latest terms related COPD.(Chronic obstructive pulmonary disease)

Anticholinergics

These medications work to relax the muscles in airways through the parasympathetic pathway, by relaxing the tense state of the muscles. These are available as controllers.

Beta-agonists

These medicines work to relax the muscles in your airways through the sympathetic pathway. These are available as rescue relievers and controllers.

Bronchodilators

A medicine used for relaxing muscles around the lungs’ airways allowing the airways to open up and expand. These include anticholinergics and Beta-agonists.

Cannula

Plastic tubing used to supply oxygen through the nose.

Corticosteroids

Medicines that mimic the action of a group of hormones produced by adrenal glands. They are anti-inflammatory. This medicine can be inhaled or taken by mouth.

Dyspnea

Shortness of breath. Difficult or labored breathing.

Exacerbations

Flare-ups of Chronic Obstructive Pulmonary Disease in which symptoms get worse. Changes in medical treatment may be needed.

Hyperventilation

Rapid breathing often caused by being nervous or panicked.

Hypoxia

Too little oxygen in the body.

Inhaler

A portable device to take inhaled medicine in a couple of breaths.

Liquid Oxygen (LOX)

This is oxygen condensed into a liquid state by extreme cold. A small amount of liquid oxygen is a very large amount of oxygen gas. The big tank at your house can also fill easy-to-carry smaller tanks when you leave your house. Nebulizer

This is a device that delivers medicines in a fine spray or mist. It requires no special coordination. It is a good method for getting drugs directly into the lungs.

Oxygen Concentrator

A machine used for oxygen therapy. It has a pump that takes oxygen from the air, and moves it through a long narrow tube into the nose. It concentrates the amount of oxygen taken from the air. There are now portable oxygen concentrators available.

Oxygen Therapy

A medically prescribed system of providing supplemental oxygen to the body. It is prescribed when diseased lungs are not able to meet the body’s oxygen needs.

Pulse Oximetry

This test measures how much oxygen is in your blood. The test is easy, and the result is a percentage. The doctor will put a sensor on your finger or ear and a light will be used to measure the oxygen content in your blood. The result of this test may show if you need oxygen therapy.

Spirometry

This is a part of a Pulmonary Function Test. It measures the amount of air able to be breathed out forcefully. It is used to help diagnose lung diseases.

Sputum

Mucus, usually loose in the lungs. It may be coughed up.

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Study of Impact the growing international trade and travel increased the risk of spreading zoonoses infectious disease like EBOLA, MERS and AIDS, SARS OR highly pathogenicAVIAN influenza, all originated in wild animals and were spred person to person.

Dr. Aleem sarwar

Abstract:
Influenza’ A (H1N1) virus is a subtype of influenza A virus and was the most common cause of human influenza (flu) in humans.  The two dominant proteins found on the virus surface are known as Hemagglutinin (often referred to as “H” or “HA”) and Neuraminidase (“N” or “NA”). 
The three types of influenza virous generally differ in the severity of illness that they cause.
Type-A.
It is a virus that most commonly causes the most severe flu symptoms.
Type- B and -C.

Type B is weaker and Type C is the weakest of all, rarely causing any symptoms.

In the midst of all the worries and concerns relating to the recent outbreak of Type A H1N1 influenza some truly striking data about influenza viruses in general are often forgotten. Every year in the United States more than 30,000 people die as a result of infection with “seasonal influenza”, and more than 200,000 people require hospitalization for treatment.

The three main types of influenza virus generally differ in the severity of illness that they cause. Type A influenza is the virus that most commonly causes the most severe flu symptoms, while Type B is weaker and Type C is the weakest of all, rarely causing any symptoms.

What Do the H and the N Mean in the Name of the Virus

Influenza viruses can be identified based on the chemical structure of specific proteins found on the outer surface coat of the virus particle. The two dominant proteins found on the virus surface are known as Hemagglutinin (often referred to as “H” or “HA”) and Neuraminidase (“N” or “NA”). Both of these proteins play critical roles in the lifespan of an influenza virus.

