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Survey on Non-Infectious and Blood-Borne Diseases

Multiple myeloma

Multiple myeloma, a cancer of the plasma cell, is a progressive hematological disease that is a treatable but incurable B-cell malignancy (Multiple myeloma, Multiple About 20000 new cases are diagnosed in the US every year. The plasma cell, which forms a significant part of the body’s defense mechanism by the production of immunoglobulins, is found in excessive numbers. The characteristic features are the large numbers of abnormal forms of the plasma cell in the bone marrow, excessive production of intact clonal immunoglobulin or Bence-Jones protein. Multiple myeloma ranks second in the most prevalent of blood cancers and is found as 1% of cancers in the US. No cause has been identified. Possible associations have been noted in the decline of the immune system for whatever cause, genetic, some occupations (like agriculture, petroleum, leather industries, cosmetology), exposure to some chemicals containing Agent Orange and exposure to irradiation (Multiple Myeloma, Multiple About 96% are diagnosed in people over 45 years of age. Other features include chromosomal changes in the Ig heavy chain genes. Laboratory tests show the presence of M-protein in the blood. 15-20% of patients show the Bence –Jones proteins which are the incomplete immunoglobulins containing only the light chain portion. Diagnosis is made by a combination of findings even though the essential finding is the M-protein which is found more in the urine. Kidney damage is caused due to the presence of these M proteins which block the renal tubules. A routine urine test may not detect the Bence –Jones protein: immunoelectrophoresis is required. Treatment need not be given in the inactive asymptomatic period. The active phase requires some initial therapy, biophsphonates and supportive care (Multiple myeloma, Multiple A lady with chemo-resistant multiple myeloma was given immunotherapy with the Wilm’s tumour gene W1 peptide-based vaccination; weekly intradermal injections for 12 weeks (Tsuboi et al p. 414). The response was surprising but minimal: a reduction of myeloma cells was brought down from 85% to 26%, reduction of M-protein in the urine from 0.6gms/day and bone scintigram showed an obvious change. The durable efficacy of a prolonged relapse is not possible with the present management of multiple myeloma. The management would hopefully change with the advent of a new drug. The potent and selective proteasome inhibitor called Bortezomib with a new mechanism of action has been studied (Tobinai, p. 318). This product was found to have high efficacy, acceptable toxicities and impressive pharmacokinetic profiles. Further studies should indicate the problems in usage.

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Myelodysplastic syndromes (MDS)

The myelodysplastic syndrome consists of a group of malignancies in which the haemopoiesis is dysplastic and ineffective. The risk of transforming into acute leukemias is there. Fatigue, a lack of energy, difficulty in breathing and exertional dyspnoea are some of the symptoms. Generally, the patients are too weak and their performance level is low (Scott p.1). Petechiae and bruises are found usually on the legs. The MDS forms a heterogenous group of illnesses (Bowen p.89). Laboratory findings show a low haematocrit value (Scott p. 1). Anaemia is a macrocytic one. A low reticulocyte level is seen. Anisocytosis, poikilocytosis and acanthocytosis are features seen in the blood picture. Nucleated RBCs, Howell Jolly bodies and basophilia are noticed (Scott p.2). Neutropenia and hypogranular cells with chromatin condensation are also found. Monocyte count will be elevated. The invasion of bacteria cannot be met with in this condition of weakness. Growth factors have less effect on the cells. Thrombo- cytopenia will be found. A hypercellular marrow will be seen making the differential diagnosis from aplastic anaemia difficult. Microscopic examination shows single and multi-linear dysplasia. Clonal cytogenetic abnormalities are seen in 40-50% of the de novo patients of MDS and 90% of the secondary or treatment-related MDS (Scott p.4). Ballieri has shown that haemopoietic growth factors, erythropoietin and granulocyte colony-stimulating factor, in combination may be used to treat the anaemia of the myelodysplastic syndromes of low risk than when they are used alone (p. 174). Tilak et al have shown the uniqueness of paediatric MDS which runs an aggressive course of 9.9. months of clinical illness terminating fatally. The researchers have called for a paediatric approach to the classification and management of paediatric MDS.

Agnogenic myeloid dysplasias

Agnogenic myeloid dysplasia or idiopathic myelofibrosis belongs to the group of chronic myeloproliferative disorders (Michiels p. 133). The aetiology could be radiation from atomic bombs, exposure to benzene compounds, clonal changes in stem cells, or the fibrosis of bone marrow (Small, Buffalo University). Clinical features or presentations are those of anaemia and splenomegaly and bone pain. The patient would come with pallor and fatigue or with frequent infections. The blood picture or smear would be leukoerythroblastic or a normochromic, normocytic one. Tear drop erythrocytosis is a classic feature. Nucleated RBCs and leucocytosis are also seen but platelet count may be high or low (Small, Buffalo Universuity). Blood chemistry would show higher levels for uric acid and LDH (Lactic dehydrogenase). Chromosomes are abnormal in one-third of cases and show a change in the C group. Fibrosis of the reticulin and the collagen and optional osteomyelofibrosis in the bone is another feature (Tefferi 2000). Megakaryocytes are found in the bone. The early stages are marked by the hyperplastic prefibrotic stage (Georgi et al 1998). The WHO classification has helped to identify the diagnostic criteria for this illness. The Cologne criteria have been used for making a diagnosis from the bone marrow morphology. The trend now is to diagnose according to both the clinical and bone morphological parameters. When the disease is on the verge of transition to myelodysplastic syndrome or acute leukemia, there will be an increase of blasts in the peripheral blood (Michiels p.143). Treatment would be palliative. Prevention may not be possible but remaining aware of the condition when a patient presents with anaemia is important. Splenectomy is indicated in cases of severe pain due to splenic infarction, refractory anaemia, thrombocytopenia due to hypersplenism and portal hypertension.

