Tag: Red blood cell

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Ailmemts & Remedies

Polycythemia

Definition:
Polycythemia is the increase of the RBC count, hemoglobin, and total RBC volume, accompanied by an increase in total blood volume. This must be distinguished from relative erythrocytosis secondary to fluid loss or decreased intake; this distinction can be made easily on a clinical basis. Polycythemia accompanies increased total blood volume, whereas relative erythrocytosis does not. Two basic categories of polycythemia are recognized:
...click to see…the picture..
* Primary polycythemias are due to factors intrinsic to red cell precursors and include the diagnoses of primary familial and congenital polycythemia (PFCP) and polycythemia vera (PV).
* Secondary polycythemias are caused by factors extrinsic to red cell precursors.

In normal hematopoiesis, myeloid stem cells give rise to erythrocytes, platelets, granulocytes, eosinophils, basophils, and monocytes. The production of each lineage is a function of cell proliferation, differentiation, and apoptosis. These various stages of differentiation rely on multiple interrelated processes. Protein growth factors, known as cytokines, stimulate proliferation of the multilineage cells (eg, interleukin [IL]-3, granulocyte-macrophage colony-stimulating activity [GM-CSF]). Other factors primarily stimulate the growth of committed progenitors (eg, GM-CSF, macrophage colony-stimulating factor [M-CSF], erythropoietin [Epo]).

Erythropoiesis is a carefully ordered sequence of events. Initially occurring in fetal hepatocytes, the process is taken over by the bone marrow in the child and adult. Although multiple cytokines and growth factors are dedicated to the proliferation of the RBC, the primary regulator is Epo. Red cell development is initially regulated by stem cell factor (SCF), which commits hematopoietic stem cells to develop into erythroid progenitors. Subsequently, Epo continues to stimulate the development and terminal differentiation of these progenitors. In the fetus, Epo is produced by monocytes and macrophages found in the liver. After birth, Epo is produced in the kidneys; however, Epo messenger RNA (mRNA) and Epo protein are also found in the brain and in RBCs, suggesting that some paracrine and autocrine function is present as well.  CLICK & SEE THE PICTURES

Erythropoiesis escalates as increased expression of the EPO gene produces higher levels of circulating Epo. EPO gene expression is known to be affected by multiple factors, including hypoxemia, transition metals (Co2+, Ni2+, Mn2+), and iron chelators. However, the major influence is hypoxia, including factors of decreased oxygen tension, RBC loss, and increased oxygen affinity of hemoglobin. In fact, Epo production has been observed to increase as much as 1000-fold in severe hypoxia.

Absolute polycythemia
The overproduction of red blood cells may be due to a primary process in the bone marrow (a so-called myeloproliferative syndrome), or it may be a reaction to chronically low oxygen levels or, rarely, a malignancy.

Primary polycythemia (Polycythemia vera)
Primary polycythemia, often called polycythemia vera (PCV), polycythemia rubra vera (PRV), or erythremia, occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow.  Often, excess white blood cells and platelets are also produced. Polycythemia vera is classified as a myeloproliferative disease. Symptoms include headaches, vertigo, and an abnormally enlarged spleen and/or liver. In some cases, affected individuals may have associated conditions including high blood pressure or the formation of blood clots. Transformation to acute leukemia is rare. Phlebotomy is the mainstay of treatment. A hallmark of polycythemia is an elevated hematocrit, with Hct > 55% seen in 83% of cases. Mutations in JAK2 are found in 95% of cases, though also present in other myeloproliferative disorders.

Secondary polycythemia
Secondary polycythemia is caused by either natural or artificial increases in the production of erythropoietin, hence an increased production of erythrocytes. In secondary polycythemia, there may be 6 to 8 million and occasionally 9 million erythrocytes per cubic millimeter (microliter) of blood. Secondary polycythemia resolves when the underlying cause is treated.

Secondary polycythemia in which the production of erythropoietin increases appropriately is called physiologic polycythemia. This physiologic (meaning normal) polycythemia is a normal adaptation to living at high altitudes (see altitude sickness). Many athletes train at high altitude to take advantage of this effect — a legal form of blood doping. Similarly, athletes with primary polycythemia may have a competitive advantage due to greater stamina.

Other causes of secondary polycythemia include smoking, renal or liver tumors, hemangioblastomas in the central nervous system, heart or lung diseases that result in hypoxia, and endocrine abnormalities including pheochromocytoma and adrenal adenoma with Cushing’s syndrome. People whose testosterone levels are high because of the use anabolic steroids, including athletes who abuse steroids and people whose doctors put them on doses that are too high, as well as people who take erythropoietin may develop secondary polycythemia.

Secondary polycythemia can be induced directly by phlebotomy to withdraw some blood, concentrate the erythrocytes, and return them to the body.

Chuvash polycythemia
Chuvash polycythemia refers to a familial form of erythrocytosis different from classical polycythemia vera. This involved patients from Chuvashia and is associated with a C598T mutation in the von Hippel-Lindau gene (VHL).[6] A cluster of patients with Chuvash polycythemia have been found in other populations, such as on the Italian island of Ischia, located in the Bay of Naples.

