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Andreea Daniela



Immune Irregularities And Autism

According to the latest research, the new treatment target for children with autism may be the immune system. The link between immunity and autism was made some time ago but until now researchers have not been able to prove it. Studies performed on mice by researchers at the California Institute of Technology (Caltech) have shown that immune system abnormalities are associated with autism spectrum disorder. The work, which will be published this week in Proceedings of the National Academy of Sciences (PNAS), was based on  epidemiological studies that have shown that maternal infection during the first trimester of pregnancy leads to behavioral disorders such as autism spectrum disorders.



To implement and to verify this fact, researchers have  infected female mice to simulate the immune response that would be triggered by a viral infection. The result was that the offspring born from infected mothers had behavioral problems  autism-like. It was found that the offspring had a different behavior than usual mice, that is they prefered to play alone rather than interacting with other mice, were communicating less.

Furthermore, researchers have analyzed the immune system of mice and found that abnormalities occurring in mice born from infected mothers during pregnancy are similar to those seen in children with autism. The change observed was decreased levels of regulatory T lymphocytes. What is even more interesting is that researchers were able to correct the autistic behavior by transplantation of bone marrow in mice. Therefore, by correcting immune system abnormalities could improve autistic behavior . But what researchers do not know yet is whether bone marrow transplant or stem cells are those that to correct autism. Although the link between autism and immune system abnormalities was found in experiments on mice, researchers say this can not yet be extrapolated to humans. However, further works on autism are  under research.

Future studies aim to link between autism and microbiota, gastrointestinal microbial flora. Autism is a neurodevelopmental disorder characterized by impairment in social development, communication and repetitive behavior. These behavioral problems of children are usually seen by parents  until the age of 3 years. It may happen that children develop normally and then  autistic behavior occur. Although autism is a disease that does not heal, there have been cases where children have been recovered. Genetic factors play  an important role in autism, but there are also other factors that have been incriminated, such as abnormal immunity, vaccines, pesticides, etc.. Lately, special attention was given to the immune system and, although further studies are necessary,  it seems this is the new target in the management of autism.



According to a study published in The New England Journal Of Medicine, targeted therapy with MEK inhibitors improved survival in patients with BRAF-mutated melanoma. So far studies have shown that only ipilimumab, a monoclonal antibody, and vemurafenib, a BRAF inhibitor, prolonged survival of patients with metastatic melanoma. Recently, another drug, trametinib (MEK inhibitor) was shown to prolong survival in BRAF-mutated melanoma.

Researchers conducted a randomized, controlled, phase 3  clinical trial, in which 1022 patients were included initially from 103 centers worldwide. Following investigations, only 322 were eligible, that is they had BRAF V600E and V600K mutations present. Also, another eligibility criterion was stage melanoma: the study included only patients with stage IIIC and IV melanoma skin. Demographic characteristics of patients included in the study were related to  age, male gender, skin melanoma extension, presence of metastases, lactate dehydrogenase level, etc.. They were divided randomly into two study groups: first group (214 patients) received oral trametinib and the second (108) received intravenous chemotherapy consisting of either dacarbazine or paclitaxel every 3 weeks. Side effects occurred in approximately 15% of patients in each study group.

The adverse effects of patients who received trametinib, include diarrhea, rash, peripheral edema and dermatitis acneiform. In 14 patients in group trametinib were observed adverse cardiac effects (decreased ejection fraction or ventricular dysfunction). 2 patients who received trametinib were excluded from the study due to severe cardiac side effects. The most common adverse reactions in patients who received chemotherapy were the gastrointestinal (nausea, constipation, vomiting), fatigue and alopecia.



Trametinib is an inhibitor of mitogen-activated protein kinase. Trametinib specifically binds MEK1 and MEK2,  which are involved in the MAP kinase pathway , and inhibits cancer cell proliferation. Vemurafenib is a BRAF inhibitor approved by FDA in August 2011 to treat metastatic melanoma. In clinical studies, vemurafenib was associated  to prolong survival of patients with BRAF-mutated metastatic melanoma. It seems that both agents improve survival in patients with metastatic melanoma compared with chemotherapy. However, the results of a previous study shows that vemurafenib is  superior to trametinib.  90% of patients treated with vemurafenib had some tumor regression, while only 74% of patients  treated with trametinib had tumor regression . Also, the objective response rate was 48% for vemurafenib while for trametinib was only 22%. However, there  have been reported treatment-related squamous-cell carcinomas among patients who received vemurafenib. This side effect may be due to the fact that BRAF inhibitor stimulates proliferation of skin lesions. Although both drugs appear to be useful in prolonging survival of metastatic melanoma patients, future studies to include those two will show which is best.


New Therapy Overcomes Drug-Resistant Leukemia

Researchers at The Institute of Cancer Research (ICR) in London made a new discovery that may represent a new treatment for patients with acute myeloid leukemia. Researchers discovered a new drug that can block tumor proliferation and prevent from resistance development of cancer cells.

