Diseases and Conditions that Begin with Letter “L”

Written by on March 15, 2011 in Diseases & Issues, Health -
Diseases and conditions that begin with letter L

Here is the list of most common diseases that start with letter “L“:

Labyrinthitis is an inflammation of the inner ear. It derives its name from the labyrinths that house the vestibular system (which sense changes in head position). Labyrinthitis can cause balance disorders.
In addition to balance control problems, a labyrinthitis patient may encounter hearing loss and tinnitus. Labyrinthitis is usually caused by a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy or as a reaction to a particular medication. Both bacterial and viral labyrinthitis can cause permanent hearing loss, although this is rare. Labyrinthitis often follows an upper respiratory tract infection (URI).
A prominent and debilitating symptom of labyrinthitis is severe vertigo. The vestibular system is a set of sensory inputs consisting of three semicircular canals, sensing changes in rotational motion, and the otoliths, sensing changes in linear motion. The brain combines visual cues with sensory input from the vestibular system to determine adjustments required to retain balance.
Recovery from acute labyrinthine inflammation generally takes from one to six weeks. However, it is not uncommon for residual symptoms (disequilibrium and/or dizziness) to last for many months or even years if permanent damage occurs.

Lafora disease, also called Lafora progressive myoclonic epilepsy, is a fatal autosomal recessive genetic disorder characterized by the presence of inclusion bodies, known as Lafora bodies, within neurons and the cells of the heart, liver, muscle, and skin.
Most patients with this disease do not live past the age of twenty-five, and death within ten years of symptoms is usually inevitable. At this time there is no cure or treatment for this disease.
Patients develop the first symptoms mainly during adolescence. Major problems include seizures, drop attacks, myoclonus, ataxia, and, most significantly, a quickly developing, progressive and severe dementia.

Langer-Giedion syndrome (LGS), also called trichorhinophalangeal syndrome type II (TRPS2) or LGCR (for “Langer-Giedion Chromosome Region”), is an uncommon autosomal dominant genetic disorder caused by a deletion of chromosomal material. It is named after the two doctors who undertook the main research into the condition in the 1960s. Diagnosis is usually made at birth or in early childhood.
The syndrome occurs when a small piece of chromosome 8’s long arm, which contains a number of genes is missing. The loss of these genes is responsible for some of the overall characteristics of Langer-Giedion syndrome.
The features associated with this condition include mild to moderate learning difficulties, short stature, unique facial features, small head and skeletal abnormalities including bony growths projecting from the surfaces of bones. Typically individuals with Langer-Giedion syndrome have fine scalp hair, ears that may be large or prominent, broad eyebrows, deep-set eyes, a bulbous nose, long narrow upper lip, and missing teeth.
While no genetic syndrome is capable of being cured, treatments are available for some symptoms. External fixators have been used for limbic and facial reconstructions.

Laron syndrome, or Laron-type dwarfism, is an autosomal recessive disorder characterized by an insensitivity to growth hormone (GH), caused by a variant of the growth hormone receptor. It causes short stature and a resistance to diabetes and cancer. The principal feature of Laron syndrome is abnormally short stature (dwarfism). Physical symptoms include: prominent forehead, depressed nasal bridge, under-development of mandible, truncal obesity and a very small penis. Seizures are frequently secondary to hypoglycemia. Some genetic variations have an impact upon intellectual capacity. The majority of reported cases have been of Arabic or Semitic origin, with numerous patients in Israel, Saudi Arabia, Egypt, Iraq, and remote villages in Ecuador with Sephardic roots.
In 2011, it was reported that people with this syndrome in the Ecuadorian villages are resistant to cancer and diabetes and are somewhat protected against aging. This is consistent with findings in mice with a defective growth hormone receptor gene. Administration of GH has no effect on IGF-1 production, therefore treatment is mainly by biosynthetic IGF-1. IGF-1 must be taken before puberty to be effective.