Relative polycythemia
Relative polycythemia is an apparent rise of the erythrocyte level in the blood; however, the underlying cause is reduced blood plasma. Relative polycythemia is often caused by loss of body fluids, such as through burns, dehydration and stress.

Polycythemia vera
Earlier diagnostic criteria for polycythemia vera included the following (based on the Polycythemia Vera Study Group Diagnostic Criteria):1

* Red cell mass greater than 36 mL/kg for men and greater than 32 mL/kg for women
* Arterial oxygen saturation greater than 92%
* Splenomegaly or 2 of the following:
o Thrombocytosis greater than 400 X 109/L
o Leukocytosis greater than 12 X 109/L
o Leukocyte alkaline phosphatase activity greater than 100 U/L in adults (reference range, 30-120 U/L) without fever or infection
o Serum vitamin B-12 greater than 900 pg/mL (reference range, 130-785 pg/mL)
o Unsaturated vitamin B-12 binding capacity greater than 2200 pg/mL

The reference range for the clinician’s laboratory should be cross-correlated. The diagnostic criteria have undergone scrutiny and several revisions in recent years. In 2001, the World Health Organization (WHO) proposed a classification system for chronic myeloid neoplasms.2 The diagnosis of polycythemia vera fell under the broader category of chronic myeloproliferative diseases. This set of criteria quickly lost favor because of lack of validation3 and the discovery of JAK2 mutations in adult patients.4,5,6,7,8,9

Currently, the diagnosis of polycythemia vera is based on the 2008 WHO criteria, which has integrated molecular diagnostics into the evaluation and screening for polycythemia vera.10 A diagnosis of polycythemia vera is made when both major and one minor criterion are present or when the first major criterion is present with any two minor criteria.

The current criteria include the following:

* Major criteria
1. Hemoglobin level of more than 18.5 g/dL in men (>16.5 g/dL in women) or other evidence of increased red cell volume

or

Hemoglobin or hematocrit level higher than 99th percentile of method-specific reference range for age, sex, altitude, of residence

or

Hemoglobin level of more than 17 g/dL in men (>15 g/dL in women) if associated with a documented and sustained increase of at least 2 g/dL from an individual’s baseline value that can not be attributed to correction of iron deficiency

or

Elevated red cell mass greater than 25% above mean normal predicted value
2. Presence of JAK2V617F or similar mutation (eg, JAK2 exon 12 mutation)
* Minor criteria
1. Bone marrow trilineage myeloproliferation
2. Subnormal serum erythropoietin levels
3. Endogenous erythroid colony growth

Pathophysiology

Primary polycythemia

The disease is considered to be a form of the myeloproliferative syndromes that include polycythemia vera, essential thrombocythemia, agnogenic myeloid metaplasia, and myelofibrosis. The clonality of polycythemia vera is well established and was first demonstrated by Adamson et al in 1976.11 Subsequent studies suggest hypersensitivity of the myeloid progenitor cells to growth factors, including Epo, IL-3, SCF, GM-CSF, and insulinlike growth factor (IGF)–1, whereas other studies show defects in programmed cell death.

Until recently, the pathophysiology of polycythemia vera was unclear. In 2005, significant progress in the understanding of polycythemia vera was made with the discovery of an activating mutation in the tyrosine kinase JAK2 (JAK2V617F ), which now appears to cause most primary cases in adults.4,5,6,7,8 Several other mutations of JAK2 have since been described (eg, exon 12, JAK2H538-K539delinsI ).9,12 The JAK2 mutations are thought to possibly cause hypersensitivity to Epo via the Epo receptor, although the effects of this mutation remain to be fully characterized.

Familial clustering suggests a genetic predisposition. Whether these mutations are responsible for the development of polycythemia vera in pediatric patients is unclear. Some groups have reported lower rates of JAK2 mutations in children compared with adults,13,14,15 whereas other groups have seen similar rates with complete or near complete presence of JAK2V617F and other JAK2 mutations.12

PFCP is caused by a hypersensitivity of erythroid precursors to Epo. Several mutations (approximately 14) have been identified in the Epo receptor (EPOR) gene; however, EPOR mutations have not been identified in all PFCP kindreds. Most identified EPOR mutations (11) cause truncation of the c-terminal cytoplasmic receptor domain of the receptor. These truncated receptors have heightened sensitivity to circulating Epo due to a lack of negative feedback regulation.16

Secondary polycythemia

Secondary polycythemia may result from functional hypoxia induced by lung disease, heart disease, increased altitude (hemoglobin increase of 4% for each 1000-m increase in altitude), congenital methemoglobinemia, and other high–oxygen affinity hemoglobinopathies stimulating increased Epo production. Secondary polycythemia may also result from increased Epo production secondary to benign and malignant Epo-secreting lesions. Secondary polycythemia may also be a benign familial polycythemia.

Chuvash polycythemia, a congenital polycythemia first recognized in an endemic Russian population, has mutations in the von Hippel-Lindau (VHL) gene, which is associated with a perturbed oxygen dependent regulation of Epo synthesis.