Bone marrow histopathology has been used innovatively by Michiels and his team for diagnosing and classification into stages the Philadelphia chromosome-negative myeloproliferative disorders (Michiels p.133). This significant tool can identify early, manifest and advanced stages of essential thrombocytopenia, polycythemia vera and agnogenic myeloid metaplasia.

Essential thrombocythemia

It is a bone marrow disorder where the DNA leads to the platelets being found in large numbers in the blood (Kugler, This illness is a myeloproliferative disorder which is a clonal stem cell disease (Finazzi, p. 51). The illness has been attributed to the transformation of a multipotent progenitor. Most people have no symptoms. Others have rashes or burning sensation or itching of the skin, pain in the extremities, a mild enlargement of the spleen, headache, dizziness and weight loss. Abnormal bleeding tendencies, complications of pregnancy and complications in the clotting of blood are also seen in this condition. Strokes are known to occur (Kugler, The abnormally high level of platelets points to the diagnosis but the other conditions with high platelet counts must be eliminated. Prevention is not possible in essential thrombocythemia except for the heparin-induced type. Plateletpheresis or removal of platelets is a treatment. Regular visits to the doctor are encouraged. Higher-risk patients are treated with hydroxyurea, anagrelide or interferon-alpha (Weiss p.243). Cytogenetic studies have not been very helpful. However, in 2005, researchers found an acquired mutation called V61 7F which was identical to the JAK2 mutation (Jones p.2162). Weiss found that in heparin-induced thrombocythemia, it was possible to gauge the probability of the heparin producing the thrombocythemia. The optical density values of the Heparin PF4 ELISA.were directly related to the probability (Weiss p. 246).

Hairy cell leukemia

Hairy cell leukemia which forms 2% of all leukemias is a B-lymphoproliferative malignancy (Arons p.1100). Slow-growing leukemia, the aetiology has not been discovered yet. Chronic lymphocytic leukemia has hair-like projections on its lymphocytes, the reason for which has not been placed yet. Symptoms are an enlarged spleen causing a fullness in the left upper part of the abdomen, weight loss without cause, a general feeling of ill-health and fever and chills. The accumulation of these cells in the bone marrow obstructs the normal production of blood cells (Hairy cell leukemia, Leukemia and Lymphoma society). The features resulting are anaemia, increased risk of infections and thrombocytopenia or pancytopenia (a deficiency of all the 3 types of blood cells). Bruises may appear, without injury, due to low platelet numbers. Hairy cells accumulate in the spleen, liver and bone marrow. However, the lymph nodes are not enlarged. The diagnostic features are the enlarged spleen and the low cell counts in the blood. Hairy cells are sometimes seen in the blood. Confirmative diagnosis is possible by bone marrow tests (Hairy cell leukemia, Leukemia and Lymphoma society).

Immunophenotyping is the final diagnostic test. Prevention is not possible. Patients without symptoms need not be treated but they require follow-up. Those who have current infections, low blood cell count and enlarged spleen may have treatment with purine analogue drugs like cladribine or pentostatin (Treatment of hairy cell leukemia, American Cancer Society). The response is very good to these drugs: 80-90%. Following this treatment, ritumaxib would reduce the remaining symptoms. Rarely, the hairy cell leukemia fails to respond. The biological therapy with interferon-alpha may work. Splenectomy relieves the pain of an enlarged spleen (Treatment of hairy cell leukemia, American Cancer Society). Aron’s study focused on deciding whether the cytotoxic T-lymphocytes were related to the T-cell receptor beta variable clonal excess (p.1100)

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The conclusion was that the abnormalities in the lymphocytes represented the deficiency of immunity. Purine analogues could make the condition worse. It was indicated that patients may benefit more from biologic antibody-based treatment than purine analogues (Arons p.1100).

Machii conducted a study to evaluate the efficacy of the therapy with cladribine in the treatment of hairy cell leukemia (p. 230). The conclusion said that the drug when used as a continuous intravenous injection of 2CdA infusion for 7 days at a daily dosage of 0.09mg/kg is very effective and has acceptable toxicity (Machii p. 235).


Dyslipidaemia is the significant predictive factor for coronary artery disease (CAD).

Hypercholesterolaemia results from a rise in LDL cholesterol and can lead to atherosclerosis. Serum cholesterol if high or more than 240mg/dL is a major contributor to CAD (Foody p. 49). A 1% increase in the low-density lipoprotein (LDL-cholesterol) can cause a 2-3% increase in the risk. Intensive lipid-lowering effects in persons who possess a high risk reduce the onset of coronary artery disease. A 10% increase in serum cholesterol leads to a 20-30% increase in risk for cardiovascular disease. Hypercholesterolaemia does not produce any symptoms and can be detected by blood investigation. However, high risk can produce cardiovascular disease and acute mental stress. A linear relationship exists between serum cholesterol and cardiovascular disease (Grundy et al, 2004). The increase in free fatty acids and LDL-C saw after an epinephrine infusion (a catecholamine-induced release) has been demonstrated by Herd in 1983. A recent study has correlated panic disorder with increased morbidity and mortality due to cardiovascular disease.

