Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases called hematological neoplasms.

Leukemia is clinically and pathologically subdivided into several large groups. The first division is between its acute and chronic forms:

Additionally, the diseases are subdivided according to which kind of blood cell is affected. This split divides leukemias into lymphoblastic or lymphocytic leukemias and myeloid or myelogenous leukemias:

Combining these two classifications provides a total of four main categories:

Within these main categories, there are typically several subcategories. Finally, hairy cell leukemia and T-cell prolymphocytic leukemia are usually considered to be outside of this classification scheme.

Damage to the bone marrow, by way of displacing the normal bone marrow cells with higher numbers of immature white blood cells, results in a lack of blood platelets, which are important in the blood clotting process. This means people with leukemia may become bruised, bleed excessively, or develop pinprick bleeds (petechiae).

White blood cells, which are involved in fighting pathogens, may be suppressed or dysfunctional. This could cause the patient’s immune system to be unable to fight off a simple infection or to start attacking other body cells. Because leukemia prevents the immune system from working normally, some patients experience frequent infection, ranging from infected tonsils, sores in the mouth, or diarrhea to life-threatening pneumonia or opportunistic infections.

Finally, the red blood cell deficiency leads to anemia, which may cause dyspnea and pallor.

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