The array of flu viruses that have been characterized over the years can carry different versions of H or N, and thus the numbering system. There are more than 10 known forms of H and as many as 9 versions of N. Thus different strains can be characterized by the type of H or N that they carry e.g. H1N1, or H3N2, etc. The avian flu that focused the world’s attention several years ago was known as H5N1.

What Do the H and N Proteins Do?

The H protein is important in allowing the virus to adhere to cells and gain entry so that the virus can be replicated. The name “hemagglutinin” means that the protein can cause red blood cells to clump together, one of the features originally associated with the flu virus when tested in laboratory dishes. The N protein, “neuraminidase”, is an enzyme that helps the virus to escape from cells once new viral particles have been replicated. This enzyme can cleave specialized sugar molecules that are often associated with the proteins found on the surface of cells. This is the protein that is targeted by flu medications such as Tamiflu and Relenza.

Flu Viruses Can Change Quickly

Unlike many other viruses, the nucleic acid that is found inside the influenza virus family is RNA not DNA, making them “RNA viruses”. Additionally, the instructions for making a new virus are carried in 8 separate fragments of RNA and not in one large contiguous piece of DNA as is true for many other viruses like chickenpox. The presence of the multiple fragments means that if a cell is infected simultaneously with two different versions of influenza, the fragments can be shuffled to generate a new form.

Fighting Flu Virus

Fortunately, seasonal influenza can be combated by vaccinations, since flu specialists are often able to predict the strain of flu that will predominate during an upcoming flu season. New technologies that are being developed for generating vaccines against influenza will likely substantially decrease the time between identifying a new flu strain and generating a vaccine. But remember to be vigilant, wash your hands frequently, cough or sneeze into a tissue or your sleeve (not your hand) and if you think you might have the flu contact your family physician for treatment options and advice.

Read more about the biology of Influenza viruses at the US National Institute of Allergy and Infectious Disease ( NIAID) or at the US Centers for Disease Control and Prevention (CDC).

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TOO MUCH SALT INTAKE MAY CAUSE LIVER DAMAGE.

• A high-salt diet  damages liver in adults and developing embryos.
• Results in oddly shaped cells.
• An increase in cell death.
• Decrease in cell proliferation, which can contribute to the development of fibrosis. 
• Researchers found that treating damage cell with vitamin C appeared to partially counter the ill effects of excess salt.                                    

                                                                 

                                                           USES OF SALT

1. Our bodies need a small amount of salt, one teaspoon per day for a healthy adult.
2. Sodium ions from  the savory mineral help regulate water movement within the body and conduct nerve impulses. 

                                                        THE  STUDY

• Xuesong  yang from jinan university in china and colleagues wanted to explore the potential effect at a cellular  level.
• The researchers gave adult mice a high-salt diet and exposed chick embryos to a briny environment. 
• Some research indicates that in addition to high blood pressure, over consumption  of sodium can damage the liver.  
  
  

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8 star pharmacist.

Caregiver: Pharmacists provide caring services. They must view their practice as integrated and continuous with those of the health care professionals with highest quality.

Decision-maker: The appropriate, efficacious, safe and cost-effective use of resources should be the foundation of the pharmacist’s work. At the local and national levels, pharmacists play a role in setting medicines policy. Achieving this goal requires the ability to evaluate, synthesize data and information and decide upon the most appropriate course of action.

Communicator: The pharmacist is in an ideal position to provide a link between prescriber and patient, and to communicate information on health and medicines to the public. He or she must be knowledgeable and confident while interacting with other health professionals and the public. 

Manager: Pharmacists must be able to manage resources and information effectively; they must also be comfortable being managed by others, whether by an employer or the manager/leader of a health care team. 

Life-long-learner: It is impossible to acquire in pharmacy school all the knowledge and experience needed to pursue a life-long career as a pharmacist. The concepts, principles and commitment to lifelong learning must begin while attending pharmacy school and must be supported throughout the pharmacist’s career. Pharmacists should learn how to keep their knowledge and skills up to date.

Teacher: The pharmacist has a responsibility to assist with the education and training of future generations of pharmacists and the public. Participating as a teacher not only imparts knowledge to others, it offers an opportunity for the practitioner to gain new knowledge and to fine-tune existing skills.