Secondary polycythemia of the newborn is fairly common and is a result of either chronic or acute fetal hypoxia or delayed cord clamping and stripping of the umbilical cord.17
Frequency
United States

Primary polycythemia is rare; the overall prevalence of polycythemia vera is 2 cases per 100,000 people. The median age is 60 years. Only 0.1% of cases of polycythemia vera are observed in individuals younger than 20 years. Fewer than 50 cases of pediatric polycythemia vera have been reported in the literature. Secondary polycythemia is seen in 1-5% of all newborns in the United States.
International

Polycythemia vera has a similar incidence in Western Europe as in the United States, and occurrence rates are very low in Africa and Asia (as low as 2 cases per million per year in Japan).

Mortality/Morbidity
Death rates for children are unavailable. The complications found in polycythemia vera are related to 2 primary factors. The first includes complications related to hyperviscosity. The second involves bone marrow–related complications. Untreated, the median survival time for these patients is 18 months. However, if patients are treated, survival is greatly extended, as many as 10-15 years with phlebotomy alone. The causes of death in adults are as follows:

* Thrombosis/thromboembolism (30-40%)
* Acute myelogenous leukemia (19%)
* Other malignancies (15%)
* Hemorrhage (2-10%)
* Myelofibrosis/myeloid metaplasia (4%)
* Other (25%)

In the neonatal period, polycythemia-induced hyperviscosity can lead to altered blood flow and subsequently affect organ function. Infants with polycythemia are at increased risk for necrotizing enterocolitis, renal dysfunction, hypoglycemia, and increased pulmonary vascular resistance with resultant hypoxia and cyanosis. Although initially thought to cause neurologic dysfunction, the decrease in cerebral blood flow seen in newborns with polycythemia is a physiologic response and does not appear to cause cerebral ischemia.17
Race

In the United States, higher rates of polycythemia vera are observed in the Ashkenazi Jewish population, and lower rates are seen in blacks.
Sex

The male-to-female ratio is 1.2-2.2:1 in adults and 1:1 in children.
Age

The median age for polycythemia vera is 60 years. Only 0.1% of polycythemia cases occur in people younger than 20 years.
Clinical
History

The clinical features associated with polycythemia are a direct result of the increase in red cell mass, which causes an expansion of blood volume. Signs of hyperviscosity and increased metabolism accompany polycythemia. A thorough history must be obtained for a history of cardiac, pulmonary (including sleep apnea), hepatic or renal disease in the patient and a complete family history for evidence of familial polycythemia.

Symptoms include the following:

* Headache
* Weight loss
* Weakness or malaise
* Dizziness
* Pruritus
* Bruising
* Ruddy or red appearance of the skin
* Diaphoresis/dyspnea
* Visual disturbance
* Paresthesias
* Arthropathies
* GI – Fullness, thirst, abdominal discomfort, constipation

Physical

A thorough physical must be completed and include specific evaluation for signs and symptoms of underlying disease that may cause secondary polycythemia; it must include pulse oximetry, careful cardiac and pulmonary evaluation, and evaluation for signs of renal or hepatic disease.

Signs of polycythemia include the following:

* Rubor, especially facial rubor
* Skin plethora
* Hypertension, both systolic and diastolic
* Hepatomegaly
* Splenomegaly
* Conjunctival plethora (engorged vessels in the bulbar conjunctiva)
* Ecchymosis
* Cardiac hypertrophy (rarely observed)

Causes

* Primary polycythemia
o In the past, the pathophysiology was unclear, and primary polycythemias were thought to be due to both inherited and acquired mutations in erythroid progenitors, leading to abnormal red cell proliferation. However, in 2005, an activating mutation found in the tyrosine kinase JAK2 was implicated as the causative factor in polycythemia vera (PV). Five separate groups identified this mutation in approximately 80% (56-97% reported) of patients with polycythemia vera.
o This acquired V617F mutation in JAK2 leads to constitutively activated JAK2. Activated JAK2 induces erythropoietin (Epo) hypersensitivity; although not yet completely delineated, it is thought to act through an activating EPOR.
o Additional JAK2 mutations have been identified in exon 12,9 JAK2H538-K539delinsI ,18 and others.19
o Primary familial and congenital polycythemia (PFCP), which is commonly found to have mutations in the Epo receptor (EPOR) gene. Approximately 14 mutations have been identified.
* Secondary polycythemia
o Congenital causes include high affinity hemoglobin and 2,3-Bisphosphoglycerate (2,3-BPG) deficiency.
o Chuvash polycythemia, a congenital polycythemia first recognized in an endemic Russian population, has mutations in the von Hippel-Lindau (VHL) gene, which is associated with a perturbed oxygen-dependent regulation of Epo synthesis.
o Acquired causes included hypoxemia and Epo-secreting tumors.
o Polycythemia of the newborn usually results from a poor intrauterine environment or hypoxic insult during labor or delivery.

