Meningoma

Meningiomas are the most common benign tumors of the brain (95% of benign tumors). However they can also be malignant. They arise from the arachnoidal cap cells of the meninges and represent about 15% of all primary brain tumors. They are more common in females than in males (2:1) and have a peak incidence in the sixth and seventh decades. Most cases are sporadic while some are familial. There has been some evidence that persons who have undergone radiation to the scalp are more at risk for developing meningiomas. The most frequent genetic mutations involved in meningiomas are inactivation mutations in the neurofibromatosis 2 gene (merlin) on chromosome 22q.

Pathogenesis
Meningiomas arise from arachnoidal cells, most of which are near the vicinity of the venous sinuses, and this is the site of greatest prevalence for meningioma formation. They are most frequently attached to the dura over the superior parasagittal surface of frontal and parietal lobes, along the sphenoid ridge, in the olfactory grooves, the sylvian region, superior cerebellum along the falx cerebri, cerebellopontine angle, and the spinal cord. The tumor is usually gray, well-circumscribed, and takes on the form of space it occupies. They are usually dome-shaped, with the base lying on the dura.

Histologically, the cells are relatively uniform, with a tendency to encircle one another, forming whorls and psammoma bodies (laminated calcific concretions). They have a tendency to calcify and are highly vascularized.

Clinical manifestations
Main article: brain tumor
Small tumors (e.g., < 2.0 cm) are usually incidental findings at autopsy without having caused symptoms. Larger tumors can cause symptoms depending on the size and location.

Focal seizures may be caused by meningiomas that overlie the cerebrum
Progressive spastic weakness in legs and incontinence may be caused by tumors that overlie the parasagittal frontoparietal region.
Sylvian tumors may cause a myriad of motor, sensory, aphasic, and seizure symptoms depending on the location.
Increased intracranial pressure eventually occurs, but is less frequent than in gliomas.

Diagnosis
Meningiomas are readily visualized with contrast CT, MRI with gadolinium, and arteriography, all attributed to the fact that meningiomas are highly calcified and vascularized. CSF protein is usually elevated if lumbar puncture is attempted.

Treatment
Surgical resection -- Meningiomas can usually be surgically resected with permanent cure if the tumor is superficial on the dural surface and easily accessible. Transarterial embolization has become a standard preoperative procedure in the preoperative management. For incompletely accessible tumors, recurrence is likely. These regions include the medial sphenoid bone, parasellar region, or anterior brainstem. If invasion of the adjacent bone occurs, total removal is nearly impossible. Malignant transformation is rare.
Radiation therapy, including Gamma KnifeTM or proton beam treatment, may be pursued in cases of inoperable or unresectable tumors, or if tumor shows malignant transformation. Focused radiation may also be helpful for small tumors at the base of the skull.
Conventional chemotherapy is likely not effective. Antiprogestin agents have been used, but with variable results. Recent evidence that hydroxyurea has the capacity to shrink unresectable or recurrent meningiomas is being further evaluated.

Meningoma

Leukimia

Leukemia or leukaemia (see spelling differences) 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). It is part of the broad group of diseases called hematological neoplasms.

Symptoms
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 (white blood cells etc.) to start attacking other body cells.

Finally, the red blood cell deficiency leads to anemia, which may cause dyspnea. All symptoms can be attributed to other diseases; for diagnosis, blood tests and a bone marrow examination are required.

Some other related symptoms

Fever, chills, night sweats and other flu-like symptoms
Weakness and fatigue
Loss of appetite and/or weight
Swollen or bleeding gums
Excess bleeding (from a minor cut)
Neurological symptoms (headache)
Enlarged liver and spleen
Easy bruising
Frequent infection
Bone pain
Joint pain
Swollen tonsils
The word leukemia, which means 'white blood,' is derived from the disease's namesake high white blood cell counts that most leukemia patients have before treatment. The high number of white blood cells are apparent when a blood sample is viewed under a microscope. Frequently, these extra white blood cells are immature or dysfunctional. The excessive number of cells can also interfere with the normal function of other cells.

Some leukemia patients do not have high white blood cell counts visible during a regular blood count. This less-common condition is called aleukemia. The bone marrow still contains cancerous white blood cells, and they are disrupting the normal production of blood cells. However, they are staying in the marrow instead of entering the bloodstream, where they would be visible in a blood test. For an aleukemic patient, the white blood cell counts in the bloodstream can be normal or low. Aleukemia can occur in any of the four major types of leukemia, and is particularly common in hairy cell leukemia.

Four major types
Leukemia is a broad term covering a spectrum of diseases.

Leukemia is clinically and pathologically split into its acute and chronic forms.

Acute leukemia is characterized by the rapid proliferation of immature blood cells. This crowding makes the bone marrow unable to produce healthy blood cells. Acute forms of leukemia can occur in children and young adults. (In fact, it is a more common cause of death for children in the US than any other type of malignant disease). Immediate treatment is required in acute leukemias 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. However, CNS involvement is uncommon, though the disease occasionally causes cranial nerve palsies.
Chronic leukemia is distinguished by the excessive build up of relatively mature, but still abnormal, blood cells. Typically taking months to 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. Chronic leukemia mostly occurs in older people, but can theoretically occur in any age group. Whereas acute leukemia must be treated immediately, chronic forms are sometimes monitored for some time before treatment to ensure maximum effectiveness of therapy.
Furthermore, the diseases are classified according to the type of abnormal cell found most in the blood (lymphoid cells vs. myeloid cells).

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

Acute Chronic
lymphocytic leukemia Acute lymphocytic leukemia (also known as Acute Lymphoblastic Leukemia, or ALL) is the most common type of leukemia in young children. This disease also affects adults, especially those age 65 and older. Chronic lymphocytic leukemia (CLL) most often affects adults over the age of 55. It sometimes occurs in younger adults, but it almost never affects children.
myelogenous leukemia (or "myeloid") Acute myelogenous leukemia (also known as Acute Myeloid Leukemia, or AML) occurs more commonly in adults than in children. This type of leukemia was previously called "acute nonlymphocytic leukemia". Chronic myelogenous leukemia (CML) occurs mainly in adults. A very small number of children also develop this disease.


Causes and risk factors
There is no single known cause for all of the different types of leukemia. The different leukemias likely have different causes, and very little is certain about what causes them.

Researchers have strong suspicions about four possible causes:
natural or artificial ionizing radiation
certain kinds of chemicals
some viruses
genetic predispositions
Leukemia, like other cancers, result from somatic mutations in the DNA which activate oncogenes or deactivate tumor suppressor genes, and disrupt 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. Cohort and case-control studies have linked exposure to petrochemicals, such as benzene, and hair dyes to the development of some forms of leukemia.

Viruses have also been linked to some forms of leukemia. For example, certain cases of ALL are associated with viral infections by either the human immunodeficiency virus (HIV, responsible for AIDS) or human T-lymphotropic virus (HTLV-1 and -2, causing adult T-cell leukemia/lymphoma).