Leader: In multidisciplinary caring situations or in areas where other health care providers are in short supply pharmacist should assume a leadership position in the overall welfare of the patient and the community. Leadership involves compassion and empathy as well as vision and the ability to make decisions, communicate, and manage effectively. A pharmacist whose leadership role is to be recognized must have vision and the ability to lead.

And the added function of:

Researcher: The pharmacist must be able to use the evidences effectively in order to advise on the rational use of medicines in the healthcare team. By sharing and documenting experiences, the pharmacist can also contribute to the evidence base with the goal of optimizing patient care and outcomes. As a researcher, the pharmacist is able to increase the accessibility of unbiased health and medicines-related information to the public and other healthcare professionals.

                                     

                                                                                      A WHO INTEGRATED MODEL,

                                                                                       

                                                                                    By,

                                                                                     Aleem Sarwar,

                                                                                     pharm.D.

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THERAPEUTIC GOAL OF HYPOPLASTIC ANEMIA IN PEDIATRICS HOSPITAL IN INDIA

Aleem sarwar,
Pharm.d. Interns.
Dept.of pharmacy practice,
Annamalai University,
Chidambaram,608 002,
Tamil Nadu,India
mob.9962761548.

 
 Abstract
 Aplastic anemia is acondition in which the bone marrow does not make enough new blood cells. bone marrow is the soft, fatty tissue in the center of  bones.
Most acquired aplastic anemia (AA) is the result of immune-mediated

destruction of hematopoietic stem cells causing pancytopenia and an empty bone marrow, which

can be successfully treated with either immunosuppressive therapy (IST) or hematopoietic stem-

cell transplantation (HSCT).the aplastic anemia is a rare and serious disease.It happens when your bone marrow fails to make enough blood cells (low blood cell counts).

Keywords
  aplastic anemia; anti-thymocyte globulin; bone marrow failure; stem cell transplantation;

cyclosporine; pancytopenia

Itroduction

 Aplastic anemia (AA) is a life-threatening bone marrow failure disorder

which, if untreated, is associated with very high mortality. Hematopoietic stem cell

transplantation (HSCT) offers an opportunity for cure, but most patients are not suitable

candidates for this procedure due to advanced age, comorbidities, or lack of a

histocompatible donor. For these patients, comparable long term survival is attainable with

immunosuppressive treatment (IST) with anti-thymocyte globulin (ATG) and cyclosporine

(CsA). Although several etiopathogenic triggers have been proposed in AA, the majority of

cases are idiopathic, with a small percentage of cases occurring after an episode of

seronegative hepatitis.

 Epidemiology and etiology

Each year, approximately between  800 to 1200 indian learn that they have aplastic anemia.the disease can strike people of any age, race, and gender. But it more common among children, teenagers, and young adults.

About 1 in 4 cases aplastic anemia can be linked to one of sveral causes. 

These include.

• Toxins, such as pesticides, arsenic, and benzene.
• Treatments for other autoimmune disease such as rheumatoid arthritis.
• Pregnancy. some times this aplastic anemia improves on its own after the woman give birth.                                                                                                                                            AA was attributed to an idiosyncratic reaction to drug or chemical
  exposure. The association of medical drug use to AA is of great importance, as it is
  devastating to patients and physicians and presents serious legal consequences and problems
  in pharmaceutical drug development. However, the study of idiosyncratic drug reactions,
  by definition extremely rare, is difficult and the only clear predisposition to abnormal drug
  metabolism underlying susceptibility is one study of a single individual exposed to
  carbamazepine published over 20 years ago. Overrepresentation of drug metabolizing
  glutathione-S-transferase gene deletions have been observed in some series  but no
  reasonable mechanism has been developed for chloramphenicol.
  Pregnancy and eosinophilic fasciitis are linked to AA. Five to ten percent of cases of AA
  follow an episode of seronegative hepatitis, but despite intensive efforts, an infectious
  agent has not been identified.

Pathophysiology                                                                                                                                     
 In most cases, AA behaves as an immune-mediated disease. An immune response

dominated by oligoclonal expanded cytotoxic T-cells targets hematopoietic stem and

progenitor cells, inducing their death via apoptosis and hematopoietic failure.