Treatment
Medical Care

* Primary polycythemia: The goals of therapy are to maximize survival while minimizing the complications of therapy as well as of the disease itself.
o Phlebotomy and myelosuppressive chemotherapy are the cornerstones of therapy and have produced a median survival time of 9-14 years after the beginning of treatment. The goal of phlebotomy is to maintain normal red cell mass and blood volume, with a target hematocrit of 45%. The mean survival time of adult patients treated solely with phlebotomy is 13.9 years; however, a high risk of thromboembolic complications is observed.
o In the past, patients have been treated with chlorambucil and other alkylating agents such as pipobroman and busulfan. However, these patients exhibited the highest rates of secondary malignancy including acute leukemia, lymphocytic lymphomas, and skin and GI carcinomas. The rates of malignancy appear lower with busulfan than with the other alkylating agents. Currently, these agents are rarely used.
o Patients treated with phosphorus-32 (32 P) tolerate treatment well and have prolonged periods of remission. However, these patients also exhibit increased rates of acute leukemias (10-15%). The mean survival time with32 P treatment is 10.9 years.
o Studies suggest that the use of interferon alfa decreases the need for phlebotomy and decreases the risk of thrombotic events. Its use is limited by side effects, cost, and route of administration.
o Recent studies using hydroxyurea as a myelosuppressive agent also show promise, reducing the need for phlebotomy. However, similarly to those treated with chlorambucil, these patients also experience higher rates of malignancy. Early clinical studies using imatinib are currently underway and are thus far inconclusive.
o Current recommendations for treatment of young patients rely primarily on phlebotomy because the thrombosis is far less likely to occur in children and the long-term risks of leukemia over a longer life span are increased.
o In the past, the use of anticoagulants, including antiplatelet drugs such as aspirin and dipyridamole (Persantine) had demonstrated increased risk of bleeding without an associated decrease in thrombotic events; therefore, anticoagulants have not previously been recommended. However, a large European study, results of which were published in the New England Journal of Medicine by Landolfi et al (2004),20 showed a decrease in thrombotic events in those patients receiving low-dose aspirin therapy and recommended aspirin therapy for those patients for whom no contraindications existed. This issue continues to remain under debate in the field of polycythemia treatment.
* Secondary polycythemia: Phlebotomy is used for symptomatic hyperviscosity. The goal is to treat the underlying cause of polycythemia.

Surgical Care
Surgery is not typically indicated. Occasionally, splenectomy is performed late in the course of the disease if massive splenomegaly causes adverse effects such as early satiety, anemia, or thrombocytopenia from sequestration.

Please note that these patients have a high risk of complications during surgical procedures.
Consultations

Consult a neurologist and neurosurgeon if evidence of a stroke is present.
Diet

Diet is unrestricted.
Activity

Contact sports and other activities should be limited for individuals in hypercoagulable and hypocoagulable states.
Medication

Current recommendations for treatment of young patients rely primarily on phlebotomy.
Antineoplastic agents

The following medications are not approved for pediatric polycythemia but are extrapolated from other pediatric treatment regimens, including leukemia and myelodysplastic syndrome.

Interferon alfa 2a and 2b (Roferon-A [alfa-2a], Intron A [alfa-2b])

A recombinant purified protein used IV for CML, hairy cell leukemia, and Kaposi sarcoma. Inhibits cellular growth and alters cell differentiation.

Dosing
Adult
CML: 9 million U/d IM/SC; initiate with 3 million U/d, increase by 3 million U every third day; not to exceed 9 million U/d
Pediatric: 2.5-5 million U/d IM/SC

Interactions:Theophylline may increase toxicity; cimetidine may increase antitumor effects; zidovudine and vinblastine may increase toxicity.

Contraindictions : Documented hypersensitivity.

Precautions:
Pregnancy
C – Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus.

Precautions
Caution in brain metastases, severe hepatic or renal insufficiencies, seizure disorders, multiple sclerosis, or compromised CNS; use has been associated with depression, suicidal ideation and suicide attempts, and GI hemorrhage

Chlorambucil (Leukeran)
Antineoplastic alkylating agent of nitrogen mustard type used for CLL, giant follicular lymphoma, Hodgkin lymphoma, and lymphosarcoma.

Dosing:
Adult
0.1-0.2 mg/kg/d PO; adjust dose according to blood count

Pediatric
Not established; limited data available

Intractions:Live virus vaccines (eg, MMR) may result in severe or fatal infection when used in immunosuppressed patients

Contraindictions :Documented hypersensitivity; previous resistance to medication

Precautions:
Pregnancy
D – Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions
Caution in history of seizure disorders or current bone marrow suppression

Busulfan (Myleran)
Potent cytotoxic drug that, at recommended dosage, causes profound myelosuppression. As alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Dosing:
Adult
4-8 mg/d PO; may administer up to 12 mg/d; maintenance dosing range is 1-4 mg/d to 2 mg/wk; discontinue regimen when WBC reaches 10,000-20,000 cells/mL; resume therapy when WBC reaches 50,000/mL

Pediatric
0.06-0.12 mg/kg/d or 1.8-4.6 mg/m2/d PO; titrate dose to maintain WBC >40,000/mL; reduce dose by 50% if WBC is 30,000-40,000/mL; discontinue if WBC <20,000/mL

Pipobroman (Vercyte, Vercite)
The mechanism of action is not fully understood; however, the drug is considered to be an alkylating agent. Pipobroman has been used with some success for treatment of polycythemia vera and chronic granulocytic leukemia. The product was discontinued by the manufacturer in the United States in 1996 but is available in Europe.