Larsen syndrome, is a autosomal dominant congenital disorder. Its symptoms include hypermobility, congenital dislocations, brachycephaly and cleft palate. It may rarely be recessive. The condition was first described in a 1950 journal report by L. J. Larsen, et al. It is caused by a resistance to Growth hormone (GH) secondary to a defect in GH receptors. Investigations reveal high levels of GH and low levels of Insulin like growth factor-1 (IGF-1). A more complete list of symptoms includes: Multiple joint dislocations;  Foot deformities;  Non-tapering, cylindrical shaped fingers; Unusual facial appearance; Less commonly occurring: Short stature; Additional skeletal abnormalities; Cleft palate; Heart defects; Hearing impairment; Mental retardation; Pulmonary hypoplasia.

Laryngeal cancer may also be called cancer of the larynx or laryngeal carcinoma. Most laryngeal cancers are squamous cell carcinomas, reflecting their origin from the squamous cells which form the majority of the laryngeal epithelium. Cancer can develop in any part of the larynx, but the cure rate is affected by the location of the tumor. For the purposes of tumour staging, the larynx is divided into three anatomical regions: the glottis (true vocal cords, anterior and posterior commissures); the supraglottis (epiglottis, arytenoids and aryepiglottic folds, and false cords); and the subglottis.
Most laryngeal cancers originate in the glottis. Supraglottic cancers are less common, and subglottic tumours are least frequent.
Laryngeal cancer may spread by direct extension to adjacent structures, by metastasis to regional cervical lymph nodes, or more distantly, through the blood stream. Distant metastates to the lung are most common.
Smoking is the most important risk factor for laryngeal cancer. Death from laryngeal cancer is 20 times more likely for heaviest smokers than for nonsmokers. Heavy chronic consumption of alcohol, particularly alcoholic spirits, is also significant. When combined, these two factors appear to have a synergistic effect. Some other quoted risk factors are likely, in part, to be related to prolonged alcohol and tobacco consumption. These include low socioeconomic status, male sex, and age greater than 55 years. People with a history of head and neck cancer are known to be at higher risk (about 25%) of developing a second cancer of the head, neck, or lung.

Laryngocele refers to a congenital anomalous air sac communicating with the cavity of the larynx, which may bulge outward on the neck. It may also be acquired, seen in glassblowers due to continual forced expiration producing increased pressures in the larynx which leads to dilatation of the laryngeal ventricle. It is also seen in people with chronic obstructive airway disease.

Laryngomalacia (literally, “soft larynx”) is a very common condition of infancy, in which the soft, immature cartilage of the upper larynx collapses inward during inhalation, causing airway obstruction. It can also be seen in older patients, especially those with neuromuscular conditions resulting in weakness of the muscles of the throat. However, the infantile form is much more common. In infantile laryngomalacia, the supraglottic larynx (the part above the vocal cords) is tightly curled, with a short band holding the cartilage shield in the front (the epiglottis) tightly to the mobile cartilage in the back of the larynx (the arytenoids). These bands are known as the aryepiglottic folds; they create the movements that opens and closes the vocal cords for phonation. The shortened aryepiglottic folds cause the epiglottis to be furled on itself. This is the well known “omega shaped” epiglottis in laryngomalacia.
Laryngomalacia results in partial airway obstruction, most commonly causing a characteristic high-pitched squeaking noise on inhalation (inspiratory stridor). Some infants have feeding difficulties related to this problem. Rarely, children will have significant life threatening airway obstruction. The vast majority, however, will only have stridor without other more serious symptoms.
Time is the only treatment necessary in more than 99% of infant cases. In other cases, surgery may be necessary. Most commonly, this involves cutting the aryepiglottic folds to let the supraglottic airway spring open.

Lassa fever is an acute viral hemorrhagic fever first described in 1969 in the town of Lassa, in Borno State, Nigeria located in the Yedseram river valley at the south end of Lake Chad. Clinical cases of the disease had been known for over a decade earlier but not connected with this viral pathogen. The infection is endemic in West African countries, and causes 300,000–500,000 cases annually with approximately 5,000 deaths. Outbreaks of the disease have been observed in Nigeria, Liberia, Sierra Leone, Guinea, and the Central African Republic, but it is believed that human infections also exist in Democratic Republic of the Congo, Mali, and Senegal. Its primary animal host is the Natal Multimammate Mouse (Mastomys natalensis), an animal indigenous to most of Sub-Saharan Africa. the virus is probably transmitted by the contact with the feces and urine of animals accessing grain stores in residences.
In 80% of cases the disease is inapparent, but in the remaining 20% it takes a complicated course. It is estimated that the virus is responsible for about 5,000 deaths annually. The fever accounts for up to one third of deaths in hospitals within the affected regions and 10 to 16% of total cases. After an incubation period of six to twenty-one days, an acute illness with multiorgan involvement develops. Non-specific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding.