T-Cell-mediated destruction of the bone marrow

Recovery of autologous hematopoiesis in patients who failed to engraft after stem cell

transplant and responsiveness to immunosuppressive therapies are the major clinical

evidences supporting an immune pathophysiology underlying acquired AA. Although a

nonimmune pathophysiology has been inferred from a failure to respond to

immunosuppression, refractoriness to therapy is also consistent with very severe stem cell

depletion, a “spent” immune response, or immunological mechanisms resistant to current

therapies.

Removal of lymphocytes from aplastic bone marrows improves colony numbers in tissue

culture, and their addition to normal marrow inhibited hematopoiesis in vitro. The

effector cells within the lymphocyte subset are activated cytotoxic T cells bearing a

profile, expressing and secreting interferon-γ. 

T-bet, a transcription factor that binds tothe interferon-γ

promoter region and is critical for Th1 polarization, is up-regulated in T-

cells of patients with AA. Specific CD8+CD28− cell clones are expanded in AA

peripheral blood, as manifest by skewed usage of the Vβ repertoire; and oligoclones

recognize and induce apoptosis of autologous myeloid cells. Regulatory T cells, which

control and suppress auto-reactive T cells, are decreased at presentation in almost all

patients with AA. In a mouse model of immune-mediated marrow failure, addition of T

regulatory cells abrogated pancytopenia induced by the infusion of lymph node cells.

Why T-cells are activated in AA is unclear. HLA-DR2 is over-represented among patients,

suggesting a role for antigen recognition, and its presence is predictive of a better response

to cyclosporine. Polymorphisms in cytokine genes, associated with an increased

immune response, also are more prevalent, such as for tumor necrosis factor-α(TNF2)

promoter at −308, interferon-γ, and interleukin 6 genes. These alterations in

nucleotide sequence and in gene regulation suggest a genetic basis for aberrant T cell

activation in bone marrow failure.

Hematopoiesis

Immune attack leads to marrow failure. The targets, mainly CD34+ cells, are very few or

absent in the aplastic bone marrow, and minimal numbers of colonies derive from

committed progenitors in semisolid media, all reflecting the severe reduction in

hematopoietic progenitor cells that defines the disease. The reduced number and function of

the marrow is secondary to cell destruction, and apoptosis is prevalent among the few

remaining elements. Microarray analysis of the remaining CD34+ cells shows a

transcriptome shifted towards apoptosis, cell death, and immune regulation.

A minority of AA cases may share pathophysiologic basis with inherited marrow failure

syndromes. One peculiar feature of white blood cells in AA is short telomeres, observed in

approximately a third of cases. Although initially blamed on excessive stem cell

turnover, telomere shortening in some cases of acquired AA and in dyskeratosis congenita, a

constitutional marrow failure syndrome is due to mutations in components of the telomerase

complex, causing low telomerase activity, progressive telomere erosion, and a deficient

proliferative capacity of hematopoietic stem cells. Family members who share the

mutation, despite normal or near normal blood counts, have hypocellular marrows, reduced

CD34+ cell counts and poor hematopoietic colony formation, increased hematopoietic

growth factor levels, and of course short telomeres; some affected relatives may present with

pulmonary fibrosis or liver cirrhosis in isolation. A few adult AA patients also have

heterozygous mutations in the Shwachman-Bodian-Diamond syndrome (SBDS) gene

(Shwachman-Diamond syndrome occurs when patient carries biallelic mutations).

Clonal evaluation

AA may coexist or evolve to clonal disorders, as paroxysmal nocturnal hemoglobinuria

(PNH), myelodysplasia (MDS), or acute myeloid leukemia (AML).

Paroxysmal nocturnal hemoglobinuria (PNH)

About 40–50% of patients with acquired AA have expanded populations of PNH cells,

easily detected by flow cytometry due to the absence of glycosylphosphatidylinositol-linked

membrane proteins, the result of somatic PIG-A gene mutations arising in hematopoietic

stem cells. Most clones are small and do not lead to clinical manifestations of

hemolysis or thrombosis, but classic PNH can evolve to marrow failure (the AA/PNH

syndrome) and all PNH patients show evidence of underlying hematopoietic deficiency. The

global absence of large number of cell surface proteins in PNH has been hypothesized to

allow escape and survival of a pre-existing mutant clone.

