Idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura (ITP) is the condition of having a short platelet count of no known cause. As most causes appear to be associated to antibodies against platelets, ITP is also recognized as immune thrombocytopenic purpura or immune-mediated thrombocytopenic purpura. Often ITP is asymptomatic, however a very little platelet count can lead to visible symptoms, such as purpura, or more seriously, bleeding diathesis. In many cases, ITP's cause is not idiopathic but autoimmune, with antibodies beside platelets being detected in approximately 60 percent of patients. Most often these antibodies are against platelet covering glycoproteins IIb-IIIa or Ib-IX, and are of the IgG type. The famous Harrington Hollingsworth experiment recognized the immune pathogenesis of ITP.

The covering of platelets with IgG renders them liable to opsonization and phagocytosis by splenic macrophages. The IgG autoantibodies are also thought to injure megakaryocytes, the precursor cells to platelets, but this is thought to contribute only slightly to the reduce in platelet numbers. The stimulus for auto-antibody making in ITP is probably abnormal T cell activity Preliminary findings suggest that these T cells can be influenced by drugs that target B cells, such as rituximab. The diagnosis of ITP is a procedure of exclusion. First, the clinician has to determine that there are no blood abnormalities other than small platelet count, and no physical signs except for signs of bleeding. Then, the secondary reason should be excluded. Secondary causes could be leukemia, medications, lupus erythematosus, cirrhosis, HIV, hepatitis C, inborn causes, and others.

In approximately one percent of cases, autoimmune hemolytic anemia and ITP coexist, a state referred to as Evans syndrome. A platelet count below 20,000 is usually an indication for treatment. Patients with a count between 20,000 and 50,000 are usually estimated on a case-by-case basis, and, with rare exceptions, there is usually no need to treat patients with a count above 50,000. Hospitalization may be recommended in cases of very low counts, and is highly desirable if the patient presents with significant internal or mucocutaneous bleeding. A count below 10,000 is potentially a medical emergency, as the patient may be susceptible to subarachnoid or intracerebral hemorrhage as a result of moderate head trauma. In most cases, treatment will be administered under the way of a hematologist.

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Mycoplasma Infection

Mycoplasma infection is respiratory sickness caused by Mycoplasma pneumoniae, a microscopic organism related to bacteria. Anyone can get the disease, but it mainly often affects older children and young adults. Mycoplasma infections occur periodically throughout the year. Extensive community outbreaks may occur at intervals of four to eight years. Mycoplasma disease is most common in late summer and fall. Mycoplasma is spread through contact with droplets from the nose and throat of impure people particularly when they cough and sneeze.

Transmission is thought to need prolonged close contact with an infected person. Extend in families, schools and institutions occur slowly. The infectious period is probably fewer than 10 days and occasionally longer. Typical symptoms contain fever, cough, bronchitis, sore throat, headache and tiredness. A general result of mycoplasma infection is pneumonia. Infections of the center ear also can result. Symptoms may continue for a few days to more than a month. Symptoms usually begin 15 to 25 days after exposure.

The symptoms generally expand slowly, over a time of two to four days. Antibiotics such as erythromycin, clarithromycin or azithromycin are efficient treatment. However, because mycoplasma infection usually resolves on its own, antibiotic action of mild symptoms is not always necessary. At this time, there are no vaccines for the avoidance of mycoplasma infection and there are no reliably effective measures for control. As with any respiratory disease, all people should coat their face when coughing or sneezing.

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Genetic fault Tied to Autoimmune Diseases

Rare variations in a single gene can lead to a wide variety of autoimmune disorders, including diabetes, lupus and rheumatoid arthritis, a new study shows. The gene in question encodes an enzyme called sialic acid acetylesterase or SIAE, which regulates the activity of the protected system’s antibody-producing B cells. About 2 percent to 3 percent of people with autoimmune disorders have defects in the enzyme that allow B cells to run amok and make antibodies that attack the body.

A team led by Shiv Pillai of Massachusetts General Hospital in Charlestown and Harvard Medical School reports online June 16 in Nature. “It’s a seminal paper because it is so applicable to a wide multiplicity of autoimmune diseases, says Judy Cho, a Yale geneticist not associated with the study. The finding suggests that enhancing the enzyme’s activity could help pleasure disease in people with autoimmune disorders.

Previously, Pillai’s group showed that mice missing SIAE develop a lupuslike disease in which high levels of antibodies attack the body’s own proteins. The researchers decided to examine the enzyme in people who, like the mice, make high levels of autoimmune antibodies. “One hundred percent, I was sure that we would find nothing,” Pillai says.


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