Leber’s hereditary optic neuropathy (LHON) or Leber optic atrophy is a mitochondrially inherited (mother to all offspring) degeneration of retinal ganglion cells (RGCs) and their axons that leads to an acute or subacute loss of central vision; this affects predominantly young adult males. However, LHON is only transmitted through the mother as it is primarily due to mutations in the mitochondrial (not nuclear) genome and only the egg contributes mitochondria to the embryo. LHON is usually due to one of three pathogenic mitochondrial DNA (mtDNA) point mutations.
Clinically, there is an acute onset of visual loss, first in one eye, and then a few weeks to months later in the other. Onset is usually young adulthood, but age range at onset from 7-60 is reported. This typically evolves to very severe optic atrophy and permanent decrease of visual acuity. In the acute stage, lasting a few weeks, the affected eye demonstrates an edematous appearance of the nerve fiber layer especially in the arcuate bundles and enlarged or telangectatic and tortuous peripapillary vessels (microangiopathy). These main features are seen on fundus examination, just before or subsequent to the onset of visual loss. A pupillary defect may be visible in the acute stage as well. Examination reveals decreased visual acuity, loss of color vision and a cecocentral scotoma on visual field examination.

Legionellosis is a potentially fatal infectious disease caused by Gram negative, aerobic bacteria belonging to the genus Legionella. Over 90% of legionellosis cases are caused by Legionella pneumophila, a ubiquitous aquatic organism that thrives in temperatures between 25 and 45 °C (77 and 113 °F), with an optimum around 35 °C (95 °F).
Legionellosis takes two distinct forms: Legionnaires’ disease, also known as “Legion Fever“, is the more severe form of the infection and produces pneumonia and Pontiac fever is caused by the same bacterium but produces a milder respiratory illness without pneumonia that resembles acute influenza.
Legionnaires’ disease acquired its name in July 1976 when an outbreak of pneumonia occurred among people attending a convention of the American Legion at the Bellevue-Stratford Hotel in Philadelphia. On January 18, 1977 the causative agent was identified as a previously unknown bacterium, subsequently named Legionella. Some people can be infected with the Legionella bacterium and have only mild symptoms or no illness at all.
Outbreaks of Legionnaires’ disease receive significant media attention. However, this disease usually occurs as single, isolated cases not associated with any recognized outbreak. When outbreaks do occur, they are usually in the summer and early autumn, though cases may occur at any time of year. The fatality rate of Legionnaires’ disease has ranged from 5% to 30% during various outbreaks. “The death rate for patients who develop Legionnaire’s disease while in the hospital is close to 50%, especially when antibiotics are started late,” according to the NIH and U.S. National Library of Medicine service’s MedlinePlus. Most infections occur in those who are middle-age or older.

Leiomyoma (plural is ‘leiomyomata’) is a benign smooth muscle neoplasm that is not premalignant. They can occur in any organ, but the most common forms occur in the uterus, small bowel and the esophagus. Leiomyoma is the most common benign tumor of small bowel. Approximately 50% of cases are found in the jejunum, followed by the ileum in 31% of cases. Almost one half of all lesions are less than 5 centimeters. GnRH antagonists for 3–6 months are used to reduce the size of the myomas. It usually reduces the size by 60% to 70%, but once the medication is stopped the myomas will grow back. Myomectomy is a choice to remove myomas. It is usually done when the patient wants to preserve their fertility. This can be performed with either traditional surgery or through laparoscopy.
Total Abdominal or Vaginal hysterectomy with Bilateral Salpingo-oophorectomy is the definitive treatment.