Fanconi anemia is also a risk factor for developing acute myelogenous leukemia.

Until the cause or causes of leukemia are found, there is no way to prevent the disease. Even when the causes become known, they may prove to be things which are not readily controllable, such as naturally occurring background radiation, and therefore not especially helpful for prevention purposes.

Treatment options for leukemia by type

Acute Myelogenous Leukemia (AML)
It is most common for adults; more men than women are affected. Many different chemotherapeutic plans are available for the treatment of AML. Overall, the strategy is to control bone marrow and systemic (whole-body) disease while offering specific treatment for the central nervous system (CNS), if involved. In general, most oncologists rely on combinations of drugs for the initial, induction phase of chemotherapy. Such combination chemotherapy usually offers the benefits of early remission (lessening of the disease) and a lower risk of disease resistance. Consolidation or "maintenance" treatments may be given to prevent disease recurrence once remission has been achieved. Consolidation treatment often entails a repetition of induction chemotherapy or the intensification chemotherapy with added drugs. By contrast, maintenance treatment involves drug doses that are lower than those administered during the induction phase.

In addition, specific treatment plans may be used, depending on the type of leukemia that has been diagnosed. Whatever the plan, it is important for the patient to understand the treatment that is being given and the decision-making process behind the choice.


Initial treatment of AML
Initial treatment of AML usually begins with induction chemotherapy using a combination of drugs such as daunorubicin (DNR), cytarabine (ara-C), idarubicin, thioguanine, etoposide, or mitoxantrone, anabolic steroids.

Follow-up treatment
Follow-up therapy for such patients may involve:

supportive care, such as intravenous nutrition and treatment with oral antibiotics (e.g., ofloxacin, rifampin), especially in patients who have prolonged granulocytopenia; that is too few mature granulocytes (neutrophils), the bacteria-destroying white blood cells that contain small particles, or granules (< 100 granulocytes per cubic millimeter for 2 weeks)
injection with colony-stimulating factors such as granulocyte colony-stimulating factor (G-CSF), which may help to shorten the period of granulocytopenia that results from induction therapy
transfusions with red blood cells and platelets
Patients with newly diagnosed disease also may be considered for stem cell transplantation (SCT), either from the bone marrow or other sources. Allogeneic bone marrow transplant (alloBMT) is reserved primarily for patients under 55 years of age who have a compatible family donor. Approximately half of newly diagnosed AML patients are in this age group, with 75% achieving a complete remission (CR) after induction and consolidation therapy. Allogeneic bone marrow transplant is available for about 15% of all patients with AML. Unfortunately, it is estimated that only 7% of all AML patients will be cured using this procedure.

People who receive stem cell transplantation (SCT, alloBMT) require protective isolation in the hospital, including filtered air, sterile food, and sterilization of the microorganisms in the gut, until their total white blood cell (WBC) count is above 500.

Treatment of central nervous system leukemia, if present, may involve injection of chemotherapeutic drugs (e.g., cytarabine or ara-C, methotrexate) into the areas around the brain and spinal cord.

Consolidation or maintenance therapy
Once the patient is in remission, he or she will receive consolidation or maintenance therapy, for example, consolidation therapy with high-dose ara-C (HDAC) with/without anthracycline drugs).

If, however, the AML patient has resistant disease (about 15%) or relapses (about 70%), second remissions sometimes are achieved by treating them with:

conventional induction chemotherapy
high-dose ara-C (HDAC), with/without other drugs
etoposide or other single chemotherapeutic agents
Elderly AML patients have special treatment concerns. They may be less able to tolerate the septicemia (blood poisoning) associated with granulocytopenia, and they often have higher rates of myelodysplastic ('preleukemia') syndrome (MDS). Individuals who are over age 75 or who have significant medical conditions can be treated effectively with low-dose ara-C. High-dose post-induction chemotherapy is unlikely to be tolerated by elderly patients.

Until recently, the treatment plans and responses of children with AML did not differ much from those of adults. Yet new, more intensive induction and consolidation treatments have resulted in higher remission rates and prolonged survivals. Many induction trials have produced good results using combinations of cytarabine (ara-C) plus an anthracycline (e.g., daunorubicin, doxorubicin). In children under 3 years of age, the anthracycline used for induction should be chosen with care, since doxorubicin produces more toxicity and related deaths than daunorubicin.

Consolidation therapy is complex, but it should include at least two courses of high-dose ara-C (HDAC). Children who have hyperleukocytosis (too many white blood cells), especially monocytic M5 leukemia, have a poor prognosis.

Chronic Myelogenous Leukemia (CML)
The challenge of treating newly diagnosed CML is to determine the best overall strategy to control the disease. General strategies for management include a variety of options:

Leukapheresis, also known as a peripheral blood stem cell transplant, with stem cell cryopreservation (frozen storage) prior to any other treatment. The patient's blood is passed through a machine that removes the stem cells and then returns the blood to the patient. Leukapheresis usually takes 3 or 4 hours to complete. The stem cells may or may not be treated with drugs to kill any cancer cells. The stem cells then are stored until they are transplanted back into the patient.

HLA (human leukocyte antigen) typing of all patients under age 60, as well as typing of siblings, parents, and children, if available. This procedure will determine whether a compatible donor is available for stem cell transplantation.

Pre-treatment fertility measures (e.g., cryopreservation of semen prior to treatment; completion of a pregnancy prior to treatment) in young patients who have not completed their families.

Interferon-alpha (INF-a) therapy'.

Chemotherapy with drugs such as hydroxyurea (Hydrea®), busulfan (Myleran®) or imatinib mesylate (Gleevec(tm)).

In general, CML treatment options are divided into two groups: those that do not increase survival and those that do. Chemotherapeutic drugs such as hydroxyurea (Hydrea®) and busulfan (Myleran®) can normalize the blood count for a period of time, but they do not increase survival. They often are used to control blood counts in patients who cannot undergo SCT or who do not respond to interferon therapy because of age or medical considerations.

Gleevec, is one of a new class of cancer drugs that disables an abnormal enzyme in the cancerous cell, kills it, but leaves healthy cells virtually untouched. Other cancer therapies, such as chemotherapy, attack healthy cells as well as cancer cells, leaving patients with unpleasant and often severe side effects.

In June of 2006, the Food and Drug Administration (FDA) approved the oral tyrosine kinase inhibitor dasatinib (Sprycel(tm)) to treat CML that does not respond to other therapy.

One treatment that does impact on CML survival is allogeneic bone marrow transplantation, the use of high dose chemotherapy and radiation followed by infusion of a donor bone marrow. This procedure removes the chromosomal abnormality in a large percentage of patients and for them is curative. In addition, there is treatment with interferon (INF). About 20% to 30% of patients taking interferon show elimination of the abnormal chromosome and improved survival. Recent findings also suggest that low-dose cytarabine (ara-C), in combination with interferon, may be more beneficial than interferon alone. For patients who do not respond to interferon, autologous or allogeneic stem cell transplantation is the only alternative.

