Mesothelium derives from the embryonic mesoderm cell layer, that lines the coelom (body cavity) in the embryo. It develops into the layer of cells that covers and protects most of the internal organs of the body.
A layer of mesothelial cells grown in cell culture, featuring the typical “cobblestone” appearance

Structure

The mesothelium forms a monolayer of flattened squamous-like epithelial cells resting on a thin basement membrane supported by connective tissue. Cuboidal mesothelial cells may be found at areas of injury, the milky spots of the omentum, and the peritoneal side of the diaphragm overlaying the lymphatic lacunae. The luminal surface is covered with microvilli. The proteins and serosal fluid trapped by the microvilli provide a frictionless surface for internal organs to slide past one another.

Function

The mesothelium is composed of an extensive monolayer of specialized cells (mesothelial cells) that line the body’s serous cavities and internal organs. The main purpose of these cells is to produce a lubricating fluid that is released between layers, providing a slippery, non-adhesive and protective surface to facilitate intracoelomic movement.

The mesothelium is also implicated in the transport and movement of fluid and particulate matter across the serosal cavities, leukocyte migration in response to inflammatory mediators, synthesis of pro-inflammatory cytokines, growth factors and extracellular matrix proteins to aid in serosal repair, and the release of factors to promote the disposition and clearance of fibrin (such as plasminogen). It is an antigen presenting cell. Furthermore, the secretion of glycosaminoglycans and lubricants may protect the body against infection and tumor dissemination.

Role in disease

* Mesothelioma: (cancer of the mesothelium) is a disease in which cells of the mesothelium become abnormal and divide without control or order. They can invade and damage nearby tissues and organs. Cancer cells can also metastasize (spread) from their original site to other parts of the body. Most cases of mesothelioma begin in the pleura or peritoneum. More than 90% of mesothelioma cases are linked to asbestos exposure.

* Intra-abdominal adhesions: Normally, the mesothelium secretes plasminogen, which removes fibrin deposits. During surgical procedures, the mesothelium may be damaged. Its fibrinolytic capacity becomes insufficient and fibrin accumulates, causing fibrous adhesions between opposing surfaces. These adhesions cause intestinal obstruction and female infertility if it occurs in the abdomen, and may impair cardiac and lung function in the thorax.

* Ultrafiltration failure: The peritoneal mesothelium is implicated in the long-term development of ultrafiltration failure in peritoneal dialysis patients. The presence of supra-physiological glucose concentrations, acidity, and glucose degradation products in peritoneal dialysis fluids contribute to the fibrosis of the peritoneal mesothelium, either by epithelial-mesenchymal transition or increased proliferation of existing fibroblasts. A fibrosed peritoneum results in the increased passage of solutes across the peritoneum and ultrafiltration failure.

Sources

* Mesothelioma: Questions and Answers (National Cancer Institute).
* Histology at KUMC epithel-epith01 “Mesothelium”
* Histology at BU 00102loa – “Tissues, Layers, and Organs: transverse section of rat gut”
* Mutsaers SE. “Mesothelial cells: Their structure, function, and role in serosal repair.” Respirology 2002; 7:171-191

Myoglobinuria is the presence of myoglobin in the urine, usually associated with rhabdomyolysis or muscle destruction. Myoglobin is present in muscle cells as a reserve of oxygen.

Trauma, vascular problems, venoms, certain drugs and other situations can destroy or damage the muscle, releasing myoglobin to the circulation and thus to the kidneys.

Under ideal situations myoglobin will be filtered and excreted with the urine, but if too much myoglobin is released into the circulation or in case of renal problems, it can occlude the renal filtration system leading to acute tubular necrosis and acute renal insufficiency.

Other causes of myoglobinuria include:

After centrifuging, the serum of myoglobinuria is clear, where the serum of hemoglobinuria after centrifuge is pink.[citation needed]

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In medicine (cardiology), myocarditis is inflammation of the myocardium, the muscular part of the heart. It is generally due to infection (viral or bacterial). It may cause chest pain, rapid signs of heart failure, or sudden death.

The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium, or the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include:[1]

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever,rash, diarrhea, joint pains, and easy fatigueability.

Myocarditis is often associated with pericarditis, and many patients present with signs and symptoms that suggest concurrent myocarditis and pericarditis.

In myocarditis, the process of inflammation is the cause of the injury, and not the response to it. As a result, inflammation of the myocardium by itself is not enough to be diagnostic for myocarditis[3].