Dosing
Adult
1 mg/kg/d PO initially for at least 30 d; if refractory, may increase to 1.5-3 mg/kg/d
Maintenance: 0.1-0.2 mg/kg/d PO; typically initiated when hematocrit has decrease by 50-55%
Pediatric

<15 years: Not established
>15 years: Administer as in adults

Follow-up
Inpatient & Outpatient Medications

* Allopurinol for hyperuricemia or gout
* Iron supplementation to manage the increased red cell production that may produce a functional iron deficiency that can cause red cell rigidity and increase the risk of stroke
* Folate
* Cimetidine for pruritus and upper GI distress

Complications

* Vascular occlusive events – Splenic infarcts, thrombosis (cerebral, portal vein, pulmonary embolus)
* Hemorrhage
* Marrow fibrosis resulting in pancytopenia
* Malignancy – Acute myelogenous leukemia (AML), chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), lymphoma
* Hyperuricemia – Renal stones, nephropathy, gout
* Budd-Chiari syndrome

Prognosis

* The median survival time for patients with polycythemia vera (PV) is 18 months for untreated patients and 9-14 years for treated patients.

Patient Education

* Inform patients that they are prone to surgical complications and are at high risk in trauma situations secondary to coagulopathies.

Miscellaneous
Medicolegal Pitfalls<%2

Categories
Healthy Tips

Olive Oil Protects Against Heart Attack

Portuguese researchers have identified a vital component of olive oil that gives greatest protection from heart attack and stroke.
……..CLICK & SEE THE PICTURES
No wonder why heart attack rates are relatively lower and human lifetime is over world averages in the Mediterranean islands.

Olive oil, which is an essential part of Mediterranean cuisine, is full of monounsaturated fats.  It lowers bad LDL cholesterol and reduces your risk of developing heart disease.
Lead researcher Fatima Paiva-Martins from University of Porto has discovered an antioxidant called DHPEA-EDA that protects red blood cells from damage more than any other part of olive oil.

“These findings provide the scientific basis for the clear health benefits that have been seen in people who have olive oil in their diet,” said Paiva-Martins.

During the study, research team led by Paiva-Martins compared the effects of four related polyphenolic compounds on red blood cells subjected to oxidative stress by a known free radical generating chemical.

Heart disease is caused partly by reactive oxygen, including free radicals, acting on LDL or “bad” cholesterol and resulting in hardening of the arteries. Red blood cells are particularly susceptible to oxidative damage because they are the body’s oxygen carriers.

They found that DHPEA-EDA was the most effective and protected red blood cells even at low concentrations.

The new discovery, Paiva-Martins believes, can lead to the production of “functional” olive oils specifically designed to reduce the risk of heart disease.


Sources: http://www.anyhealthydiet.com/diet-and-nutrition/eat-healthy-food-protect-your-heart/

and The study  published in Molecular Nutrition & Food Research.

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Ailmemts & Remedies

Amebic Liver Abscess

Alternative Names:Hepatic amebiasis; Extraintestinal amebiasis; Abscess – amebic liver
Definition :
Amebic liver abscess is a collection of pus in the liver caused by an intestinal parasite.Organisms that carry disease can travel through the blood stream into the liver and form an abscess, a collection of infected tissue and pus.

YOU MAY CLICK TO SEE THE PICTURES
….
Amebic liver abscess is an extraintestinal manifestation caused by a protozoa Entamoeba histolytica. The disease spreads through the ingestion of cysts in fecally-contaminated food or water. The infection is worldwide, most common in tropical areas usually in developing countries where poor sanitation exist.

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This is an Abscess (walled area of infection/pus) in the liver that is caused by the organism Entamoeba histolytica.  It is common in tropical and subtropical areas (southeast Asia, Africa, India, Latin America).  In the U.S., it is most common in young Hispanic adults.  It is also seen in those with recent travels to tropical areas, homosexuals, and among the inhabitants of institutions for the mentally ill.

Causes :-
Travel to endemic areas (as above), where the cysts of the parasite may be ingested by consuming water or food contaminated by fecal matter.
Amebic liver abscess is caused by Entamoeba histolytica, the same organism that causes amebiasis, an intestinal infection. The organism is carried by the blood from the intestines to the liver.

The disease spreads through ingestion of cysts in fecally-contaminated food or water, use of human waste as fertilizer, and person-to-person contact.

The infection occurs worldwide, but is most common in tropical areas where crowded living conditions and poor sanitation exist. Africa, Latin America, Southeast Asia, and India have significant health problems associated with this disease.