Patients with advanced-phase disease may be treated with cytotoxic drugs. For example, individuals showing myeloid transformation may be given drugs that are used to induce remission in AML - that is, daunorubicin and cytarabine, with or without 6-thioguanine or etoposide. Blast cell numbers will be reduced temporarily, but they will increase again within 3 to 6 weeks. Individuals showing lymphoid transformation have a slightly better outlook. They are treated with drugs used in the management of acute lymphocytic leukemia (ALL) - that is, prednisone, vincristine, and daunorubicin, with or without L-asparaginase.

New drugs that are being studied in clinical trials of CML include homoherringtonine with interferon-alpha (INF-a), paclitaxel (Taxol®), QS21 (a plant extract that heightens immune responses), and amifostin (a chemical that lessens some side effects of chemotherapy). In addition, clinical trials are evaluating the potential benefits of substances such as vaccines, monoclonal antibodies (immunologic substances that can direct the patient's immune system to kill cancer cells), and hormones (e.g., growth factors, interleukins).

Acute Lymphocytic Leukemia (ALL)
Proper management of ALL focuses on control of bone marrow and systemic (whole-body) disease as well as prevention of cancer at other sites, particularly the central nervous system (CNS). In general, ALL treatment is divided into several phases:

Induction chemotherapy to bring about remission - that is, leukemic cells are no longer found in bone marrow samples. For adult ALL, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L-asparaginase or cyclophosphamide. For children with low-risk ALL, standard therapy usually consists of three drugs (prednisone, L-asparaginase, and vincristine) for the first month of treatment. High-risk children may receive these drugs plus an anthracycline such as daunorubicin.

Consolidation therapy (1-3 months in adults; 4-8 months in children) to eliminate any leukemia cells that are still "hiding" within the body. A combination of chemotherapeutic drugs is used to keep the remaining leukemia cells from developing resistance. Patients with low- to average-risk ALL receive therapy with antimetabolite drugs such as methotrexate and 6-mercaptopurine (6-MP). High-risk patients receive higher drug doses plus treatment with extra chemotherapeutic agents.

CNS prophylaxis (preventive therapy) to stop the cancer from spreading to the brain and nervous system. Standard prophylaxis may consist of:

Cranial (head) irradiation plus spinal tap or intrathecal (IT) delivery (into the space around the spinal cord and brain) of the drug methotrexate.
High-dose systemic and IT methotrexate, without cranial irradiation
IT chemotherapy.
Only children with T-cell leukemia, a high white blood cell count, or leukemia cells in the cerebrospinal fluid (CSF) need to receive cranial irradiation as well as IT therapy.

Maintenance treatments with chemotherapeutic drugs (e.g., prednisone + vincristine + cyclophosphamide + doxorubicin; methotrexate + 6-MP) to prevent disease recurrence once remission has been achieved. Maintenance therapy usually involves drug doses that are lower than those administered during the induction phase. In children, an intensive 6-month treatment program is needed after induction, followed by 2 years of maintenance chemotherapy.

Follow-up therapy for ALL patients usually consists of:

supportive care, such as intravenous nutrition and treatment with oral antibiotics (e.g., ofloxacin, rifampin), especially in patients with prolonged granulocytopenia; that is, too few mature granulocytes (neutrophils), the bacteria-destroying white blood cells that contain small particles, or granules (< 100 granulocytes per cubic millimeter for 2 weeks)
transfusions with red blood cells and platelets
A laboratory test known as polymerase chain reaction (PCR) is advisable for ALL patients, since it may help to identify specific genetic abnormalities. Such abnormalities have a large impact upon prognosis and, consequently, treatment plans. PCR testing is especially important for patients whose disease is B-cell in type. B-cell ALL usually is not cured by standard ALL therapy. Instead, higher response rates are achieved with the aggressive, cyclophosphamide-based regimens that are used for non-Hodgkin's lymphoma.

Among ALL patients, 3-5% children and 25-50% of adults are positive for the Philadelphia chromosome (Ph1)[citation needed]. Because these patients have a worse prognosis than other individuals with ALL, many oncologists recommend allogeneic bone marrow transplantation (alloBMT), since remission may be brief following conventional ALL chemotherapy.

People who receive bone marrow transplantation will require protective isolation in the hospital, including filtered air, sterile food, and sterilization of the microorganisms in the gut, until their total white blood cell (WBC) count is above 500.

Recurrent ALL patients usually do not benefit from additional chemotherapy alone. If possible, they should receive re-induction chemotherapy, followed by allogeneic bone marrow transplant (alloBMT).

Alternatively, patients with recurrent ALL may benefit from participation in new clinical trials of alloBMT, immune system agents, and chemotherapeutic agents, or low-dose radiotherapy, if the cancer recurs throughout the body or CNS.

Chronic Lymphocytic Leukemia (CLL)
CLL is probably "incurable" by present treatments. But, fortunately, a large group of CLL patients do not require therapy. Studies suggest that people with Stage A CLL (that is, individuals who have fewer than three areas of enlarged lymphoid tissue) do not benefit from early treatment. They may, in fact, suffer drawbacks because of it. Therefore, most oncologists base CLL treatment upon both the stage and symptoms of the patient.

For example, in older patients (60+ years) who have low-risk early stage disease (Rai Stage 0) a conservative "watch and wait" approach may be taken.

By contrast, older individuals with CLL-related complications or more advanced disease (Rai Stage III or IV) may benefit from chemotherapy and treatment with a corticosteroid (e.g., prednisone, prednisolone).

Corticosteroids are first-line agents for people in whom the immune systems has been altered by CLL. CLL may cause autoimmune syndromes in which the patient's immune system attacks and destroys his or her own blood cells. When the red blood cells are affected, the condition is known as immunohemolytic anemia, characterized by decreased numbers of red blood cells, which may cause fatigue, dizziness, and shortness of breath. When the blood platelets are affected, it is called immune-mediated thrombocytopenia, in which a decreased numbers of platelets may lead to bleeding.

For younger patients who are experiencing symptoms, the physician may consider early chemotherapy, plus allogeneic or autologous bone marrow transplantation (alloBMT; autoBMT).

In general, the indications for treatment are:

falling hemoglobin or platelet count
progression to a later stage of disease
painful, disease-related overgrowth of lymph nodes or spleen
lymphocyte doubling time (an indicator of lymphocyte reproduction) of fewer than 12 months

Transformation of CLL to high-grade disease or aggressive non-Hodgkin's lymphoma
If the patient experiences blood flow problems caused by high numbers of leukemia cells in the circulation, the physician may recommend leukapheresis, also known as apheresis, to separate out white blood cells, prior to chemotherapy. Symptoms that are related to enlargement of the lymph nodes in one area or an overgrown spleen may be treated by localized, low-dose radiotherapy, or surgical management by splenectomy (removal of the spleen). But if leukemia has invaded the lymph nodes at many different sites, total body irradiation (TBI) may be needed.