Myelodysplasia (MDS)

Aneuploidy develops in a minority of patients treated with immunosuppression over time,

usually monosomy 7 and trisomy 8. AA patients who develop trisomy 8 usually respond

to IST. T-cell oligoclones appear to recognize the aneuploid cells and specifically WT1

 as an antigen, but target cells are not killed due to their expression of anti-apoptotic genes.

Immunosuppressive therapy

Horse anti-thymocyte globulin (ATGAM (R); h-ATG) is the only drug approved by the

Food and Drug Administration for the treatment of AA. While it is generally believed that h-ATG administration leads to depletion of immune competent cells, its exact mechanism of

action remains unclear. H-ATG preparations contain a variety of antibodies recognizing

human T-cell epitopes, many directed against activated T-cells or activation antigens.

Both refractory and relapsed patients are frequently treated with further courses of ATG. In

these settings, rabbit ATG (r-ATG) + CsA has been frequently used. R-ATG is similar to h-ATG except that gamma immune globulin is obtained by immunization of rabbits with

human thymocytes. Clinically, r-ATG appears to be more immunosuppressive as a more

prolonged lymphopenia is observed with this agent compared to h-ATG. This enhanced

lymphocytotoxicity of r-ATG may be explained by higher affinity IgG subtype to human

lymphocytes, less batch-to-batch variability, longer half-life, and more efficient lymphocyte

depletion. In addition, r-ATG may promote immune regulation as suggested by an in

vitro assay where CD4+CD25− were converted to CD4+CD25+ regulatory T cells in the

presence of r-ATG but not h-ATG. For the 1/3 of patients who are refractory to h-ATG/CsA, repeated courses of immunosuppression have yielded response rates varying from 30 –70%. For relapsed patients, re-introduction of CsA commonly result in

improvement in blood counts, however, CsA-dependence is frequent and the dose of CsA

usually is tapered slowly with hematologic monitoring. Re-treatment with ATG/CsA in

relapsed AA has resulted in response rates of 50–60%. In our experience, relapse

 does not correlate to a poor prognosis, as patients often respond to re-introduction of CsA and/or re-treatment with ATG

 In moderate AA, the clinical course is variable: some patients progress to severe disease,

others remain stable and may not require intervention; regular transfusions may not be

required. Very few clinical trials have specifically addressed moderate disease.

Immunosuppression can reverse moderate pancytopenia and alleviate transfusion

requirements; ATG and cyclosporine are more effective in combination. Daclizumab, a

humanized monoclonal antibody to the interleukin-2 receptor, improved blood counts and

relieved transfusion requirements in 6 of 16 evaluable patients; the outpatient regimen had

little toxicity.

Allogeneic Hematopoietic Stem Cell Transplantation

Allogeneic bone marrow transplantation from a histocompatible matched sibling is curative

therapy in the majority of SAA patients who undergo this procedure . The most recent

cohort reported to the IBMTR showed 77% 5-year survival, and in children and patients

who were minimally transfused, survival of 80–90% may be routinely achieved. Acute

grade II–IV graft-versus-host-disease (GVHD) occurs in about 20–30% of patients and

chronic GVHD in 30–40%. Chronic GVHD has been a major cause of morbidity

and mortality in patients who survived more than 2 years post graft, with the necessity of

long term immunosuppressive therapy common. Graft rejection, a historic problem in

the application of transplant to SAA is now infrequent, likely a benefit of less immunogenic

blood products (leukocyte-depleted erythrocytes, for example) from fewer donors (platelets

collected by cytoapheresis). Also, better radiation-free conditioning regimens have

 improved the tolerability of HSCT and allowed for engraftment in heavily transfused (and in

some cases alloimmunized) patients who were refractory to IST. The frequently

employed conditioning regimen of cyclophosphamide + ATG was compared to

cyclophosphamide in a prospective randomized study  no differences in engraftment,

GVHD, and survival rates were observed between the two groups, suggesting that the better

outcome with HSCT over time relates to advances in supportive care. The main source of

stem cells up to 2000 has been bone marrow cells; in recent years, G-CSF peripheral blood

(PB) mobilized CD34+ have become more widely used. In a retrospective analysis, the use

of PB progenitor cell graft has been correlated to a worse outcome and more chronic GVHD

in younger patients (less than 20) compared to those who receive a bone marrow graft in

HLA-matched sibling donor transplants. This difference was not observed in older

patients.