The physiological and neurochemical changes following a panic attack have been found associated with an increase in LDL-C (Perez-Parada p. 334). It was surmised that a stress-induced model supports the release of fatty acids from adipose tissue. These fatty acids reach the liver where they are converted into LDL particles (Perez-Parada p. 334). In another study molecular imprinting was studied by Soares (p.79). The methods employed to reduce cholesterol in food include extraction with solvents, supercritical fluid extraction, steam distillation and treatment with cyclodextrin or saponin. Complexing cholesterol with beta-CD is the method used in the dairy industry as the selected cheapest method. This last method was used for the study of imprinting hydrophobic silica matrix in an attempt to discover an adsorbent for the other organic materials so that cholesterol can be removed (Soares p. 79).


Haemachromatosis is an iron overload disease caused by an inherited disorder whereby the body absorbs and stores plenty of iron which damages the various organs (Haemachromatosis, NDDIC). The main function of iron is when it becomes part of Haemoglobin, the substance that allows the transport of oxygen in the blood. The defect of hereditary haemachromatosis is in the gene HFE. This regulates the amount of iron absorbed from food into the body. Iron in excess damages the liver in alcoholism, autoimmune hepatitis, porphyria cutanea tarda, heart disease and diabetes. One striking feature is that only some of the patients with the gene HFE get haemachromatosis (Haemachromatosis, NDDIC). Juvenile and neonatal haemachromatosis are not caused by the genetic defect and have no known cause. Symptoms include joint pain, fatigue, lack of energy, abdominal pain, loss of sex drive and heart problems. If detection is late, serious consequences are arthritis, cirrhosis liver, cancer, damage to the pancreas, cardiovascular abnormalities and abnormal pigmentation of the skin (Haemachromatosis, NDDIC). Laboratory tests show the level of iron in the body. The transferrin saturation test indicates the amount of iron bound to protein in the blood. The total iron-binding capacity measures the capacity of the blood to transport iron. The level of iron in the liver is indicated by the serum ferritin test. A positive result for any of the tests can be further confirmed by a liver biopsy. Phlebotomy is the treatment and it is done once or twice a week for months or one year by drawing blood as if for donation (Haemachromatosis, NDDIC). Blood ferritin levels will be tested frequently to keep the level at 25-50 micrograms per liter. Maintenance therapy is started when iron levels reach normal level by giving blood transfusions every 2-4 months. If therapy is started before damage to organs has occurred, complications are prevented. Prevention is not possible but relatives of a patient detected with haemachromatosis must undergo a genetic test confirmation or have two consecutive blood tests for transferring saturation (Haemachromatosis, NDDIC). Drug management is also done but venesection forms 98% of procedures (Charles p. 792). Sartori investigated the heterozygous beta-globin gene mutations as a risk factor for iron accumulation and liver fibrosis in chronic hepatitis C. It was found that heterozygosis for beta-globin mutations is a novel risk factor for both hepatic iron accumulation and the progression to fibrosis in patients with CHC (Sartori et al p.613). Gehrke and his team studied the role of haemochromatosis and transferrin receptor gene polymorphisms in chronic hepatitis C: the impact on iron status, liver injury and HCV genotype. The conclusion was that heterozygosity for the C282Y mutation in HFE contributes to iron accumulation and fibrosis progression in chronic hepatitis C (Gehrke p. 740).


The blood does not clot normally in this rare bleeding disorder (Hemophilia, NHLBI).

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Bleeding is prolonged following injuries and internal bleeding in joints is possible. A protein called the clotting factor is either present in minimal quantities or totally absent. In normal circumstances, the clotting factor together with the platelets forms the clot. Hemophilaia A is due to the absence of factor 8 and hemophilia B is due to factor 9. Depending on the amount of factors, the illness can be a mild, moderate or severe form (Hemophilia, NHLBI). The disease is usually inherited but rarely can it be acquired also. It is seen usually in males. The X chromosome carries the genes which decide the presence of the factors. So the abnormality on the X chromosome decides the illness. The female has hemophilia only if she has the abnormalities on both X chromosomes. The female is usually a carrier. Mutations can give rise to children born of normal parents. Mild hemophila does not usually show symptoms unless following dental extractions or accidents or surgeries (Hemophilia, NHLBI). The moderate and severe forms have bleeding from the gums, a bite, nosebleeds, minor cuts all of which produce excessive bleeding. Small knocks and hits can produce large amounts of internal bleeding leading to serious complications. Bleeding and clotting times will decide that there is a problem. Special blood tests will show the type of hemophilia. Replacement therapy with the absent clotting factor is done intravenously as an injection. Preventive therapy is by taking the factors at regular intervals (Hemophilia, NHLBI). Precautions of screening blood before donation to hemophilic patients must be taken. Hepatitis A and B vaccines must be taken. Desmopressin is used to treat mild and moderate cases. Antifibrinolytic measures must be taken before dental extractions and surgeries. Bogdanova investigated the number of women who had reduced factor 8 activity and negative family history to discover whether they carried mutations of F8. The study revealed that 15% of studied patients had pathogenic mutations. Mutations were not seen in 85% of the patients. Theoretically, these patients were expected to be having deletions in the regulatory regions of the F8. El-Maarri studied the underlying reasons for Factor 8 deficiency in Hemophilia A patients with undetectable mutations in the F8 gene (p. 109). 27 patients had severe problems at the F8 gene while 13 patients had minor problems. 1 had moderate activity.

12 cases had a history of hemophilia in the family. 36 patients had no inhibitors while one had.

A quantitative expression of the mutation may be responsible for the absence of hemophilia and these expression levels may be affected by genetic and epigenetic factors. However, there is not much information on the epigenetic factors that influence the expression of a specific allele (El-Maarri, p. 112).