Chemotherapy for CLL
The chemotherapeutic plans that are used most often for CLL are:
combination chemotherapy with chlorambucil (Leukeran®) or cyclophosphamide (Cytoxan®) plus a corticosteroid drug such as prednisone, or
single-agent treatments with nucleoside drugs such as fludarabine, pentostatin, or cladribine (2-chlorodeoxyadenisine; 2-CDA). However, such drugs usually are reserved for cases in which CLL is resistant (unresponsive to treatment) or returns after chemotherapy with chlorambucil or cyclophosphamide.
People with intermediate (Rai Stage I and II) or advanced (Rai Stage III or IV) disease may be helped by participation in a clinical trial. At the present time, clinical trials are being conducted using immunologic compounds (e.g., interferons, monoclonal antibodies) as well as new chemotherapeutic agents (e.g., bryostatin, dolastatin 10, and PSC 83 - a cyclosporine drug given with chemotherapy to overcome drug resistance).

Hairy Cell Leukemia (HCL)
Hairy cell leukemia is an incurable, indolent blood disorder in which mutated, partly matured B cells accumulate in the bone marrow. Its name is derived from the shape of the cells, which look like they are covered with short, fine, hair-shaped projections. Unlike any other leukemia, HCL is characterized by low white blood cell counts.

Patients with hairy cell leukemia who are symptom-free typically do not receive immediate treatment. They engage in "watchful waiting" with routine bloodwork and exams every three to six months to monitor disease progression and identify any new symptoms.

Treatment is generally considered necessary when the patient shows signs and symptoms such as low blood cell counts (e.g., infection-fighting neutrophil count below 1.0 K/ul), frequent infections, unexplained bruises, anemia, or fatigue that is significant enough to disrupt the patient's everyday life.

Patients who need treatment, which includes most newly diagnosed HCL cases, usually receive either cladribine or pentostatin, which are both in a class of chemotherapeutic drugs known as purine analogs or nucleosides. In most cases, one round of treatment will produce a prolonged remission.

Other treatments include rituximab infusion or self-injection with Interferon-alpha. In limited cases, the patient may benefit from splenectomy (removal of the spleen). These treatments are not typically given as the first treatment for a new patient because their success rates are lower than cladribine or pentostatin.

In the short term, especially when neutrophil counts are low, an immune system hormone called granulocyte colony-stimulating factor may be taken to increase white blood cell counts. This is believed to help prevent or treat an infection. Many patients also take antibiotics until their white blood cell counts have recovered to normal levels.

Clinical trials are being conducted with high-dose chemotherapy followed by stem cell transplantation.

Research

Açaí Palm
In 2006, a study performed at the University of Florida showed that açaí fractions containing polyphenolics could reduce proliferation of HL-60 leukemia cells in vitro. This was most likely due to increased rapid cell death (apoptosis) as fractions were also found to activate caspase-3 (an enzyme important in apoptosis) which was inversely correlated to cell death. (Pozo-Insfran et al., 2006). This is a very preliminary study, but indicates a need for more research on the possible anti-cancer effects of açaí.

Leukimia

Hepatitis a Diseas Medicine

Hepatitis (plural hepatitides) implies injury to liver characterised by presence of inflammatory cells in the liver tissue. Etymologically from ancient Greek hepar (ηπαρ) or hepato- (ηπατο-) meaning 'liver' and suffix -itis denoting 'inflammation' (c.1727[1]). The condition can be self limiting, healing on its own or can progress to scarring of liver. Acute hepatitis is when it lasts less than 6 months and chronic hepatitis is when it persists longer. A group of viruses known as the hepatitis viruses cause most liver damages worldwide. Hepatitis can also be due to toxins (notably alcohol), other infections or from autoimmune process. It may run a subclinical course when the affected person may not feel ill. The patient becomes unwell and symptomatic when the disease impairs liver functions that include among other things, screening of harmful substances, regulation of blood composition and production of bile to help digestion.

Causes
Acute hepatitis
Viral Hepatitis: Hepatitis A to E (more than 95% of viral cause), Herpes simplex, Cytomegalovirus, Epstein-Barr, yellow fever virus, adenoviruses.
Non viral infection: toxoplasma, Leptospira, Q fever, rocky mountain spotted fever
Alcohol
Toxins: Amanita toxin in mushrooms, Carbon tetrachloride, asafetida
Drugs: Paracetamol, amoxycillin, anti tuberculosis medicines, minocycline and many others

Circulatory insufficiency
pregnancy
Auto immune conditions e.g. SLE
Metabolic diseases e.g. Wilson's disease
Chronic hepatitis
Viral Hepatitis: Hepatitis B with or without hepatitis D, Hepatitis C (Hepatitis A and E do not lead to chronic disease)
Autoimmune: Autoimmune hepatitis
Alcohol
Drugs: methyl-dopa, nitrofurantoin, isoniazide, ketoconazole
Non-alcoholic steatohepatitis
Heredity: Wilson's disease, alpha 1-antitrypsin deficiency
Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis

Signs and symptoms
Acute Hepatitis

Clinically the course of acute hepatitis varies widely from mild symptoms requiring no treatment to fulminant hepatic failure needing liver transplantation. Acute viral hepatitis are more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7 to 10 days, with the total illness lasting 2 to 6 weeks.

Initial features are of nonspecific flu-like symptoms, common to almost all acute viral infections and may include: malaise, muscle and joint aches, fever, feeling sick or vomiting, diarrhea and headache. More specific symptoms, which can be present in acute hepatitis from any cause are: profound loss of appetite, aversion of smoking among smokers, dark urine, yellowing of the eyes and skin i.e. jaundice and abdominal discomfort. Physical findings are usually minimal, apart from jaundice (33%) and tender hepatomegaly (10%). There can be occasional lymphadenopathy (5%) or splenomegaly (5%).

Chronic Hepatitis

Majority of patients will remain asymptomatic or mildly symptomatic, abnormal blood tests being the only manifestation. Features may be related to extent of liver damage or the cause of hepatitis. Many experience return of symptoms related to acute hepatitis. Jaundice can be a late feature and may indicate extensive damage. Other features include abdominal fullness from enlarged liver or spleen, low grade fever and fluid retention (ascites). Extensive damage and scarring of liver i.e. cirrhosis leads to weight loss, easy bruising and bleeding tendencies. Acne, abnormal menstruation, lung scarring, inflammation of the thyroid gland and kidneys may be present in women with autoimmune hepatitis.

Findings on clinical examination are usually those of cirrhosis or are related to aetiology.

Types of hepatitis
Please see the respective articles for more detailed information.
See also infectious canine hepatitis.

Viral
Most cases of acute hepatitis are due to viral infections:

Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis B with D
Hepatitis E
Hepatitis F (existence unknown)
Hepatitis G
In addition to the hepatitis viruses (please note that the hepatitis viruses are not all related). Other viruses can also cause hepatitis, including cytomegalovirus, Epstein-Barr virus, yellow fever, etc.