Matched unrelated donor transplant

A matched sibling donor is available in only 20–30% of cases. As the outcome in aplastic

patients who have failed a single round of ATG has been poor, alternative sources of

hematopoietic stem cells have been sought, usually from now very large donor registries.

Data from large retrospective studies suggest that the outcome for an unrelated donor HSCT

remains less favorable compared to a matched-related transplant, due to more GVHD, a

mortality rate that is about twice that observed in matched sibling transplants, and long term

survival of about 50%  Older patients with poor performance status have the

worst outcome and better results are obtained in children than for adults. Progress in donor

selection through high-resolution HLA typing technology has likely contributed to

decreased graft rejection and better survival  and recently reported outcomes for MUD

rival those for an HLA-matched sibling transplant in children and young adults.

Conclusion

In recent years, further evidence has accumulated to strengthen the hypothesis that bone

marrow failure in AA results from immunologic destruction of hematopoietic stem and

progenitor cells. In a minority of patients with shortened telomeres, a qualitative disorder

may accompany the numerical diminution of CD34+ cells in the bone marrow. Current

research is aimed at investigating the mechanisms that lead to T cell activation and, whether

it is antigen driven or a result of immunological disarray. The clinical implication of

telomere shortening in AA is being investigated for prognostic significance. Most patients

with AA are now expected to survive regardless of the treatment modality employed.

Advances in supportive care and better salvage therapies have produced significantly

increased survival among initial non-responders to ATG+ CsA; the decrease in allo-

sensitization (through routine leucodepletion of blood products) and better donor selection

(through high molecular HLA-typing) have improved the outcomes of both related and

unrelated HSCT; long term survival in pediatric patients who respond to IST is excellent and

 ATG based regimen should be offered as initial therapy to those who lack a matched sibling

donor. Our practice has been to consider an alternative donor HSCT in suitable pediatric

patients who have failed an initial course of ATG + CSA or in adults who have failed two

courses of IST. Refractory patients who are not suitable candidates for alternative donor

HSCT can be supported through a combination of transfusions, androgens and/or

administration of hematopoietic growth factors. In chronically transfused patients, iron

overload can now be managed with more convenient oral agents (deferasirox, Exjade) and,

the prospect of approval of newer oral thrombopoietic drugs is likely to ease platelet

transfusion requirements especially in AA patients who are refractory to IST.

ATG based regimen should be offered as initial therapy to those who lack a matched sibling

donor. Our practice has been to consider an alternative donor HSCT in suitable pediatric

patients who have failed an initial course of ATG + CSA or in adults who have failed two

courses of IST. Refractory patients who are not suitable candidates for alternative donor

HSCT can be supported through a combination of transfusions, androgens and/or

administration of hematopoietic growth factors. In chronically transfused patients, iron

overload can now be managed with more convenient oral agents (deferasirox, Exjade) and,

the prospect of approval of newer oral thrombopoietic drugs is likely to ease platelet

transfusion requirements especially in AA patients who are refractory to IST.

References

1. Kaufman, DW.; Kelly, JP.; Levy, M.; Shapiro, S. The Drug Etiology of Agranulocytosis and

Aplastic Anemia. Oxford; New York: 1991.

*2. Issaragrisil S, Kaufman D, Anderson T, Chansung K, Leaverton P, Shapiro S, Young NS, The

Aplastic Anemia Study G. The epidemiology of aplastic anemia in Thailand. Blood. 2006;

107:1299–1307. [PubMed: 16254144] This large epidemiologic study enrolled more than 500

patients and 2,000 case controls; an accurate incidence rate was obtained, and there were

environmental associations with the disease that were familiar (chemicals and drugs) and others

that were unexpected (water source, animal exposure).