This is the pressure in the arteries and is signified by systolic pressure and diastolic pressure. Normal pressure is 120/80 mm Hg. The 120 represents the pressure in the arteries when the heart contracts. The 80 represents the pressure when the heart relaxes. The pressure increases the risk of developing heart disease, eye damage, renal disease and brain damage (High blood pressure, Chronic or long-duration diseases cause end-organ damage. Both systolic and diastolic pressures are significant. Essential hypertension accounts for 90% of hypertension. Secondary hypertension occurs because of damage in any of the organs. 30% of cases of essential hypertension are due to genetic factors. The arteries would be stiff without elasticity.

Essential hypertension is associated with genetic factors, obesity, overuse of salt and aging. The presence of C reactive protein appears to be a predictor in hypertension so an inflammatory cause has been stipulated (High blood pressure, The presence of atherosclerotic plaques is believed by some researchers to be the cause of narrowing of the arteries and stiffness. Secondary blood pressure is due to disease in the kidney, adrenal gland or aortic artery. Management for hypertension is by using the angiotensin-converting enzyme inhibitors or angiotensin receptor blocker drugs. A study by Sakuta in Japanese middle-aged men investigated the prevalence rates of metabolic disorders like diabetes and hypertension in patients with asymptomatic colonic diverticulum (p. 97). The rates of both were found elevated (Sakuta p. 97). Another study found that genetically modified animals could not be used effectively for hypertension research for eliciting a new therapeutic strategy (Stingl p. 41).

Polycythemia Vera (PV)

This illness is characterized by the abnormal increase in the blood cells produced by the bone marrow especially the red cells (Dugdale, US National Library of Medicine). It is a disorder of the bone but the exact cause is unknown. Symptoms include breathing difficulty on lying down, giddiness, fullness in the region of the splenic region, redness of the face and symptoms of phlebitis. The skin may have a bluish discoloration and the patient may have fatigue. Laboratory tests confirm the diagnosis by the total blood count, differential count, ESR, erythropoietin level and Vit B12 level. Bone marrow biopsy can help diagnose the condition. Reducing the thickness of the blood and preventing bleeding and clotting are the goals of treatment. Phlebotomy is done to reduce the thickness of blood. Chemotherapy with hydroxyurea can suppress the bone marrow. Interferon can lower blood counts (Dugdale, US National Library of Medicine). Anegrelide can reduce the platelets. Aspirin is used as a blood thinner but it can cause gastritis. Patients usually do not have many problems even after diagnosis. The prognosis is bad only when complications like stroke or heart attack occur. A study by Dai investigated the “hypersensitivity of bone marrow erythroid, granulocyte-macrophage, and megakaryocyte progenitor cells to interleukin-3 and granulocyte-macrophage colony-stimulating factor” (Dai, Pubmed). The studies showed that just like PV blood BFU-E, the hypersensitivity of marrow hematopoietic progenitor cells to rIL-3 and rGM-CSF was obvious. The hypersensitivity of PV progenitor cells to IL-3 and GM-CSF could be a primary factor in the pathogenesis of PV. The underlying mechanism does not appear to be caused by the enhanced binding of rIL-3 (Dai, Pubmed). A study by Michiel showed slight hypercellularity of the bone marrow and proliferation of all cells called panmyelosis which a diagnostic is finding (p. 135). Megakaryocytes are found clustered especially when the platelet count is increased. They also show a pleiomorphic picture which is a grouping of a giant to small megakaryocytes: lobulated nuclei would be seen but obvious anomalies may be absent. Secondary polycythemia does not have the typical picture of panmyelosis of PV and cellularity and megakaryopoiesis are not seen but an inflammatory reaction may be present (Michiels p. 138).

Human Immunodeficiency syndrome

Diagnosis of this condition usually results from suspicion of illness and laboratory testing. HIV illness results from getting infected with organisms from an infected person mostly through sexual contact (Perlmutter p.535). An ELISA may not be positive but if the HIV-1 RNA level is seen to be more than 50,000 copies per mL, the diagnosis is positive. Confirmation is done through a Western Blot antibody test. Delay in disease progression is through patient education and treatment. Symptoms are not characteristic features of HIV: presenting symptoms are those of the opportunistic infections that occur in HIV infection. Infectious mononucleosis, influenza, streptococcal infection, an acute infection may present as symptoms (Perlmutter, p. 535). Triple combination anti-retroviral therapy (HAART) must be started as soon as the diagnosis is made. The drugs combined would be a nucleoside reverse transcriptase inhibitor (NRTI), a nonthymidine NRT and a protease inhibitor. The treatment would be beneficial and resistance would not be developed if compliance is met. The viral load subsides with the treatment. Recovery of the immune system is reflected in the CD4 and CD8 lymphocytes. HIV infection produces an acute syndrome when the patient presents with any acute symptoms of pneumonia, fever, fatigue, rash, lympadenopathy, nausea or vomiting. The person may not test positive yet. Transmission of the virus is through sexual contact, shared injections and blood transfusions. A study investigated the efficacy of Raltegravir in the treatment of patients having resistance to the other retroviral drugs (Cocohoba p. 1747). It was indicated to be a potent and well-tolerated antiretroviral agent that would be significant in treating a patient who has developed resistance. Another study on the pharmacology, efficacy, and tolerability of Maraviroc was done by Lieberman-Blum. Maraviroc has been found to be a CCR5-receptor antagonist for the treatment of HIV-1 infection and is a promising agent for treating patients who have developed resistance to multiple drugs (Lieberman-Blum p. 1228).

Hepatitis B

This is a viral infection that is transmitted through contact with the blood or other fluids of an infected person (Hepatitis B WHO 2009). It affects the liver and could be an acute or chronic illness. Six hundred thousand persons die from complications every year. 25% develop cancer of the liver through chronic infection early in childhood. This virus is 50-100 times more infectious than HIV. This is an occupational hazard for staff working in hospitals especially.