Hepatitis A
Hepatitis A or infectious jaundice is caused by a picornavirus. It is transmitted by the orofecal route, transmitted to humans through methods such as contaminated food. It causes an acute form of hepatitis and does not have a chronic stage. The patient's immune system makes antibodies against hepatitis A that confer immunity against future infection. People with hepatitis A are advised to rest, stay hydrated and avoid alcohol. A vaccine is available that will prevent infection from hepatitis A for life. Hepatitis A can be spread through personal contact, consumption of raw sea food or drinking contaminated water. This occurs primarily in third world countries. Strict personal hygiene and the avoidance of raw and unpeeled foods can help prevent an infection. Infected people excrete the hepatitis A virus with their stool two weeks before and one week after the appearance of jaundice. The time between the infection and the start of the illness can run from 15 to 45 days, and approximately 15% of sufferers may experience relapsing symptoms from six months to a year following initial diagnosis.

Hepatitis B
Hepatitis B is caused by a hepadnavirus, which can cause both acute and chronic hepatitis. Chronic hepatitis develops in the 15% of patients who are unable to eliminate the virus after an initial infection. Identified methods of transmission include blood (blood transfusion, now rare), tattoos (both amateur and professionally done), sexually (through sexual intercourse or through contact with blood or bodily fluids), or in utero (from mother to her unborn child, as the virus can cross the placenta). However, in about half of cases the source of infection cannot be determined. Blood contact can occur by sharing syringes in intravenous drug use, shaving accessories such as razor blades, or touching wounds on infected persons. Needle-exchange programmes have been created in many countries as a form of prevention. In the United States, 95% of patients clear their infection and develop antibodies against hepatitis B virus. 5% of patients do not clear the infection and develop chronic infection; only these people are at risk of long term complications of hepatitis B.

Patients with chronic hepatitis B have antibodies against hepatitis B, but these antibodies are not enough to clear the infection that establishes itself in the DNA of the affected liver cells. The continued production of virus combined with antibodies is a likely cause of immune complex disease seen in these patients. A vaccine is available that will prevent infection from hepatitis B for life. Hepatitis B infections result in 500,000 to 1,200,000 deaths per year worldwide due to the complications of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Hepatitis B is endemic in a number of (mainly South-East Asian) countries, making cirrhosis and hepatocellular carcinoma big killers. There are six FDA-approved treatment options available for persons with a chronic hepatitis B infection: alpha-interferon, pegylated interferon adefovir, entecavir, telbivudine and lamivudine. About 45% of persons on treatment achieve a sustained response.

Hepatitis C
Hepatitis C (originally "non-A non-B hepatitis") is caused by a Flavivirus. It can be transmitted through contact with blood (including through sexual contact where the two parties' blood is mixed). Hepatitis C may lead to a chronic form of hepatitis, culminating in cirrhosis. It can remain asymptomatic for 10-20 years. Patients with hepatitis C are prone to severe hepatitis if they contract either hepatitis A or B, so all hepatitis C patients should be immunized against hepatitis A and hepatitis B if they are not already immune. The virus can cause cirrhosis of the liver. HCV viral levels can be reduced to undetectable levels by a combination of interferon and the antiviral drug ribavirin. The genotype of the virus determines the rate of response to this treatment regimen. Genotype 1 is more resistant to interferon therapy than other HCV genotypes.

Hepatitis D
Hepatitis D is considered a subviral satellite, as it can only propagate in the presence of the Hepatitis B virus.

Hepatitis E
Hepatitis E produces symptoms similar to hepatitis A, although it can take a fulminant course in some patients, particularly pregnant women; it is more prevalent in the Indian subcontinent.

Hepatitis F
Hepatitis F is a hypothetical virus linked to hepatitis. Several hepatitis F candidates emerged in the 1990s; none of these reports have been substantiated.

Hepatitis G
Another type of hepatitis, hepatitis G, has been identified, and is probably spread by blood and sexual contact. There is, however, doubt about whether it causes hepatitis, or is just associated with hepatitis, as it does not appear to be primarily replicated in the liver.
Other viruses can cause infectious hepatitis:

Mumps virus
Rubella virus
Cytomegalovirus
Epstein-Barr virus
Other herpes viruses

Alcoholic Hepatitis
Ethanol, mostly in alcoholic beverages, is a significant cause of hepatitis. Usually alcoholic hepatitis comes after a period of increased alcohol consumption. Alcoholic hepatitis is characterized by a variable constellation of symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen ascites, and modest elevation of liver blood tests. Alcoholic hepatitis can vary from mild with only liver test elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both categories is 50% within 30 days of onset.

Alcoholic hepatitis is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C. The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis in Western countries.

Drug induced hepatitis
A large number of drugs can cause hepatitis. The anti-diabetic drug troglitazone was withdrawn in 2000 for causing hepatitis. Other drugs associated with hepatitis:
Allopurinol
Amitriptyline (antidepressant)
Amiodarone (antiarrhythmic)
Azathioprine[11][12]
Halothane (a specific type of anesthetic gas)
Hormonal contraceptives
Ibuprofen and indometacin (NSAIDs)
Isoniazid (INH), rifampicin, and pyrazinamide (tuberculosis-specific antibiotics)
Ketoconazole (antifungal)
Methyldopa (antihypertensive)
Minocycline (tetracycline antibiotic)
Nifedipine (antihypertensive)
Nitrofurantoin (antibiotic)
Phenytoin and valproic acid (antiepileptics)
Zidovudine (antiretroviral i.e. against AIDS)
Some herbs and nutritional supplements

The clinical course of drug-induced hepatitis is quite variable, depending on the drug and the patient's tendency to react to the drug. For example, halothane hepatitis can range from mild to fatal as can INH-induced hepatitis. Hormonal contraception can cause structural changes in the liver. Amiodarone hepatitis can be untreatable since the long half life of the drug (up to 60 days) means that there is no effective way to stop exposure to the drug. Statins can cause elevations of liver function blood tests normally without indicating an underlying hepatitis. Lastly, human variability is such that any drug can be a cause of hepatitis.

Other toxins that cause hepatitis
Toxins and drugs can cause hepatitis:

Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel (Amanita ocreata), and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).
White phosphorus, an industrial toxin.
Paracetamol (acetaminophen in the United States) can cause hepatitis when taken in an overdose. The severity of liver damage can be limited by prompt administration of acetylcysteine.
Carbon tetrachloride ("tetra", a dry cleaning agent), chloroform, and trichloroethylene, all chlorinated hydrocarbons, cause steatohepatitis (hepatitis with fatty liver).
Cylindrospermopsin, a toxin from the cyanobacterium Cylindrospermopsis raciborskii and other cyanobacteria.

Metabolic disorders
Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.

Obstructive
"Obstructive jaundice" is the term used to describe jaundice due to obstruction of the bile duct (by gallstones or external obstruction by cancer). If longstanding it leads to destruction and inflammation of liver tissue.

Autoimmune
Anomalous presentation of human leukocyte antigen (HLA) class II on the surface of hepatocytes—possibly due to genetic predisposition or acute liver infection—causes a cell-mediated immune response against the body's own liver, resulting in autoimmune hepatitis.