Risk Factors :-
*Malnutrition
*Old age
*Pregnancy
*Steroid use
*Cancer
*Immunosuppression
*Alcoholism
*Recent travel to a tropical region
*Homosexuality, particularly in males

Symptoms :-
There may or may not be symptoms of intestinal infection. Symptoms may include:
*Right upper abdominal pain
*Right sided chest pain worse on a deep breath
*Intense, continuous, or stabbing pain
*Chills
*Diarrhea precedes infection in 20% of patients
*Fever
*General discomfort, uneasiness, or ill feeling (malaise)
*Jaundice
*Joint pain
*Loss of appetite
*Sweating
*Weight loss
*malaise

Nature of the disease:-
Most infected people, perhaps 90%, are asymptomatic, but this disease has the potential to make the sufferer dangerously ill. It is estimated by the World Health Organization that about 70,000 people die annually worldwide.

Infections can sometimes last for years. Symptoms take from a few days to a few weeks to develop and manifest themselves, but usually it is about two to four weeks. Symptoms can range from mild diarrhoea to dysentery with blood and mucus. The blood comes from amoebae invading the lining of the intestine. In about 10% of invasive cases the amoebae enter the bloodstream and may travel to other organs in the body. Most commonly this means the liver, as this is where blood from the intestine reaches first, but they can end up almost anywhere.

Onset time is highly variable and the average asymptomatic infection persists for over a year. It is theorised that the absence of symptoms or their intensity may vary with such factors as strain of amoeba, immune response of the host, and perhaps associated bacteria and viruses.

In asymptomatic infections the amoeba lives by eating and digesting bacteria and food particles in the gut, a part of the gastrointestinal tract. It does not usually come in contact with the intestine itself due to the protective layer of mucus that lines the gut. Disease occurs when amoeba comes in contact with the cells lining the intestine. It then secretes the same substances it uses to digest bacteria, which include enzymes that destroy cell membranes and proteins. This process can lead to penetration and digestion of human tissues, resulting first in flask-shaped ulcers in the intestine. Entamoeba histolytica ingests the destroyed cells by phagocytosis and is often seen with red blood cells inside when viewed in stool samples. Especially in Latin America,  a granulomatous mass (known as an amoeboma) may form in the wall of the ascending colon or rectum due to long-lasting immunological cellular response, and is sometimes confused with cancer.

Theoretically, the ingestion of one viable cyst can cause an infection.

Diagnosis:
Exams and Tests
Tests that may be done include:
*Abdominal ultrasound
*Abdominal CT scan or MRI
*Complete blood count
*Liver biopsy – rarely done due to high risk of complications
*Liver scan
*Liver function tests
*Serology for amebiasis

Treatment
A medicine called metronidazole (Flagyl) is the usual treatment for liver abscess. Medications such as paromomycin must also be taken to remove intestinal amebiasis to prevent recurrence of the disease.

In rare cases, the abscess may need to be drained to help relieve some of the abdominal pain.

Prognosis:
Without treatment, the abscess may rupture and spread into other organs, leading to death. Persons who receive treatment have a very high chance of a complete cure or having only minor complications.
Possible Complications :In the majority of cases, amoebas remain in the gastrointestinal tract of the hosts. Severe ulceration of the gastrointestinal mucosal surfaces occurs in less than 16% of cases. In fewer cases, the parasite invades the soft tissues, most commonly the liver. Only rarely are masses formed (amoebomas) that lead to intestinal obstruction.

The abscess may rupture into the abdominal cavity, the lining of the lungs, the lungs, or the sac around the heart. The infection can also spread to the brain.

When to Contact a Medical Professional
Call your health care provider if symptoms develop after travel to an area where the disease is known to occur.

Prevention:
To help prevent the spread of amoebiasis around the home :
*Wash hands thoroughly with soap and hot running water for at least 10 seconds after using the toilet or changing a baby’s diaper, and before handling food.
*Clean bathrooms and toilets often; pay particular attention to toilet seats and taps.
*Avoid sharing towels or face washers.

To help prevent infection:
*Avoid raw vegetables when in endemic areas, as they may have been fertilized using human feces.
*Boil water or treat with iodine tablets.
*When traveling in tropical countries where poor sanitation exists, drink purified water and do not eat uncooked vegetables or unpeeled fruit.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://www.nlm.nih.gov/medlineplus/ency/article/000211.htm
http://www.ecureme.com/emyhealth/data/Amebic_Liver_Abscess.asp
http://organizedwisdom.com/Amebic_Liver_Abscess
http://organizedwisdom.com/helpbar/index.html?return=http://organizedwisdom.com/Amebic_Liver_Abscess&url=en.wikipedia.org/wiki/Amoebiasis#Diagnosis_of_human_illness

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Diagnonistic Test

Bone Marrow Biopsy

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Introduction: Bone marrow is the spongy material found in the center of most large bones in the body. The different cells that make up blood are made in the bone marrow. Bone marrow produces red blood cells, white blood cells, and platelets. Along with a biopsy (the sampling of mostly solid tissue or bone), an aspiration (the sampling of mostly liquid) is often done at the same time.

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Doctors can diagnose many problems that cause anemia, some infections, and some kinds of leukemia or lymphoma cancers by examining a sample of your bone marrow (the tissue where blood cells are made). A bone marrow biopsy is the procedure to collect such a sample. It is done using a large needle inserted through the outside surface of a bone and into the middle of the bone, where the marrow is.