Leishmaniasis is a disease caused by protozoan parasites that belong to the genus Leishmania and is transmitted by the bite of certain species of sand fly (subfamily Phlebotominae). Although the majority of the literature mentions only one genus transmitting Leishmania to humans (Lutzomyia) in the Americas, a 2003 study by Galati suggested a new classification for the New World sand flies, elevating several subgenera to the genus level. Elsewhere in the world, the genus Phlebotomus is considered the vector of leishmaniasis.
Most forms of the disease are transmissible only from animals (zoonosis), but some can be spread between humans. Human infection is caused by about 21 of 30 species that infect mammals. These include the L. donovani complex with three species (L. donovani, L. infantum, and L. chagasi); the L. mexicana complex with four main species (L. mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Viannia with four main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L. (V.) peruviana). The different species are morphologically indistinguishable, but they can be differentiated by isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies. Cutaneous leishmaniasis is the most common form of leishmaniasis. Visceral leishmaniasis is a severe form in which the parasites have migrated to the vital organs.

Lennox–Gastaut syndrome (LGS), also known as Lennox syndrome, is a difficult-to-treat form of childhood-onset epilepsy that most often appears between the second and sixth year of life, and is characterized by frequent seizures and different seizure types; it is often accompanied by mental retardation and psychological and behavioral problems.
As a general rule, the age of seizure onset in LGS patients is between the ages of two and six; however, this does not exclude the possibility that seizures can begin before age two, or after age six. The syndrome shows clear parallels to West syndrome, enough to suggest a connection. Daily multiple seizures are typical in LGS. Also typical is the broad range of seizures that can occur, larger than that of any other epileptic syndrome. The most frequently occurring seizure types are: tonic, which are often nocturnal (90%); the second most frequent are myoclonic seizures, which often occur when the patient is over-tired.
Approximately 5% of children with epilepsy have LGS, and it is more common in males than females. Whereas some children seem perfectly normal prior to the development of seizures, others already had some form of epilepsy, such as West syndrome, which is seen in 20% of patients before (symptomatic) LGS. West syndrome is characterized by Blitz Nick Salaam seizures, and typically evolves into LGS in the second year of life.

Leprosy or Hansen’s disease (HD), is a chronic disease caused by the bacteria Mycobacterium leprae and Mycobacterium lepromatosis. Named after physician Gerhard Armauer Hansen, leprosy is primarily a granulomatous disease of the peripheral nerves and mucosa of the upper respiratory tract; skin lesions are the primary external sign. Left untreated, leprosy can be progressive, causing permanent damage to the skin, nerves, limbs and eyes. Contrary to folklore, leprosy does not cause body parts to fall off, although they can become numb or diseased as a result of infection; infection results in tissue loss, so fingers and toes become shortened and deformed as the cartilage is absorbed into the body.
Although the mode of transmission of Hansen’s disease remains uncertain, most investigators think that M. leprae is usually spread from person to person in respiratory droplets. The minimum incubation period reported is as short as a few weeks and this is based on the very occasional occurrence of leprosy among young infants. The maximum incubation period reported is as long as 30 years, or over, as observed among war veterans known to have been exposed for short periods in endemic areas but otherwise living in non-endemic areas. It is generally agreed that the average incubation period is between three and five years. Leprosy is now known to be neither sexually transmitted nor highly infectious after treatment. Approximately 95% of people are naturally immune and sufferers are no longer infectious after as little as 2 weeks of treatment.
Leprosy has affected humanity for over 4,000 years, and was well-recognized in the civilizations of ancient China, Egypt, and India. DNA taken from the shrouded remains of a man discovered in a tomb next to the Old City of Jerusalem shows him to be the earliest human proven to have suffered from leprosy. In 1995, the World Health Organization (WHO) estimated that between 2 and 3 million people were permanently disabled because of leprosy at that time. In the past 20 years, 15 million people worldwide have been cured of leprosy.

Leptospirosis (also known as Weil’s disease, Weil’s syndrome, canicola fever, canefield fever, nanukayami fever, 7-day fever, Rat Catcher’s Yellows, Fort Bragg fever, and Pretibial fever) is a bacterial zoonotic disease caused by spirochaetes of the genus Leptospira that affects humans and a wide range of animals, including mammals, birds, amphibians, and reptiles. The disease was first described by Adolf Weil in 1886 when he reported an “acute infectious disease with enlargement of spleen, jaundice and nephritis”. Leptospira was first observed in 1907 from a post mortem renal tissue slice. In 1908, Inada and Ito first identified it as the causative organism and in 1916 noted its presence in rats. It is recognized among the world’s most common zoonoses.