Autoimmune hepatitis has an incidence of 1-2 per 100,000 per year, and a prevalence of 15-20/100,000. As with most other autoimmune diseases, it affects women much more often than men (8:1). Liver enzymes are elevated, as is bilirubin. Autoimmune hepatitis can progress to cirrhosis. Treatment is with steroids and disease-modifying antirheumatic drugs (DMARDs).

The diagnosis of autoimmune hepatitis is best achieved with a combination of clinical and laboratory findings. A number of specific antibodies found in the blood (antinuclear antibody (ANA), smooth muscle antibody (SMA), Liver/kidney microsomal antibody (LKM-1) and anti-mitochondrial antibody (AMA)) are of use, as is finding an increased Immunoglobulin G level. However, the diagnosis of autoimmune hepatitis always requires a liver biopsy. In complex cases a scoring system can be used to help determine if a patient has autoimmune hepatitis, which combines clinical and laboratory features of a given case.

Four subtypes are recognised, but the clinical utility of distinguishing subtypes is limited.

Positive ANA and SMA, raised immunoglobulin G (classic form, responds well to low dose steroids)
Positive LKM-1 (typically female children and teenagers; disease can be severe)
All antibodies negative, positive antibodies against soluble liver antigen (SLA)(now designated SLP/LP). This group behaves like group 1.
No autoantibodies detected (~13%)

Alpha 1-antitrypsin deficiency
In severe cases of alpha 1-antitrypsin deficiency (A1AD), the accumulated protein in the endoplasmic reticulum causes liver cell damage and inflammation.

Nonalcoholic steatohepatitis
Non-alcoholic steatohepatitis (NASH) is a type of hepatitis which resembles alcoholic hepatitis on liver biopsy (fat droplets, inflammatory cells, but usually no Mallory's hyalin) but occurs in patients who have no known history of alcohol abuse. NASH is more common in women and the most common cause is obesity or the metabolic syndrome. A related but less serious condition is called "fatty liver" (steatosis hepatis), which occurs in up to 80% of all clinically obese people. A liver biopsy for fatty liver shows fat droplets throughout the liver, but no signs of inflammation or Mallory's hyalin.

The diagnosis depends on history, physical exam, blood tests, radiological imaging and sometimes a liver biopsy. The initial evaluation to identify the presence of fatty infiltration of the liver is radiologic imaging including ultrasound, computed tomographic imaging, or magnetic resonance imaging. However, radiologic imaging cannot readily identify inflammation in the liver. Therefore, the differentiation between steatosis and NASH often requires a liver biopsy. It can also be difficult to distinguish NASH from alcoholic hepatitis when the patient has a history of alcohol consumption. Sometimes in such cases a trial of abstinence from alcohol along with follow -up blood tests and a repeat liver biopsy are required.

NASH is becoming recognized as the most important cause of liver disease second only to Hepatitis C in numbers of patients going on to cirrhosis.

Hepatitis awareness
World Hepatitis Awareness Day is an annual event organised by several worldwide hepatitis advocacy groups to raise awareness of infectious hepatitis and demand action to curb the spread of the disease and treat people who are infected.

Hepatitis a Diseas Medicine

5th Dease

Fifth disease is also referred to as erythema infectiosum (meaning infectious redness) and as slapped cheek syndrome, slapcheek, slap face or slapped face. The name "fifth disease" derives from its historical classification as the fifth of the classical childhood skin rashes or exanthems. In 1975, the cause of Fifth disease was discovered to be parvovirus B19.

Symptoms
The bright red cheeks are a defining symptom of the infection in children (hence the name "slapped cheek disease"). Occasionally the rash will extend over the bridge of the nose or around the mouth. In addition to the red cheeks, children often develop a red, lacy rash on the rest of the body, with the upper arms and legs being the most common locations. The rash can last a couple of weeks (some cases lasting for several months) and may itch. Patients are usually no longer infectious once the rash has appeared.

Teenagers and adults may present with a self-limited arthritis.

The disease is usually mild, but in certain risk groups it can have serious consequences:

In pregnant women, infection in the first trimester has been linked to hydrops fetalis, causing spontaneous abortion
In people with Sickle-cell disease or other forms of chronic hemolytic anemia, infection can precipitate an aplastic crisis

Epidemiology
Any age may be affected although it is most common in children aged five to fourteen years. By the time adulthood is reached about half the population will have become immune following infection at some time in their past. Outbreaks can arise especially in nurseries and schools.

5th Dease

DSM Categories

The Diagnostic and Statistical Manual of Mental Disorders (DSM) is a handbook for mental health professionals that lists different categories of mental disorder and the criteria for diagnosing them, according to the publishing organization the American Psychiatric Association. It is used worldwide by clinicians and researchers as well as insurance companies, pharmaceutical companies and policy makers. It has attracted controversy and criticism as well as praise.

The DSM has gone through five revisions since it was first published in 1952. The last major revision was the DSM-IV published in 1994, although a "text revision" was produced in 2000. The DSM-V is currently in consultation, planning and preparation, due for publication in approximately 2012. The mental disorders section of the International Statistical Classification of Diseases and Related Health Problems (ICD) is another commonly-used guide, and the two classifications use the same diagnostic codes.

History
The Diagnostic and Statistical Manual of Mental Disorders was first published in 1952, by the American Psychiatric Association. It was developed from an earlier classification system adopted in 1918 to meet the need of the federal Bureau of the Census for uniform statistics from psychiatric hospitals; from categorization systems in use by the United States military; and from a survey of the views of 10% of APA members. The manual was 130 pages long and contained 106 categories of mental disorder. The DSM-II was published in 1968, listed 182 disorders, and was 134 pages long. These manuals reflected the predominant psychodynamic psychiatry. Symptoms were not specified in detail for specific disorders, but were seen as reflections of broad underlying conflicts or maladaptive reactions to life problems, rooted in a distinction between neurosis and psychosis (roughly, anxiety/depression broadly in touch with reality, or hallucinations/delusions appearing disconnected from reality). Sociological and biological knowledge was also incorporated, in a model that did not emphasize a clear boundary between normality and abnormality.

In 1974, the decision to create a new revision of the DSM was taken, and Robert Spitzer was selected as chairman of the task force. The initial impetus was to make the DSM nomenclature consistent with the International Statistical Classification of Diseases and Related Health Problems (ICD), published by the World Health Organization. The revision took on a far wider mandate under the influence and control of Spitzer and his chosen committee members. One goal was to improve the reliability of psychiatric diagnosis. The practices of mental health professionals, especially in different countries, was not uniform. The establishment of specific criteria was also an attempt to facilitate mental health research. The multiaxial system attempts to yield a more complete picture of the patient, rather than just a simple diagnosis. The criteria and classification system of the DSM-III was based on a process of consultation and committee meetings. An attempt was made to base categorization on description rather than assumptions of etiology, and the psychodynamic view was abandoned, perhaps in favor of a biomedical model, with a clear distinction between normal and abnormal.