Why the procedure is performed: A bone marrow aspiration and biopsy procedure is done for many reasons.

*The test allows the doctor to evaluate your bone marrow function. It may aid in the diagnosis of low numbers of red blood cells (anemia), low numbers of white blood cells (leukopenia), or low numbers of platelets (thrombocytopenia), or a high number of these types of blood cells.

*The doctor can also determine the cause of some infections, diagnose tumors, determine how far a disease, such as lymphoma, has progressed, and evaluate the effectiveness of chemotherapy or other bone marrow active drugs.

*Where the procedure is performed: Bone marrow aspirations and biopsies can be performed in doctor’s offices, outpatient clinics, and hospitals. The procedure itself takes 10-20 minutes.

Preperation for the test:
You will need to sign a consent form giving your doctor permission to perform this test. Because you will probably receive some pain medicines or anti-anxiety medications that can make you drowsy, you will need to arrange a ride home.

Tell your doctor if you have ever had an allergic reaction to lidocaine or the numbing medicine used at the dentist’s office. Also talk with your doctor before the test if you are taking insulin, or if you take aspirin, nonsteroidal anti-inflammatory drugs, or other medicines that affect blood clotting. It may be necessary to stop or adjust the dose of these medicines before your test. Most people need to have a blood test done some time before the procedure to make sure they are not at high risk for bleeding complications.

*You may receive instructions about not eating food or drinking liquids before the procedure.

*Be sure to tell your doctor about any prescription medications, over-the-counter medications, as well as herbal supplements you are taking.

*Notify your doctor about all allergies, previous reactions to medications, if you have had any bleeding problems in the past, or if you are pregnant.

*Before the procedure, you will be asked to change into a patient gown.

*Your vital signs-blood pressure, heart rate, respiratory rate, and temperature-will be measured.

*Depending on your doctor, you may have an IV placed or your blood drawn.

*You may be given some medicine to help you relax.

*You may be asked to position yourself on your stomach or your side depending on the site the doctor chooses to use.

Risk Factors:
You will be asked to sign a consent form before the procedure. You will be notified of the alternatives as well as the potential risks and complications of this procedure.

Risks are minimal.

Possible risks include these:

*Persistent bleeding and infection

*Pain after the procedure

*A reaction to the local anesthetic or sedative

Having a sample taken is not harmful for your bone or bone marrow. Injury of nearby tissue from the biopsy is very uncommon. You might have some buttock soreness for a few days, and you may have some bruising at the biopsy site. A few individuals have an allergy or a side effect from the pain medicine or anti-anxiety medicine.

What happens when the test is performed?
Most patients have this test done by a hematologist in a clinic procedure area. You wear a hospital gown during the procedure. A sedative may be injected at this time. (If you are prescribed a sedative in pill form, you will be instructed to take it ahead of time.)

*Most patients have bone marrow sampled from the pelvis. You lie on your stomach and the doctor feels the bones at the top of your buttock. An area on your buttock is cleaned with soap. A local anesthetic is injected to numb the skin and the tissue underneath the skin in the sampling area. This causes some very brief stinging.

*The doctor will choose a place to withdraw bone marrow. Often this is the hip (pelvic bone), but it also can be done from the breastbone (sternum), lower leg bone (tibia), or backbone (vertebra).

*The chosen site will be cleaned with a special soap (iodine solution) or alcohol. After the skin is clean, sterile towels will be placed around the area. It is important that you do not touch this area once it has become sterile.

*Local anesthetic, usually lidocaine, will be injected with a tiny needle at the site. Initially, there may be a little sting followed by a burning sensation. After a few minutes, the site will become numb. A needle is then placed through the skin and into the bone. You may feel a pressure sensation.

*For the bone marrow aspiration, a small amount of bone marrow is then pulled into a syringe.

*A bone marrow biopsy is then usually performed. A somewhat larger needle is then put in the same place and a small sample of bone and marrow is taken up into the needle.

*After taking the liquid sample, the doctor carefully moves the needle a little bit further into the bone marrow to collect a second sample of marrow called a core biopsy. This core biopsy is a small solid piece of bone marrow, with not just the liquid and cells but also the fat and bone fibers that hold them together. After the needle is pulled out, this solid sample can be pushed out of the needle with a wire so that it can be examined under a microscope. Pressure is applied to your buttock at the biopsy location for a few minutes, until you are not at risk of bleeding. A bandage is placed on your buttock.
Must you do anything special after the test is over?
You will feel sleepy from the medicines used to reduce pain and anxiety.
After the local anesthetic wears off over the next few hours, you may have some discomfort at the biopsy site. Your doctor will advise you about pain medication.Once these medicines have worn off (a few hours after the test), you can return to normal activities, but you should not drive or drink alcohol for the rest of the day.

You should keep the bandage on for 48 hours, and then it should be removed.

After the test:
The samples taken from your bone marrow will be sent to a laboratory and the pathologist for analysis. Several tests are done including looking at the bone marrow under a microscope. The results of these tests will usually be available in a few days. Your doctor will give you instructions for follow-up.