Myocardial inflammation can be suspected on the basis of electrocardiographic results (ECG), elevated CRP and/or ESR and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.[1]

The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).[1]

The gold standard is still biopsy of the myocardium, generally done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy and—if necessary—immunochemistry and special staining methods. Histopathological features are: myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.[1]

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Myeloperoxidase deficiency is a common genetic disorder featuring deficiency, either in quantity or function, of myeloperoxidase, an enzyme found in certain phagocytic immune cells, especially polymorphonuclear leukocytes.

It can appear similar to chronic granulomatous disease on some screening tests.[1]

Although MPO deficiency classically presents with immune deficiency (especially candida albicans infections), the majority of individuals with MPO deficiency show no signs of immunodeficiency.

The lack of severe symptoms suggest that role of myeloperoxidase in the immune response must be redundant to other mechanisms of intracellular killing of phagocytosed bacteria.[2]

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A myeloid sarcoma (chloroma, granulocytic sarcoma, extramedullary myeloid tumor), is a solid tumor composed of immature malignant white blood cells called myeloblasts. A chloroma is an extramedullary manifestation of acute myeloid leukemia; in other words, it is a solid collection of leukemic cells occurring outside of the bone marrow.

The condition now known as chloroma was first described by the British physician A. Burns in 1811[1], although the term chloroma did not appear until 1853.[2] This name is derived from the Greek word chloros (green), as these tumors often have a green tint due to the presence of myeloperoxidase. The link between chloroma and acute leukemia was first recognized in 1902 by Dock and Warthin.[3] However, because up to 30% of these tumors can be white, gray, or brown rather than green, the more correct term granulocytic sarcoma was proposed by Rappaport in 1967[4] and has since become virtually synonymous with the term chloroma.

Currently, any extramedullary manifestation of acute myeloid leukemia can be termed a granulocytic sarcoma or chloroma. Specific terms which overlap with granulocytic sarcoma include:

In recent years, the term “myeloid sarcoma” has been favored.[5]

Chloromas are rare; exact estimates of their incidence are lacking, but they are uncommonly seen even by physicians specializing in the treatment of leukemia. Chloromas may be somewhat more common in patients with the following disease features:[6]

However, even in patients with the above risk factors, chloroma remains an uncommon complication of acute myeloid leukemia.

Rarely, a chloroma can develop as the sole manifestation of relapse after apparently successful treatment of acute myeloid leukemia. In keeping with the general behavior of chloromas, such an event must be regarded as an early herald of a systemic relapse, rather than as a localized process. In one review of 24 patients who developed isolated chloromas after treatment for acute myeloid leukemia, the mean interval until bone marrow relapse was 7 months (range, 1 to 19 months).[7]

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Mycetoma, is a chronic, specific, granulomatous,[1] progressive inflammatory disease. It mainly affects the foot; and Mycetoma pedisis also known as Madura foot. This infection is endemic in Africa, India, and Central and South America.[2]

It usually involves the subcutaneous tissue after a traumatic inoculation of the causative organism. Mycetoma may be caused by true fungi or by higher bacteria and hence it is usually classified into eumycetoma and actinomycetoma respectively. Tumefaction and formation of sinus tracts characterize mycetoma. The sinuses usually discharge purulent and seropurulent exudate containing grains. It may spread to involve the skin and the deep structures resulting in destruction, deformity and loss of function, very occasionally it could be fatal.

There are two known forms of mycetoma. The two forms of mycetoma are bacterial mycetoma and fungal mycetoma: bacterial mycetoma is known as actinomycetoma while the fungal form is called eumycetoma. Even at the level of electron microscopy the two forms of mycetoma are difficult to distinguish from one another.

The true incidence and the geographical distribution of mycetoma throughout the world is not exactly known due to the nature of the disease which is usually painless, slowly progressive which may lead to the late presentation of the majority of patients. Mycetoma has a worldwide distribution but this is extremely uneven. It is endemic in tropical and subtropical regions. The African continent seems to have the highest prevalence. It prevails in what is known as the mycetoma belt stretching between the latitudes of 15 south and 30 north. The belt includes Sudan, Somalia, Senegal, India, Yemen, Mexico, Venezuela, Colombia, Argentina and others.

The geographical distribution of the individual mycetoma organism shows considerable variations, which can be convincingly explained on an environmental basis. Areas where mycetoma prevails are relatively arid zones with a short rainy season with a relative humidity.