Leukemia or leukaemia is a type of cancer of the blood or bone marrow characterized by an abnormal increase of white blood cells. 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.
In 2000, approximately 256,000 children and adults around the world developed some form of leukemia, and 209,000 died from it. About 90% of all leukemias are diagnosed in adults.
Clinically and pathologically, leukemia is subdivided into a variety of large groups. The first division is between its acute and chronic forms:
* Acute leukemia is characterized by a rapid increase in the numbers of immature blood cells. Crowding due to such cells makes the bone marrow unable to produce healthy blood cells. Immediate treatment is required in acute leukemia due to the rapid progression and accumulation of the malignant cells, which then spill over into the bloodstream and spread to other organs of the body. Acute forms of leukemia are the most common forms of leukemia in children.
* Chronic leukemia is characterized by the excessive build up of relatively mature, but still abnormal, white blood cells. Typically taking months or years to progress, the cells are produced at a much higher rate than normal cells, resulting in many abnormal white blood cells in the blood. Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy. Chronic leukemia mostly occurs in older people, but can theoretically occur in any age group.
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 easily 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.
Some patients experience other symptoms. These symptoms might include feeling sick, such as having fevers, chills, night sweats and other flu-like symptoms, or feeling fatigued. Some patients experience nausea or a feeling of fullness due to an enlarged liver and spleen; this can result in unintentional weight loss. If the leukemic cells invade the central nervous system, then neurological symptoms (notably headaches) can occur. All symptoms associated with leukemia can be attributed to other diseases. Consequently, leukemia is always diagnosed through medical tests.
No single known cause for all of the different types of leukemia exists. The known causes, which are not generally factors within the control of the average person, account for relatively few cases. The different leukemias likely have different causes.
Leukemia, like other cancers, results from somatic mutations in the DNA. Certain mutations produce leukemia by activating oncogenes or deactivating tumor suppressor genes, and thereby disrupting the regulation of cell death, differentiation or division. These mutations may occur spontaneously or as a result of exposure to radiation or carcinogenic substances, and are likely to be influenced by genetic factors.
Most forms of leukemia are treated with pharmaceutical medications, typically combined into a multi-drug chemotherapy regimen. Some are also treated with radiation therapy. In some cases, a bone marrow transplant is useful.

Leukodystrophy refers to a group of disorders characterized by progressive degeneration of the white matter of the brain. The leukodystrophies are caused by imperfect growth or development of the myelin sheath, the fatty covering that acts as an insulator around nerve fibers. Myelin, from which the white matter of the brain takes its colour, is a complex substance made up of at least ten different chemicals. Each of the leukodystrophies is the result of a defect in the gene that controls the production or metabolism of one (and only one) of the component molecules of myelin.
The word leukodystrophy comes from the Greek roots leuko, white, dys, lack of, and troph, growth. Thus leukodystrophy describes a set of diseases that affect the growth or maintenance of the white matter.

Leukoplakia is a clinical term used to describe patches of keratosis. It is visible as adherent white patches on the mucous membranes of the oral cavity, including the tongue, but also other areas of the gastro-intestinal tract, urinary tract and the genitals. 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. It is sometimes described as precancerous. It is also associated with smoking.
Tobacco, either smoked or chewed, is considered to be the main culprit in its development. (1998-2010 Mayo Foundation for Medical Education and Research (MFMER). The term “candidal leukoplakia” is sometimes used to describe certain types of oral candidiasis. Although the term “leukoplakia” often applies to conditions of the mouth, it can also be used to describe conditions of the genitals and urinary tract.