When to Seek Medical Care:
Call your doctor if you notice signs of spreading redness, continued bleeding, fever, worsening pain, or if you have other concerns after this procedure.

Go to a hospital’s emergency department if these conditions develop:

*If your bleeding will not stop with direct pressure
*If you see thick discharge from the wound
*If you have a persistent fever
*If you feel lightheaded

How long is it before the result of the test is known?
Some parts of your bone marrow biopsy report may be available within a day, but some tests require special stains or tests that can take longer, in some cases up to one week.

Resources:
https://www.health.harvard.edu/fhg/diagnostics/bone-marrow-biopsy.shtml
http://www.emedicinehealth.com/bone_marrow_biopsy/article_em.htm

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Ailmemts & Remedies

Jaundice-A Royal Disease

Jaundice, icterus, hepatitis.” These three terms are interchanged by people to describe what they believe is a single common affliction, a disease that causes the skin and eyes to turn yellow. The word “jaundice” is actually a corrupted anglicised version of the French jaune coined in the 19th century by French physicians to describe what they thought was a single disease entity. Unaware of cause or cure, the discolouration was also called the morbus regius (the regal disease), with the belief that only the touch of a king could cure it.

Times have now changed and medicine has become evidence based. Tests can be done if a person becomes “jaundiced” to evaluate the “when, where and why”. Once the cause is removed, the disease will disappear.

The yellow colour is due to a pigment called bilirubin, normally produced in the spleen and liver when old red blood cells are broken down. The pigment is then metabolised in the liver and excreted. The level of bilirubin is usually 0.3 to 1.9mg/dl (milligrams per decilitre). The human eye can discern the yellow colour imparted by bilirubin when the level is three times or more than the normal 3mg/dl in the blood.

Infectious diseases can interfere with the ability of the liver cells to metabolise bilirubin. The most common infections are viral, commonly caused by the hepatitis group of viruses. There are several of these — some are transmitted through contaminated food or water, others through unprotected sex or unsterile injections.

Jaundice owing to viral hepatitis A is the commonest form of jaundice in young people. It is usually a mild self-limited disease that recovers spontaneously in one or two months. No specific treatment is required. Hepatitis B, C or E can be more severe, relapsing, fatal or chronic.

Out of this group, hepatitis A and B are preventable. Vaccination against hepatitis B is offered in a 3-dose schedule before the age of one year (it can be given later to anyone who missed it). Hepatitis A vaccine is given after the age of two years as a 2-dose schedule. Protection is almost 100 per cent.

Other infections caused by the herpes group of viruses, leptospirosis, cytomegalovirus, malaria or even severe bacterial sepsis can also cause jaundice. These diseases are not preventable by immunisation.

Jaundice is not always due to an infection. If for any reason the number of red blood cells destroyed is greater than normal, the liver is unable to cope with the overload of pigment and the person becomes jaundiced. This occurs in some hereditary blood disorders like thalassaemia, and sickle cell disease, or a hereditary metabolic defect like G6PD deficiency.

Sometimes, the liver cells themselves are defective and unable to cope with even the normal amount of bilirubin produced in the body. This occurs in certain inherited conditions like the Dubin-Johnson or the Gilbert syndrome. Several members of a family are affected, the jaundice is mild and fluctuating and it is not fatal.

Medications can be toxic to the liver and cause jaundice. Common examples are an overdose of paracetamol or even oestrogens. Alcohol is a direct toxin, poisonous to the liver cells. Consumption on a regular basis over many years can damage the liver and can result in jaundice.

Even when the bilirubin is adequately metabolised and produced in normal quantities, jaundice can occur, if the drainage ducts are blocked by stones, strictures and primary or secondary cancer deposits.

Sixty per cent of newborns can develop a “physiological” or normal self-limited jaundice. There is a rapid cell turnover in newborns and they produce bilirubin at a rate of 6 to 8 mg per kg per day, (more than twice the production rate in adults). The immature liver cells are initially unable to cope but the bilirubin production and level typically decline to the adult level within 10 to 14 days. Sometimes the jaundice is due to a mother-baby blood group incompatibility. The mother forms antibodies to the infant’s blood. This too is self limited and treatable.

The sudden appearance of jaundice in any age group should not be self diagnosed, ignored, treated with diet restrictions or herbs without a diagnosis. After consultations with a physician, appropriate blood and urine tests and, if necessary, scans or a laproscopy should be done to arrive at a diagnosis.

Eighty per cent of the jaundice in young adults is due to hepatitis A. As this disease is self-limited, quackery and miracle cures (like the touch of the king, amulets and bracelets) abound and appear successful.

Secondary jaundice recovers once the causative factor is removed. Abstaining from alcohol and discontinuing offending drugs may reverse jaundice. If a correctable obstruction is seen on scanning or a laparoscopy, surgical treatment provides relief.

The tragedy of jaundice is that ignorance and superstition stand in the way. Some treatable and curable forms of jaundice are not diagnosed or tackled till it is too late.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Sources: The Telegraph (Kolkata, India)

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