The organisms are usually present in the soil in the form of grains. The infecting agent is implanted into the host tissue through a breach in the skin produced by trauma caused by sharp objects such as thorn pricks, stone or splinters.

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Myasthenia gravis (literally “serious muscle-weakness”; from Greek µ?? “muscle”, ?s???e?a “weakness”, and Latin gravis “serious”; abbreviated MG) is a neuromuscular disease leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the post-synaptic neuromuscular junction,[1] inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. At 200–400 cases per million it is one of the less common autoimmune disorders.[1]

The most widely accepted classification of myasthenia gravis is the Myasthenia Gravis Foundation of America Clinical Classification:[2]

The hallmark of myasthenia gravis is fatiguability. Muscles become progressively weaker during periods of activity and improve after periods of rest. Muscles that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are especially susceptible. The muscles that control breathing and neck and limb movements can also be affected. Often the physical examination is within normal limits.[3]

The onset of the disorder can be sudden or rapid. Often symptoms are intermittent. The diagnosis of myasthenia gravis may be delayed if the symptoms are subtle or variable.

In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in MG varies greatly among patients, ranging from a localized form, limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles – sometimes including those that control breathing – are affected. Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech, often nasal due to weakness of the velar muscles).

In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress.[4] Since the heart muscle is stimulated differently, it is never affected by MG.

Myasthenia gravis is a autoimmune channelopathy: it features antibodies directed against the body’s own proteins. While in various similar diseases the disease has been linked to a cross-reaction with an infective agent, there is no known causative pathogen that could account for myasthenia. There is a slight genetic predisposition: particular HLA types seem to predispose for MG (B8 and DR3 with DR1 more specific for ocular myasthenia). Up to 75% of patients have an abnormality of the thymus; 25% have a thymoma, a tumor (either benign or malignant) of the thymus, and other abnormalities are frequently found. The disease process generally remains stationary after thymectomy (removal of the thymus).

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Mumps or epidemic parotitis is a viral disease of the human species, caused by the mumps virus. Prior to the development of vaccination and the introduction of a vaccine, it was a common childhood disease worldwide, and is still a significant threat to health in the third world.[1]

Painful swelling of the salivary glands (classically the parotid gland) is the most typical presentation.[2] Painful testicular swelling and rash may also occur. The symptoms are generally not severe in children. In teenage males and men, complications such as infertility or subfertility are more common, although still rare in absolute terms.[3][4][5] The disease is generally self-limited, running its course before receding, with no specific treatment apart from controlling the symptoms with painkillers.

The more common symptoms of mumps are:

Other symptoms of mumps can include sore face and/or ears and occasionally in more serious cases, loss of voice. In addition, up to 20% of persons infected with the mumps virus do not show symptoms, so it is possible to be infected and spread the virus without knowing it.[8]

Fever and headache are prodromal symptoms of mumps, together with malaise and anorexia.

A physical examination confirms the presence of the swollen glands. Usually the disease is diagnosed on clinical grounds and no confirmatory laboratory testing is needed. If there is uncertainty about the diagnosis, a test of saliva, or blood may be carried out; a newer diagnostic confirmation, using real-time nested polymerase chain reaction (PCR) technology, has also been developed.[9] An estimated 20%-30% of cases are asymptomatic.[10] As with any inflammation of the salivary glands, serum amylase is often elevated.[11][12]

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Multiple myeloma (also known as MM, myeloma, plasma cell myeloma, or as Kahler’s disease after Otto Kahler) is a cancer of plasma cells. The cells metastasize, often spreading to neighboring bone. These immune cells are formed in bone marrow, are numerous in lymphatics and produce antibodies. Myeloma is regarded as incurable, but remissions may be induced with steroids, chemotherapy, thalidomide and stem cell transplants. Myeloma is part of the broad group of diseases called hematological malignancies.

Because many organs can be affected by myeloma, the symptoms and signs vary greatly. A mnemonic sometimes used to remember the common tetrad of multiple myeloma is CRAB: C = Calcium (elevated), R = Renal failure, A = Anemia, B = Bone lesions.[1] Myeloma has many possible symptoms, and all symptoms may be due to other causes. They are presented here in decreasing order of incidence.