Lichen planus is a chronic mucocutaneous disease that affects the skin, tongue, and oral mucosa. The disease presents itself in the form of papules, lesions, or rashes. Lichen planus does not involve lichens; the name refers to the appearance of affected skin. It is sometimes associated with certain medications and diseases, but is basically of unknown cause.
The typical rash of lichen planus is well-described by the “5 Ps”: well-defined pruritic, planar, purple, polygonal papules. The commonly affected sites are near the wrist and the ankle. The rash tends to heal with prominent blue-black or brownish discoloration that persists for a long time. Besides the typical lesions, many morphological varieties of the rash may occur. The presence of cutaneous lesions is not constant and may wax and wane over time. Oral lesions tend to last far longer than cutaneous lichen planus lesions.
The cause of lichen planus is not known. It is not contagious and does not involve any known pathogen. Some lichen planus-type rashes (known as lichenoid reactions) occur as allergic reactions to medications for high blood pressure, heart disease and arthritis, in such cases termed drug-induced lichenoid reactions. These lichenoid reactions are referred to as lichenoid mucositis (of the mucosa) or dermatitis (of the skin). Lichen planus has been reported as a complication of chronic hepatitis C virus infection and can be a sign of chronic graft-versus-host disease of the skin (Lichenoid reaction of graft-versus-host disease). It has been suggested that true lichen planus may respond to stress, where lesions may present on the mucosa or skin during times of stress in those with the disease. Lichen planus affects women more than men (at a ratio of 3:2), and occurs most often in middle-aged adults.

Lipodystrophy is a medical condition characterized by abnormal or degenerative conditions of the body’s adipose tissue. A more specific term, lipoatrophy is used when describing the loss of fat from one area (usually the face). This condition is also characterized by a lack of circulating leptin which may lead to osteosclerosis. A lipodystrophy can be a lump or small dent in the skin that forms when a person keeps performing injections in the same spot. These types of lipodystrophies are harmless. People who want to avoid them can do so by changing (rotating) the places where they perform injections. For people with diabetes, using purified insulins may also help.

Lissencephaly, which literally means smooth brain, is a brain formation disorder caused by defective neuronal migration during the 12th to 24th weeks of gestation, resulting in a lack of development of brain folds (gyri) and grooves (sulci). It is a form of cephalic disorder. Terms such as ‘agyria’ (no gyri) or ‘pachygyria’ (broad gyri) are used to describe the appearance of the surface of the brain. Children with lissencephaly are severely neurologically impaired and often die within several months of birth.
Affected children display severe psychomotor retardation, failure to thrive, seizures, and muscle spasticity or hypotonia. Other symptoms of the disorder may include unusual facial appearance, difficulty swallowing, and anomalies of the hands, fingers, or toes. Causes of lissencephaly can include viral infections of the uterus or the fetus during the first trimester, or insufficient blood supply to the fetal brain early in pregnancy.

Loa loa filariasis (also known as loiasis, loaiasis, Calabar swellings, Fugitive swelling, Tropical swelling and African eyeworm) is a skin and eye disease caused by the nematode worm, loa loa. Humans contract this disease through the bite of a Deer fly or Mango fly (Chrysops spp), the vectors for Loa loa. The adult Loa loa filarial worm migrates throughout the subcutaneous tissues of humans, occasionally crossing into subconjunctival tissues where it can be easily observed. Loa loa does not normally affect one’s vision but can be painful when moving about the eyeball or across the bridge of the nose. The disease can cause red itchy swellings below the skin called “Calabar swellings”. The disease is treated with the drug diethylcarbamazine (DEC), and when appropriate, surgical methods may be employed to remove adult worms from the conjunctiva.
Human loiasis geographical distribution is restricted to the rain forest and swamp forest areas of West Africa, being especially common in Cameroon and on the Ogooué River. Humans are the only known natural reservoir. It is estimated that 12-13 million humans are infected with the Loa loa larvae.
An area of tremendous concern regarding loiasis is its co-endemicity with onchocerciasis in certain areas of west and central Africa, as mass ivermectin treatment of onchocerciasis can lead to serious adverse events (SAEs) in patients who have high Loa loa microfilarial densities, or loads. This fact necessitates the development of more specific diagnostics tests for Loa loa so that areas and individuals at a higher risk for neurologic consequences can be identified prior to microfilaricidal treatment. Additionally, the treatment of choice for loiasis, diethylcarbamazine, can lead to serious complications in and of itself when administered in standard doses to patients with high Loa loa microfilarial loads.