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Other high-risk groups are people with higher-risk sexual behavior, those whose households have infected people, injection drug users and people who need frequent transfusions and those who have organ transplants (Hepatitis B WHO 2009). Prevention is possible with a Hepatitis B vaccine which is 95% effective and given in 3 or 4 doses. Symptoms of the illness include jaundice, dark urine, fatigue, nausea, vomiting and abdominal pain. It has been found that 90% of persons infected with HBV are free from the virus in 6 months. Modes of transmission are perinatal, early childhood infections, unsterile or shared injections, blood transfusions and sexual contact. Spread does not occur through contaminated food or water. The incubation period is 30-90 days. Treatment is symptomatic only. Liver transplants are also done for those with cirrhosis (Hepatitis B, WHO 2009). A comparative study was done by Chen et al of anti-hepatitis B virus RNA interference by double-stranded adeno-associated virus serotypes 7, 8, and 9. A combination of the power of RNAi silencing effect and multiple treatments with different AAV serotypes could produce effective and persistent suppression of HBV (Chen p. 352). Jenke et al studied whether long-term suppression of hepatitis B virus replication is possible by short hairpin RNA expression using the scaffold/matrix attachment region-based replicating vector system pEPI-1 (p. 2355). The study concluded that this was possible (Jenke et al p. 2355).

Hepatitis C

Hepatitis C is a virus that can cause an infection just like Hepatitis B. It affects the liver. Transmission is through contact with infected blood. It is spread by the sharing of injection needles, accidental pricking or injury caused by an infected needle as an occupational hazard in hospital workers, sexual contact with an infected person and the newborn from the infected mother during delivery (Hepatitis C, NDDIC). Hepatitis C can also be obtained through unsterile tattooing. Shaking hands, kissing, hugging or sitting next to an infected person will not allow the transmission of the organism. Blood transfusions prior to 1992 were not screened for Hepatitis C.

So transfusions could have transmitted the pathogen then. Symptoms of the illness may be so mild that the patient does not get any idea of the seriousness. Only tests can reveal whether this infection has occurred (Hepatitis C, NDDIC). Laboratory tests on the blood can clinch the diagnosis and liver biopsy would further confirm it. Prevention is by taking precautions, by not sharing drug needles, wearing gloves when blood is to be touched, using a condom during sex, not using an infected person’s toothbrush, razor or anything which has blood on it or having tattoos with clean instruments. The person who is infected should not donate blood. In HIV patients co-infected with the Hepatitis C virus, HAART therapy can cause lesser liver damage in the form of necroinflammatory activity (Pascual-Pareja p.971). Another study was done to determine the severity of steatosis in combined HIV and Hepatitis C infections. The severity of steatosis has been associated with advanced fibrosis in patients with co-infections. Anti-retroviral therapy with ritonavir or stavudine has been found to modify the severity of steatosis (Pascual-Pareja p. 208).

Hepatitis D

Hepatitis D or Hepatitis Delta is caused by the delta virus which is actually a defective RNA virus (Hepatitis Delta WHO). It cannot replicate by itself: it needs hepatitis B to help it do so. Transmission is through percutaneous means or through sexual contact with an infected person’s blood. Blood will be infectious at all stages of the active infection. Chronic HBV carriers and those who have not been immunized have a risk of getting the infection. Hepatitis D in the absence of HBV cannot cause an infection. Man is the natural reservoir. It is life-threatening when infection occurs in a chronic HBV-infected person when it leads to fulminant hepatitis. Chronic hepatitis D can also cause hepatocellular carcinoma. There is no treatment for the disease: Interferon may improve the patient’s condition. There is no hyperimmune D globulin. Liver tramsplant can be done for an end-stage fulminant acute hepatitis. Prevention is through strict aseptic measures. A study done by Xiridou aimed to confirm that the presence of hepatitis D could facilitate the control of HBV. The conclusion said that control programs are to determine the co-infection of Hepatitis D with hepatitis B so that the monitoring and efficacy of the programmes are improved (Xiridou p. e5247). Another study investigated the seroprevalence of the hepatitis delta infection in the people of Chennai, India with hepatic diseases.

HDV infection was found to be of low prevalence and thereby played only a minor role as a determining factor (Saravanan p.793).

Cytomegalus virus

Cytomegalus virus infections present with nausea, as sexually transmitted anorectal lesions, parotid swellings, generalized lymphadenopathy with tender nodes, hepatosplenomegaly, seizures in children, abnormal shape of the head or recurrent fevers in children, acute hearing loss and flu-like symptoms (Disease Information, MedTech). A typical presentation is viraemia sepsis. Fever presentation in immune-compromised persons is one presentation. Cardona described a paediatric case of Menetrier’s disease or protein-losing gastropathy which is associated with cytomegalus virus infection. The child had a short period of illness from which it recovered quickly. The clinical, ultrasonographic and endoscopic findings have been described in detail for a sound diagnosis (Cardona p. 478). In another study by Megged, a series report of protein-losing gastropathy was prepared from a review of the literature (p.1217). It was concluded that CMV should be thought about in children with protein-losing gastropathy. Newer and faster diagnostic techniques like polymerase chain reaction, which are better than the serological tests, help the diagnosis. Treatment with ganciclovir is recommended for prolonged cases (Megged p.1217).