Myeloma bone pain usually involves the spine and ribs, and worsens with activity. Persistent localized pain may indicate a pathological bone fracture. Involvement of the vertebrae may lead to spinal cord compression. Myeloma bone disease is due to proliferation of tumor cells and release of Interleukin 1, IL-1, also known as osteoclast activating factor (OAF), which stimulates osteoclasts to break down bone. These bone lesions are lytic in nature and are best seen in plain radiographs, which may show “punched-out” resorptive lesions. The breakdown of bone also leads to release of calcium into the blood, leading to hypercalcemia and its associated symptoms.

The most common infections are pneumonias and pyelonephritis. Common pneumonia pathogens include S. pneumoniae, S. aureus, and K. pneumoniae, while common pathogens causing pyelonephritis include E. coli and other gram-negative organisms. The greatest risk period for the occurrence of infection is in the initial few months after the start of chemotherapy.[2] The increased risk of infection is due to immune deficiency resulting from diffuse hypogammaglobulinemia, which is due to decreased production and increased destruction of normal antibodies. A selected group of patients may benefit from replacement immunoglobulin therapy to reduce the risk of infection.[3]

Renal failure may develop both acutely and chronically. It is commonly due to hypercalcemia (see above). It may also be due to tubular damage from excretion of light chains, also called Bence Jones proteins, which can manifest as the Fanconi syndrome (type II renal tubular acidosis). Other causes include glomerular deposition of amyloid, hyperuricemia, recurrent infections (pyelonephritis), and local infiltration of tumor cells.

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Moyamoya disease is an extremely rare disorder characterized by progressive intracranial vascular stenoses of the circle of Willis, resulting in successive ischemic events. Hemorrhagic events can also occur. The condition leads to irreversible blockage of the carotid arteries to the brain as they enter into the skull. It is a disease that tends to affect children and adults in the third to fourth decades of life. In children it tends to cause strokes or seizures. In adults it tends to cause bleeding or strokes. The clinical features are cerebral ischaemia (strokes), recurrent TIAs, sensorimotor paralysis (numbness in the extremities), convulsions and/or migraine-like headaches.

The condition is believed to be hereditary and linked to q25.3, on chromosome 17[1]. In Japan the overall incidence is higher (0.35 per 100,000).[1] In North America, women in the third or fourth decade of life are most affected. These women frequently experience transient ischemic attacks (TIA), cerebral hemorrhage or no symptoms. They have a higher risk of recurrent stroke and may be experiencing a distinct underlying pathophysiology compared to patients from Japan. Data suggest a potential benefit with surgery if early diagnosis is made.[2] The pathogenesis of Moyamoya disease is unknown.

The process of blockage (vascular occlusion) once it begins tends to continue despite any known medical management. In some people this leads to repeated strokes and severe functional impairment or even death. In others, this blockage may not cause any symptoms.

Moyamoya can be either congenital or acquired. Patients with Down syndrome, neurofibromatosis, or sickle cell disease can develop Moyamoya malformations. It is more common in women than in men.[3] Brain radiation therapy in children with neurofibromatosis increases the risk of its development.

The diagnosis is initially suggested by CT, MRI, or angiogram. In fact, the name derives from its angiographic image; the “puff of smoke,” which is how moyamoya loosely translates from Japanese, refers to the appearance of multiple compensatorily dilated striate vessels seen on angiography. Contrast-enhanced T1-weighted images are better than FLAIR images for depicting the leptomeningeal ivy sign in Moyamoya disease. MRI and MRA should be performed for the diagnosis and follow-up of Moyamoya disease. Diffusion-weighted imaging can also be used for following the clinical course of children with Moyamoya disease, in whom new focal deficits are highly suspicious of new infarcts.

Often nuclear medicine studies such as SPECT (single photon emission computerized tomography) are used to demonstrate the decreased blood and oxygen supply to areas of the brain involved with Moyamoya disease. Conventional angiography provided the conclusive diagnosis of Moyamoya disease in most cases and should be performed before any surgical considerations.

There are many operations that have been developed for the condition, but currently the most favored are the in-direct procedures EDAS, EMS, and multiple burr holes and the direct procedure STA-MCA. Direct superficial temporal artery (STA) to middle cerebral artery (MCA) bypass is considered the treatment of choice, although its efficacy, particularly for hemorrhagic disease, remains uncertain. Multiple burr holes have been used in frontal and parietal lobes with good neovascularisation achieved.

The EDAS (encephaloduroarteriosynangiosis) procedure requires dissection of a scalp artery over a course of several inches and then making a small temporary opening in the skull directly beneath the artery. The artery is then sutured to the surface of the brain and the bone replaced.

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