Lung cancer is a disease which consists of uncontrolled cell growth in tissues of the lung. This growth may lead to metastasis, which is the invasion of adjacent tissue and infiltration beyond the lungs. The vast majority of primary lung cancers are carcinomas, derived from epithelial cells. Lung cancer, the most common cause of cancer-related death in men and women, is responsible for 1.3 million deaths worldwide annually, as of 2004. The most common symptoms are shortness of breath, coughing (including coughing up blood), and weight loss.
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. The most common cause of lung cancer is long-term exposure to tobacco smoke. The occurrence of lung cancer in nonsmokers, who account for as many as 15% of cases, is often attributed to a combination of genetic factors, radon gas, asbestos, and air pollution including secondhand smoke.
Lung cancer may be seen on chest radiograph and computed tomography (CT scan). The diagnosis is confirmed with a biopsy. This is usually performed by 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. Survival varies, depending on stage, overall health, and other factors, but the overall five-year survival rate for all persons diagnosed with lung cancer is 14%.

Lupus erythematosus is a category for a collection of diseases with similar underlying problems with immunity (autoimmune disease). Symptoms of these diseases can affect many different body systems, including joints, skin, kidneys, blood cells, heart, and lungs. Four main types of lupus exist — systemic lupus erythematosus, discoid lupus erythematosus, drug-induced lupus erythematosus, and neonatal lupus erythematosus. Of these, systemic lupus erythematosus is the most common and serious form of lupus.
Photosensitivity’s relationship to and influence on the systemic manifestations of lupus remain to be defined. Mechanisms for photosensitivity might include: modulation of autoantibody location, cytotoxic effects, apoptosis induction with autoantigens in apoptotic blebs, upregulation of adhesion molecules and cytokines, induction of nitric oxide synthase expression and ultraviolet-generated antigenic DNA. Tumor necrosis factor alpha also seems to play a role in the development of photosensitivity.

Lyme disease, or Lyme borreliosis, is an emerging infectious disease caused by at least three species of bacteria belonging to the genus Borrelia. Borrelia burgdorferi sensu stricto is the main cause of Lyme disease in the United States, whereas Borrelia afzelii and Borrelia garinii cause most European cases. The disease is named after the town of Lyme, Connecticut, USA, where a number of cases were identified in 1975. Although Allen Steere realized in 1978 that Lyme disease was a tick-borne disease, the cause of the disease remained a mystery until 1981, when B. burgdorferi was identified by Willy Burgdorfer.
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 a few species of the genus Ixodes (“hard ticks”). Early symptoms may include fever, headache, fatigue, depression, and a characteristic circular skin rash called erythema migrans. Left untreated, later symptoms may involve the joints, heart, and central nervous system. In most cases, the infection and its symptoms are eliminated by antibiotics, especially if the illness is treated early. Delayed or inadequate treatment can lead to the more serious symptoms, which can be disabling and difficult to treat. Lyme disease is a biosafety level 2 disease.

Lymphedema, also known as lymphatic obstruction, is a condition of localized fluid retention and tissue swelling caused by a compromised lymphatic system. The lymphatic system returns the interstitial fluid to the thoracic duct and then to the bloodstream, where it is recirculated back to the tissues. Tissues with lymphedema are at risk of infection. Symptoms may include severe fatigue, a heavy swollen limb or localized fluid accumulation in other body areas, including the head or neck, discoloration of the skin overlying the lymphedema, and eventually deformity (elephantiasis).
Lymphedema should not be confused with edema arising from venous insufficiency, which is not lymphedema. However, untreated venous insufficiency can progress into a combined venous/lymphatic disorder which is treated the same way as lymphedema (see Treatment below). Presented here is an extreme case of severe unilateral hereditary lymphedema which had been present for 25 years without treatment.

Lymphoma is a cancer in the lymphatic cells of the immune system. Typically, lymphomas present as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and can be curable depending on the histology, type, and stage of the disease. These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoesis) and do not usually form static tumors. 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 the first description of lymphoma in 1832, specifically of the form named after him, Hodgkin’s lymphoma. Since then, many other forms of lymphoma have been described, grouped under several proposed classifications. The 1982 Working formulation classification became very popular. It introduced the category non-Hodgkin lymphoma (NHL), divided into 16 different diseases. However, because 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. Although older classifications referred to histiocytic lymphomas, these are recognized in newer classifications as of B, T or NK cell lineage.


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