The bites of infected Anopheles mosquitoes transmit the parasite Plasmodium into the blood of Man (Malaria, WHO). The multiplication of the parasite occurs in the liver from where they are released into the blood. Fever, headache and vomiting appear after 15 days of the bite. It is a life-threatening disease. Every 30 seconds, a child dies of malaria. 4 types of plasmodia are involved in malaria: Plasmodium vivax, malariae, ovale and falciparum. The vectors, mosquitoes, breed in the rainy season. Some countries have been described as endemic as malaria occurs all through the year. Most cases are from Sub-Saharan Africa. People who move newly into the mosquito-infested regions are more vulnerable. Pregnant women are especially vulnerable (Malaria, WHO). Severe anaemia and impaired foetal growth are predicted even if they do not show symptoms. HIV-infected pregnant women are also at high risk. Falciparum malaria is the most dangerous of the varieties and can cause cerebral malaria which is a fatal disease. Global health development programs have made efforts to wipe out the disease. Treatment aims to radically cure the illness. The main laboratory test which is diagnostic is the examination of the thick film slide under the microscope after staining with Field’s or Giemsa stain (Malaria, WHO). The number of parasites seen till 200 white blood cells aisre counted is noted. The parasites are found among the WBCs and the platelets. Treatment is with pyrimethamine tablets. Falciparum malaria is treated with combinations of artemisinin-based drugs. Drug resistance is a common occurrence in malaria. This has been reduced with combinations of drugs. Prevention is through vector control. Challenges in the control include the resistance to DDT and pyrethroids. National efforts need to focus on insecticide resistance (Malaria, WHO). Many genes have been implicated in malaria. Ndiaye’s team of researchers investigated how a variant of the intercellular adhesion molecule 1 (ICAM1), ICAM1 (Kilifi) influenced the risk of severe malaria in Senegal (p. 474). The study found no evidence for the role of ICAM1 variability on the phenotypes (Ndiaye p. 474). Variations in the host genes encoding adhesion molecules and the susceptibility to falciparum malaria were studied by Sinha and his team in India (p.250). They investigated the association of SNPs of three adhesion molecule genes ICAM1, PECAM1 and CD36 to the severity of falciparum malaria in a malaria-endemic region (Sinha p. 250). Variations were found in all three. The PECAM 1 showed a difference in the endemic and non-endemic regions.


This zoonosis is caused by several Babesia protozoa which parasitise the red blood cells. It is an infection similar to malaria (Babesiosis IGenexInc.). Organisms Babesia microti and WA1 are both described as human pathogens. The intermediate host is the black-legged tick which also transmits the B. burgdoferi which causes the Lyme disease. Symptoms of Babesiosis are fever, chills, arthralgia, headache, malaise and myalgia. The illness is fatal for splenectomised patients. Transmission occurs through the tick bite or blood transfusion. The diagnostic tests are the indirect immunofluorescent antibody assay (IFA) and nucleic acid-based diagnostic test (Babesiosis, IGenex Inc.). For the IFA to be positive, the sero-conversion should have taken place. This therefore may not be positive when the patient is ill with the fever. Antibodies may persist for a long duration even after the symptoms have disappeared. The nucleic acid-based diagnostic test is a better test where performance is concerned. 2 tests come under this group: PCR and FISH (Fluorescent In-situ Hybridisation). The PCR-based diagnostic test is highly sensitive. However, a negative test does not rule out babesiosis; it just implies that the sample of blood does not have the parasite. Treatment is by using antibiotic and antimalarial therapy to reduce parasitaemia (Babesiosis, IGenex Inc.). However, now the combination of atovaquone and azithromycin is the first line of treatment. Clindamycin and quinine are being used for the severe symptoms (Babesiosis WebMD). A study was done to investigate the pathogenesis, clinical course and optimal treatment regimen of the disease as these are not certain yet (Krause p.370). It was found that immunocompromised people who are infected by B. microti have the risk of a persistent relapsing illness. Treatment must be given for 6 weeks or more with two weeks of non-detection of the parasite in the blood smear (Krause p.375). Another study investigated the efficacy of the alternative regimen of atovaquone and azithromycin. This has been found to be much better than the earlier treatment with clindamycin and quinine and adverse reactions are less too (Krause b, p. 1454).


This illness affects people in 88 countries in the world. It is caused by the protozoa Leishmania which is an intracellular pathogen affecting the macrophages and dendritic cells of the immune system (Leishmaniasis WHO 2009). The characteristic symptoms are disfiguring cutaneous and muco-cutaneous lesions. Human infection is through the bite of the vector sandfly breeding in forest areas or caves, 20 species of which are pathogenic to Man. Four types of illnesses have been seen. The cutaneous type which has a few skin lesions heal within a few months with no scars. The diffuse cutaneous type show disseminated and chronic lesions that look like lepromatous leprosy and are difficult to treat (Leishmaniasis WHO 2009). The muco-cutaneous variety destroys the mucous membrane of the mouth, nose, throat and surrounding areas. Visceral leishmaniasis or kala azar can be fatal if not treated. It has a high fever, heavyweight loss, hepatosplenomegaly and anaemia. The direct agglutination test for 3 species of Leishmania, donovani, tropica and brasiliensis, showed high cross-reactivity for positive cases of Leishmaniasis (Allain p.232). One study investigated the protection against experimental visceral leishmaniasis infection in dogs that were immunized with purified excreted secreted antigens of Leishmania infantum promastigotes (Lemesre p.2825). The results supported the view that a promising vaccine is possible. The efficacy of a vaccine for visceral leishmaniasis was tested in another study. “The LiESAp-MDP vaccine produced a significant, long-lasting and strong protective effect against canine visceral leishmaniasis” (Lemesre p.4223).