The criteria adopted for many of the mental disorders were expanded from the Research Diagnostic Criteria (RDC) and Feighner Criteria which had been developed for psychiatry research in the 1970s. Other criteria were established by consensus in committee meetings, as determined by Spitzer. The approach is generally seen as "Neo-Kraepelinian", after the work of the psychiatrist Emil Kraepelin. Spitzer argued that “mental disorders are a subset of medical disorders” but the task force decided on the DSM statement: “each of the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome”. The first draft of the DSM-III was prepared within a year. Many new categories of disorder were introduced. Field trials sponsored by the U.S. National Institute of Mental Health (NIMH) were conducted between 1977 and 1979 to test the reliability of the new diagnoses. A controversy emerged regarding deletion of the concept of neurosis, a mainstream of psychoanalytic theory and therapy but seen as vague and unscientific by the DSM task force. Faced with enormous political opposition, such that the DSM-III was in serious danger of not being approved by the APA Board of Trustees unless “neurosis” was included in some capacity, a political compromise reinserted the term in parentheses after the word “disorder” in some cases. In 1980, the DSM-III was published, at 494 pages long and listing 265 diagnostic categories. The DSM-III rapidly came into widespread international use by multiple stakeholders and has been termed a revolution or transformation in psychiatry.

In 1987 the DSM-III-R was published as a revision of DSM-III, under the direction of Spitzer. Categories were renamed, reorganized, and significant changes in criteria were made. Six new categories were deleted while others were added. Controversial diagnoses such as pre-menstrual dysphoric disorder and Masochistic Personality Disorder were considered and discarded. Altogether, DSM-III-R contained 292 diagnoses and was 567 pages long.

In 1994, DSM-IV was published, listing 297 disorders in 886 pages. The task force was chaired by Allen Frances. A steering committee of 27 people was introduced, including four psychologists. The steering committee created 13 work groups of 5–16 members. Each work group had approximately 20 advisers. The work groups conducted a three step process. First, each group conducted an extensive literature review of their diagnoses. Then they requested data from researchers, conducting analyses to determine which criteria required change, with instructions to be conservative. Finally, they conducted multicenter field trials relating diagnoses to clinical practice. A major change from previous versions was the inclusion of a clinical significance criterion to almost half of all the categories, which required that symptoms cause "clinically significant distress or impairment in social, occupational, or other important areas of functioning."

A "Text Revision" of the DSM-IV, known as the DSM-IV-TR, was published in 2000. The diagnostic categories and the vast majority of the specific criteria for diagnosis were unchanged. The text sections giving extra information on each diagnosis were updated, as were some of the diagnostic codes in order to maintain consistency with the ICD.

DSM and Politics
Following controversy and protests from gay activists at APA annual conferences from 1970 to 1973, the seventh printing of the DSM-II, in 1974, no longer listed homosexuality as a category of disorder. After talks led by the psychiatrist Robert Spitzer, who had been involved in the DSM-II development committee, a vote by the APA trustees in 1973, confirmed by the wider APA membership in 1974, had replaced the diagnosis with a milder category of "sexual orientation disturbance". This was replaced with the diagnosis of ego-dystonic homosexuality in the DSM-III in 1980, but this was removed in 1987 with the release of the DSM-III-R. A category of "sexual disorder not otherwise specified" continues in the DSM-IV, which may include "persistent and marked distress about one’s sexual orientation”.

The current DSM

Categorization
The DSM-IV is a categorical classification system. The categories are prototypes, and a patient with a close approximation to the prototype is said to have that disorder. DSM-IV states that “there is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries...” but isolated, low-grade and noncriterion (unlisted for a given disorder) symptoms are not given importance. Qualifiers are sometimes used, for example mild, moderate or severe forms of a disorder. For nearly half the disorders, symptoms must be sufficient to cause “clinically significant distress or impairment in social, occupational, or other important areas of functioning", although DSM-IV-TR removed the distress criterion from tic disorders and several of the paraphilias. Each category of disorder has a numeric code taken from the ICD coding system, used for health service (including insurance) administrative purposes.

Multi-axial system
The DSM-IV organizes each psychiatric diagnosis into five levels (axes) relating to different aspects of disorder or disability:

Axis I: clinical disorders, including major mental disorders, as well as developmental and learning disorders
Axis II: underlying pervasive or personality conditions, as well as mental retardation
Axis III: Acute medical conditions and Physical disorders.
Axis IV: psychosocial and environmental factors contributing to the disorder
Axis V: Global Assessment of Functioning or Children’s Global Assessment Scale for children under the age of 18. (on a scale from 100 to 0)
Common Axis I disorders include depression, anxiety disorders, bipolar disorder, ADHD, and schizophrenia.

Common Axis II disorders include borderline personality disorder, schizotypal personality disorder, antisocial personality disorder, narcissistic personality disorder, and mild mental retardation.

Cautions
The DSM-IV-TR states that, because it is produced for mental health specialists, its use by people without clinical training can lead to inappropriate application of its contents. Appropriate use of the diagnostic criteria is said to require extensive clinical training, and its contents "cannot simply be applied in a cookbook fashion." The APA notes that diagnostic labels are primarily for use as a "convenient shorthand" among professionals. The DSM advises that laypersons should consult the DSM only to obtain information, not to make diagnoses, and that people who may have a mental disorder should be referred to psychiatric counseling or treatment. Further, people sharing the same diagnosis/label may not have the same etiology (cause) or require the same treatment; the DSM contains no information regarding treatment or cause for this reason. The range of the DSM represents an extensive scope of psychiatric and psychological issues, and it is not exclusive to what one may consider "illnesses."

DSM-IV sourcebooks
The DSM-IV doesn't specifically cite its sources, but there are four volumes of "sourcebooks" intended to be APA's documentation of the guideline development process and supporting evidence, including literature reviews, data analyses and field trials. The Sourcebooks have been said to provide important insights into the character and quality of the decisions that led to the production of DSM-IV, and hence the scientific credibility of contemporary psychiatric classification.

DSM Categories

Colonectomy

Colon hydrotherapy, also known as colonic irrigation, is an alternative medical procedure, sometimes associated with naturopathy. Similar to an enema, it involves the introduction of discrete amounts of purified water, sometimes infused with minerals or other materials, such as organic coffee, into the colon using medically approved class II colon hydrotherapy devices with sanitary, disposable speculums or gravity-fed enema-like systems inserted into the rectum. The fluid is released after a short period, and the process will be repeated multiple times during the course of a treatment. A colema is a type of colon hydrotherapy performed by oneself using a bucket with an attached hose, while lying on a board positioned over a toilet, into which the contents of enema are released.

In gastroenterology, the term "colonic irrigation" is also used to refer to the practice of introducing water through a colostomy or a surgically constructed conduit as a treatment for constipation.

Though colon hydrotherapy, colemas and enemas all have features in common, there are some significant differences between the modalities in terms of depth of colon cleansing, amount of water used, and the necessity for a practitioner to be present.