3. Hamerschlak N, Maluf E, Pasquini R, Eluf-Neto J, Moreira FR, Cavalcanti AB, Okano ÍR, Falcão

RP, Pita MT, Loggetto SR, et al. Incidence of aplastic anemia and agranulocytosis in Latin

America: the LATIN study. Sao Paulo Medical Journal. 2005; 123:101–104. [PubMed: 16021270]

4. Young, NS.; Young, NS.; Alter, BP. Drugs and chemicals. In: Saunders, WB., editor. Aplastic

Anemia, Acquired and Inherited. 1994. p. 100-132.

5. Gerson WT, Fine DG, Spielberg SP, Sensenbrenner LL. Anticonvulsant-induced aplastic anemia:

increased susceptibility to toxic drug metabolites in vitro. Blood. 1983; 61:889–893. [PubMed:

6831050]

6. Sutton JF, Stacey M, Kearsey SE, Reig TS, Young NS, Liu JM. Increased risk for aplastic anemia

and myelodysplastic syndrome in individuals lacking GSTT1 gene. Pediatric Blood Cancer. 2004;

42:122–126. [PubMed: 14752874]

7. Dufour C, Syahn J, Bacigalupo A, Longoni D, Varotto S, Iori AP, Bagnasco F, Locasciulli A,

Menna G, Ramenghi U, et al. Genetic polymorphisms of CYP3A4, GSTT1, GSTM1, GSTP1 and

NQO1 and the risk of acquired idiopathic aplastic anemia in Caucasian patients. Haematologica.

2005; 90:1027–1031. [PubMed: 16079101]

8. Lu J, Basu A, Melenhorst J, Young NS, Brown KE. Analysis of T-cell repertoire in hepatitis-

associated aplastic anemia. Blood. 2004; 103:4588–4593. [PubMed: 14988156]

9. Young NS. Hematopoietic cell destruction by immune mechanisms in aquired aplastic anemia.

Seminars in Hematology. 2000; 37:3–14. [PubMed: 10676907]

10. Sloand EM, Kim S, Maciejewski JP, Tisdale J, Follmann D, Young NS. Intracellular interferon- y

in circulating and marrow T cells detected by flow cytometry and the response to

imunosuppressive therapy in patients with aplastic anemia. Blood. 2002; 100:1185–1191.

[PubMed: 12149196]

*11. Solomou EE, Keyvanfar K, Young NS. T-bet, a Th1 transcription factor, is up-regulated in T cells

from patients with aplastic anemia. Blood. 2006; 107:3983–3991. [PubMed: 16434488] The T

cell polarizing transcription factor T-bet was increased in T cells from most patients with aplastic

anemia.

12. Risitano AM, Maciejewski JP, Green S, Plasilova M, Zeng W, Young NS. In-vivo dominant

immune responses in aplastic anaemia: molecular tracking of putatively pathogenetic T-cell clones

by TCR [beta]-CDR3 sequencing. The Lancet. 2004; 364:355–364.

**13. Solomou EE, Rezvani K, Mielke S, Malide D, Keyvanfar K, Visconte V, Kajigaya S, Barrett AJ,

Young NS. Deficient CD4+ CD25+ FOXP3+ T regulatory cells in acquired aplastic anemia.

Blood. 2007; 110:1603–1606. [PubMed: 17463169] Regulatory T cells were decreased at

presentation in almost all patients; a regulatory T cell defect 16 was implicated in autoimmune.

14. Aplastic anemia and MDS international foundation.

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WHAT IS MILIARIA ?..

                      

miliaria is a caused by obstruction of the sweat gland duct during hot humid summer season.
                             

KEY POINT.

Itching, stinging and secondary infection can occur and lead to periporitis (multiple staphylococcal abscesses) superimposed on miliaria rubra in young children. Eczematization can occur.

MEDICATION AND TREATMENT.

NONPHARMACOLOGICAL 

• Avoid causal factor like heat and occlusion due to oils, creams, cosmetics etc.

• cool baths and aeration.

      PHARMACOLOGICAL

1. Emollients like anhydrous lanolin or  calamine lotion locally.   or
2. Talc or any commercially available powders.
3. For relief of itching tab. Pheniramine  25 mg 3 times a day .

• PRECAUTION

  • Frequent cool bath and aeration.
  • To stay in cool environment to minimize  the body's need to sweat.
  •    No oil application over scalp and body.                                     

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