Acute leukemia

Biological, immunological and clinical features separate the T–cell leukemias from the non-T-cell leukemias (Cooper, 2007). T cell leukemias had a worse prognosis than B-cell leukemias. However, advances in therapy have changed the situation. Nelarabine (2-amino-9beta-D-arabinosyl-6-methoxy-9H-guanine), a synthesised guanosine nucleoside, targets specific malignant cells with less toxicity. This drug has been approved by the US FDA and is effective against acute lymphatic leukemia andlymphoblastic leukemia (Cooper, 2007).

Scuto et al studied the mechanism of action of LBH589, a novel broad-spectrum HDAC inhibitor belonging to the hydroxamate class, in Philadelphia chromosome-negative (Ph(-)) acute lymphoblastic leukemia (Scuto et al, 2008). The actions were induced cell-cycle arrest, apoptosis, and histone (H3K9 and H4K8) hyperacetylation. LBH589 treatment increased mRNA levels of proapoptosis, growth arrest, and DNA damage repair genes including FANCG, FOXO3A, GADD45A, GADD45B, and GADD45G. Increased histone acetylation at the GADD45G promoter and phosphorylation of histone H2AX was also associated. Potent growth inhibitory activity against including Ph(-) ALL cells associated with up-regulation of genes critical for DNA damage response and growth arrest is seen in LBH589 (Scuto et al, 2008).