History
The practice has been known since ancient times for treating constipation which was believed to have been the root of many diseases and illnesses. The first recorded reference to colon cleansing date back more than 3000 years to the Ebers papyrus, an Egyptian medical document. This document outlines bowel and colon cleansing procedures using various herbal concoctions and water, and has been carbon dated to between 1500 and 1700 B.C.

In the early 1980s, there were a number of cases of amebiasis, leading to six deaths attributed to therapist Marissa Wright, who failed to maintain sanitary conditions. These are believed to be the only fatalities that can directly be attributed to colon hydrotherapy. There have been reports of electrolyte imbalances in children brought on by colonics using softened water. Such imbalances can also be caused by laxative use or diarrhea.

Usage
Current alternative medicine practitioners recommend it for a variety of ills stemming from accumulation of fecal matter in the large intestine, a process referred to as autointoxication (a theory no longer accepted in mainstream medicine)[5][6]. Some alternative medicine practitioners believe that autointoxication results from increased absorption of bacterial / fungal toxins as a result of an increased toxic load in the colon.

Colonic irrigation can be useful in cases of incontinence, where it is tolerable to the patient.

Colonic irrigation should not be used in people with diverticulitis, ulcerative colitis, Crohn's disease, severe or internal hemorrhoids or tumors in the rectum or colon. It also should not be used soon after bowel surgery (unless directed by one's health care provider). Regular treatments should be avoided by people with heart disease or kidney disease (renal insufficiency). Colonics are inappropriate for people with bowel, rectal or anal pathologies where the pathology contributes to the risk of bowel perforation.

Controversy and regulation
While some hydrotherapists believe colonics lead to better overall wellness, others claim it helps ease specific diseases, including chronic fatigue, arthritis, and sinusitis. It is also claimed to improve muscle tone in the colon, leading to stronger peristaltic contractions. There is limited scientific research to support these claims.

The practice is currently only regulated in some states of the United States. Some practitioners go through a voluntary certification process, and may be members of one of the colon hydrotherapy associations worldwide, such as the International Association of Colon HydroTherapy (I-ACT)or The Guild of Colon Hydrotherapists. Prospective patients should ensure that the equipment used is sterile and that the practitioner is experienced.

The American College of Gastroenterology takes the position that in the unusual case of fecal impaction complicating chronic constipation, a 5 to 10 ounce tap water enema may be of benefit, but does not otherwise recommend its use. The orthodox medical establishment perceives colon hydrotherapy to be little more than a bowel rinse, or expensive laxative.

The typical cost for a colonic treatment is about $65 to $100 in the US.

Colonectomy

Adrenal Insufficency

In medicine, adrenal insufficiency (or "hypocortisolism") is the inability of the adrenal gland to produce adequate amounts of cortisol in response to stress.

Causes can include:
Acute adrenal insufficiency
Addison's disease (autoimmune adrenalitis)
Septic shock
Waterhouse-Friderichsen syndrome
Addisonian crisis in case of:
Discontinuing corticosteroid therapy without tapering the dosage
Surgery, illness or any other form of stress in patients with long-term corticosteroid therapy
Chronic adrenal insufficiency
Addison's disease
Congenital Adrenal Hyperplasia
antiphospholipid syndrome
haemochromatosis

Hypoadrenia is a term for a hypothesised condition of the adrenal glands. The terms adrenal exhaustion or adrenal fatigue are often used (and connected to hypoadrenia) by complementary and alternative therapists, but are not formal medical terms.

The adrenal glands are part of the body's mechanism for short term stress response and management, they are involved in the production of the hormone adrenaline (also known as epinephrine), the famous fight or flight chemical released in stressful situations, which increases the body's metabolic rate and muscular contraction strength. Along with the thyroid gland they are also part of the body's metabolic energy regulation and control system, and thus control to an extent the energy available to body systems.

It has been theorized by alternative medical practitioners that under conditions of long term stress, the adrenal glands can become less responsive to circumstance, or maladapted, and cease to function optimally, leading to a wide (but slightly vague) range of fatigue and stress related conditions including a greater likelihood of psychological conditions such as depression and possibly certain other mood disorders. However, it is important to note that this theory has not yet gained acceptance within mainstream medicine.

Biological background
Main article: Stress: neurochemistry and physiology

Biologically, long term stress is a modern phenomenon in the human environment (in evolutionary terms through most of human and mammalian history, stress was a reaction to a point incident, rather than a continuing way of life). As a result, the human body and its internal regulatory mechanisms are poorly adapted to handling many aspects of the types of stress found in civilized cultures. They evolved, so to speak, to react to predator attacks, rather than (for example) constant belittlement, decades long abuse, high risk hobbies, pressure to succeed, or existential and religious inspired worries about ones life and future.

Organs such as the brain, the endocrine system-- including the sympathetic and parasympathetic systems, and the various glands contained therein, which were not evolved for, or designed to handle and respond optimally to, constant stimulation may therefore, under modern social conditions, become constantly or abnormally stimulated. Other organs which form part of the whole, such as the nervous and musculoskeletal system, are also made to work for decades under different (and comparatively abnormal) conditions than existed throughout the rest of human evolution.

It has been hypothesised by alternative medical practitioners, but not clinically proven, that under certain long term stress and physical conditions, that the body's stress management systems cease to regulate stress and stress related body systems and hormones appropriately, and instead become adapted to continual over stimulation in various inappropriate ways which can lead to the symptoms described. This is strictly hypothetical, and by no means universally accepted, particularly in mainstream medicine.

Symptoms
The theorized symptoms for adrenal exhaustion include a depletion of energy reserves and a loss of resilience. They range from fatigue, nervousness, anxiety, exacerbated PMS, depression, brain fog and carbohydrate cravings to allergies, muscular pain, tenderness, joint pain and irritable bowel syndrome.

Clinical views on hypoadrenia
"Adrenal exhaustion" and "adrenal fatigue" are common diagnoses in alternative medicine, but are not recognized in conventional medicine. The mainstream medical view of hypoadrenia is that its alleged symptoms are vague and non-specific, and that day-to-day emotional stress is highly unlikely to lead to an "exhaustion" or imbalance of the adrenal glands.

Psychological conditions and mood disorders referenced above may be linked to hypoadrenia. Symptoms of chronic fatigue and depression could result from diminished adrenal stores, caused by prolonged exposure to a particular stressor (i.e. poverty) or a series of stressful events occurring closely together (i.e. loss of job, divorce, and children ill). The adrenal gland, responsible among other functions for producing cortisol, when in constant use may produce cortisol over a long period of time, resulting in a high amount of cortisol in the bloodstream. Cortisol functions to return the body to a state of rest/repose after a stressor or fight/flight stimulus. An individual with low cortisol levels may demonstrate mood disorders as anxiety, depression or fatigue as a result of the increased cortisol present in the bloodstream. An indication that psychological conditions may be linked to the amount of cortisol is that the hypothalamus, or master gland, is shared by both the nervous system and the endocrine system; endocrine system containing the adrenal gland and hormone cortisol.

Adrenal Insufficency