  1. Allain, D.S. and Kagan, I.G. (1975). A Direct Agglutination Test for Leishmaniasis. American Journal of Tropical Medicine Hygiene, Vol. 24 No. 2 p. 232-236
  2. Arons, E. et al. (2006). Characterization of T cell repertoire in hairy cell leukemia patients before and after recombinant immunotoxin BL22 therapy. Cancer Immunological Immunotherapy, Vol. 55, p. 1100-1110
  3. Babesiosis.
  4. Bogdanova, N. (2008). Mutation detection rates in female patients with reduced factor VIII activity and negative family history for Hemophilia A. in the 37th Hemophilia symposium (Eds.) I.Scharrer and W. Schramm, Germany:Springer Verlag, Berlin Heidelberg
  5. Bowen, D.T. (2006). Management of patients with myelodysplastic syndromes: Introductory concepts in In Haematological malignancies: Myelodysplastic syndromes (Eds.) Deeg H.J, et al. Springer Berlin Heidelberg
  6. Cardona, B. et al. (2006). Ménétrier’s disease of childhood and acute cytomegalus virus infection. An Pediatr (Barc). 2006;64(5):478-80 Anales Paediatria
  7. Charles, J. et al. (2007). Management of haemachromatosis in general practice. Australian Family Physician, Vol. 36, No.10, p792-793.
  8. Chen, C.C. et al. (2009). Comparative study of anti-hepatitis B virus RNA interference by double-stranded adeno-associated virus serotypes 7, 8, and 9. Mol Ther. 2009;17(2):352-9. Epub 2008 Dec 9
  9. Cocohoba, J. and Dong, B.J. (2008). Raltegravir: the first HIV integrase inhibitor. Clinical therapy, Vol. 30, No.10, p. 1747-1765
  10. Cooper, T.M. (2007). Role of nelarabine in the treatment of T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma. Ther Clin Risk Manag. 2007 ;3(6):1135-41 Pubmed
  11. Dai, C.H. et al. (1992). Hypersensitivity of bone marrow erythroid, granulocyte-macrophage, and megakaryocyte progenitor cells to interleukin-3 and granulocyte-macrophage colony-stimulating factor. Blood. 1992;80(4):891-9
  12. Disease Information for Cytomegalus Virus.
  13. Dugdale, D.C. (2009). Polycythemia vera. US National Library of Medicine
  14. El-Maarri, O. et al. (2008). Investigating the underlying reasons of Factor VIII deficiency in hemophilia patients with undetectable mutations in the F8 gene in the 37th Hemophilia symposium (Eds.) I.Scharrer and W. Schramm, Germany:Springer Verlag, Berlin       Heidelberg
  15. Finazzi, G. (2008). Essential thrombocythemia in Rare Haematological Malignancies (Eds) Stephen M.Ansell, New York: Springer Science and Business media
  16. Gehrke, S.G. et al. (2003). Hemochromatosis and transferrin receptor gene polymorphisms in chronic hepatitis C: impact on iron status, liver injury and HCV genotype.Journal of Molecular Medicine, Vol. 81 No.12, p. 780-787
  17. Georgi et al. (1998), The histopathology of chronic myeloproliferative disorders, Bailliere’s Clinical haematology, Vol. 11, p. 721-749
  18. Haemachromatosis.
  19. Leukemia and lymphoma society
  20. Hemophilia. National Heart Lung and Blood Institute. Dept for Health and Human Services. Web.
  21. Hepatitis B. Web. WHO 2009
  22. Hepatitis C.  The National Digestive Diseases Information Clearinghouse (NDDIC), NIH
  23. Hepatitis Delta.
  24. High blood pressure.
  25. Jenke, A.C. et al. (2008). Long-term suppression of hepatitis B virus replication by short hairpin RNA expression using the scaffold/matrix attachment region-based replicating vector system pEPI-1. Antimicrob Agents Chemother. 2008; 52(7):2355-9. Epub 2008
  26. Jones, A.V. et al. (2005). Widespread occurrence of the JAK2 V617 mutation in chronic myeloproliferative disorders, Blood, Vol. 106, p. 2162-2168
  27. Krause, P.J. (2008). Persistent and relapsing babesiosis in immunocompromised patients. Clin Infect Dis. 2008;46(3):370-6
  28. Krause b, P.J. (2000). Atovaquone and azithromycin for the treatment of babesiosis. N Engl J Med. 2000;343(20):1454-8
  29. Kugler, M. (2006). Essential thrombocythemia Web.
  30. Lemesre, P.J. et al (2007) Long lasting protection against canine visceral leishmaniasis using the LiESAp-MDP vaccine in endemic areas of France: a double blind randomized efficacy field trial. Vaccine, Vol. 25 No. 21, p.4223-4234 Epub 2007
  31. Lemesre, P.J. (2005). Protection against experimental visceral leishmaniasis infection in dogs immunized with purified excreted secreted antigens of Leishmanaia infantum promastigotes. Vaccine Vol. 23, No. 22. p. 2825-2840
  32. Lieberman-Blum, S.S. et al. (2008). Maraviroc: a CCR5-receptor antagonist for the treatment of HIV-1 infection. Clinical Therapy, Vol. 30, No.7. p.1228-1250
  33. Machii, T. et al. (2005). Phase II Clinical study of Cladribine in the treatment of hairy cell Leukemia, International Journal of Haematology, Vol. 82, p. 230-235. DOI 10.1532/IJH97.04128
  34. Malaria. Web.
  35. Megged, O. and Schlesinger, Y. (2008). Cytomegalovirus-associated protein-losing gastropathy in childhood. Eur J Pediatr. 2008;167(11):1217-20. Epub 2008 Jul 24
  36. Michiels, al. (2002). Clinical and pathological criteria for the diagnosis of Essential thrombocytopenia, polycythemia vera and idiopathic myelofibrosis (Agnogenic myeloid metaplasia). International Journal of Haematology, Vol. 76, p. 133-145
  37. Multiple Myeloma.
  38. Ndiaye, al. (2005). Clinical study of ICAM1 in clinical malaria in Senegal. Tissue Antigens. 2005 ;65(5):474-80
  39. Pascual-Pareja, J.F. et al (2009) Factors affected with hepatic steatosis in human Immunedeficiency virus and hepatitis C virus co-infected patients. Med Clin (Barc). Vol.132(6). p.208-213
  40. Pascual-Pareja, J.F. et al (2009) HAART is associated with lower hepatic ncreoinflammatory activity in HIV-Hepatitis C virus co-infected patients with cell count of more than 350 cells/microL at the time of liver biopsy. AIDS. 2009;23(8):971-5
  41. Perez-Parada, al. (2007). Delayed increase in LDL cholesterol following pentagastrin- induced panic attacks. Psychopharmacology, Vol. 193, p.333-340
  42. Perlmutter, B.L. et al. (1999). How to recognise and treat HIV syndrome. American Family Physician, Vol. 60, p. 535-546
  43. Sakuta, H.and Suzuki, T. (2007). Prevalence rates of Type 2 diabetes and Hypertension are elevated among middle aged Japanese men with colonic diverticulum. Environmental Health and Prevenntive Medicine, Vol. 12, p. 97-100.
  44. Saravana, S. et al. (2008). Seroprevalence of hepatitis delta virus infection among subjects with underlying hepatic diseases in Chennai, southern India. Trans R Soc Trop Med Hyg. 2008; 102(8):793-6. Epub 2008
  45. Sartori, M. et al. (2007). Heterozygous beta-globin gene mutations as a risk factor for iron accumulation and liver fibrosis in chronic hepatitis C., Gut, Vol. 56, No.5, p. 613-614
  46. Scott, B. and Deeg, H.J. (2006). Clinical presentation. In Haematological malignancies: Myelodysplastic syndromes (Eds.) Deeg H.J, et al. Springer Berlin Heidelberg
  47. Scuto, A. et al. (2008). The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells Blood. 2008;111(10):5093-100. Epub 2008
  48. Sinha, S. et al. (2008). Variations in the host genes encoding adhesion molecules and the susceptibility to falciparum malaria. Malar J. 2008;7:250
  49. Soares, C.M.F. et al. (2007). Molecular imprinting of beta cyclodextrin/cholesterol template into a silica polymer for cholesterol separation. Journal of Inclu Phenom macrocyclic chemistry, Vol. 57, p. 79-82
  50. Stingl, L. et al. (2009). 20 years of hypertension research using genetically modified animals: No clinically promissing approaches in sight. Altex, Vol. 26, No.1, p. 41-51
  51. Tefferi, A. et al (2000). Myelofibrosis with myeloid metaplasia, New England Journal of Medicine, Vol.342, p. 1255-1265.
  52. Tilak, V. et al ( 2008). Myelodysplastic syndrome, Indian Journal of Paediatrics, Vol.75 (7), p. 729-732.
  53. Tobinai, K. (2007). Proteaosome inhibitor, bortezomib, for myeloma and lymphoma. Intenational Journal of Clinical Oncology, Vol.12, p. 318-326. Japan Society of Clinical Oncology, 2007, DOI 10.1007/s10147-007-0695-5
  54. Treatment of hairy cell leukemia.
  55. Tsuboi, al. (2007). Wilm’s tumour gene W1 peptide-based immunotherapy induced a minimal response in a patient with advanced therapy-resistant multiple myeloma. International Journal of Haematology, Vol. 86, p. 414-417, DOI 10. 1532/IJH97.07007, The Japanese Society of Haematology.
  56. Weiss, B.M. et al. (2008). Optical density values correlate with the clinical probability of heparin-induced thrombocytopenia. Journal of Thromb. Thrombolysis, Vol. 26, p. 243-246. Springer Science and Business Media, LLC
  57. Xiridou, M. et al. (2009). How hepatitis D virus can hinder the control of hepatitis B virus. PLoS ONE. 2009; 4(4):e5247. Epub 2009

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