FLT3 gene  mutation is encountered in acute leukemia with poor prognosis. The treatment of this sever forms is often ineffective because cancer cells develop resistance. Normally, FTL3 gene is involved in cell proliferation, but in patients with leukemia, FTL3 mutations cause a chaotic and uncontrolled replication of malignant cells. While drugs which are blocking the protein produced by FTL3 gene are available, cancerous cells become resistant to this drugs, making the treatment ineffective.

In order to prevent this events, scientists developed a “double hit drug”, which is blocking, on the one hand, the product of FTL3 gene and on the other hand is targeting another key protein called Aurora kinase. Aurora kinase present elevated levels in many cancer types and it was observed that is causing errors during cell division. Study of The Institute of Cancer Research (ICR) in London, funded by Cancer Research UK and Breakthrough Breast Cancer, had positive results: half of the mice treated with this drug had complete remission of the disease. Therefore, they are thinking about  introducing  this new drug in clinical trials to prove efficacy in humans.

Acute Myeloid Leukemia

Acute Myeloid Leukemia

Acute myeloid leukemia represents 80% acute leukemias in adults. Acute myeloid leukemia is characterized by uncontrolled proliferation of myeloid cells, bone marrow being occupied by cancer cells that interfere with normal production of blood cells. This events explain the signs that occur in people with acute myeloid leukemia: anemia (low red blood cells count), neutropenia (low neutrophil counts) and thrombocytopenia (low platelet count). Symptoms occurring in patients with acute myeloid leukemia are asthenia, fatigue, bruising (even after minor lesions), dyspnea, infections.

FTL3 gene encodes a protein called FTL3 (Fms-like tyrosine kinase 3) with a receptor role that is  found on the surface of hematopoietic progenitor cells. It also called CD135 and plays an important role in oncogenesis, because mutations of CD135 are promoting malignant cell development (is a protooncogene). The most common mutations of FTL3  associated with acute myeloid leukemia are represented by  internal tandem duplications.

So far, many treatments schemes that include FTL3 inhibitors, such as sunitinib, sorafenib, midostaurin, have been tried, but the results were not promising. Lead author Dr. Spiros Linardopoulos, leader of the Cancer Drug Target Discovery Team at The Institute of Cancer Research, said that there was a great interest these FTL3 inhibitors, but their effectiveness was limited because cancer cells have developed resistance due to mutations. He also added that the new drug may be a solution not only for patients aged over 60 years who can not manage chemotherapy, but also for those with relapses.


Multiple Sclerosis Gene Variant Role Discovered

Researchers at Oxford University have identified the role of a gene variant in multiple sclerosis. The study was led by a team from Oxford University, along with German, Danish and U.S. colleagues, and published in the journal Nature.

The discovery emerged by analyzing the human genome. Researchers have focused mainly on the analysis of TNFRSF1A variant gene, a  gene associated with multiple sclerosis development. After molecular analysis, researchers were able to demonstrate that this gene variant causes a short form of the TNFR1 protein. TNFR1, or p55 or the CD120 is the receptor for TNF alpha and TNF beta. After binding of TNF alpha to TNFR1 apoptosis is triggered, ie programmed cell death. Shortened form of this protein does not allow binding of TNF alpha. Medications used to treat autoimmune diseases,  inflammatory bowel disease and rheumatoid arthritishave the same mechanism of action. These drugs, monoclonal antibodies such as Infliximab, Adalimumab and Etanercept, prevents TNF alpha-receptor binding. Although these drugs are effective in treating autoimmune diseases, the researchers found no explanation why MS does not respond to such treatment.Dr Calliope Dendrou, one of the joint first authors of the paper from the Nuffield Department of Clinical Neurosciences at Oxford University, said: ” ‘Had we known this prior to the clinical trial of TNF blockers in MS patients, this could have helped to predict the poor outcome.”

Multiple Sclerosis

Multiple Sclerosis

Professor Lars Fugger of the Nuffield Department of Clinical Neurosciences at Oxford University, said that it is extremely important to understand the biological details of a gene variant. Once these details understood, researchers can figure out which patients respond to treatment and who not. Also, Professor Lars Fugger also said that while TNFRSF1A gene variant is associated with a moderate risk of developing multiple sclerosis, drugs that mimic the effect of the variant gene have a  much higher impact.

Multiple sclerosis is a chronic autoimmune inflammatory disease of the central nervous system. Multiple sclerosis  is more common in young people, especially women, and it evolves with neural multifocal demyelination and the appearance of plaques of MS. It is a condition that develops gradually with periods of flares and periods of calm. MS patients have visual disturbances, sensory disturbances (paresthesia), motor disorders (paresis), progressive muscular atrophy, etc.. Also it can occur cerebellar disorders such as ataxia, impaired balance and coordination (intentional shaking). Other symptoms may be linked to speech: MS patients may have dysarthria, slow speech. Symptoms may even  go to seizures when sclerosis plaques  affects the cortex. MS is not curable, there is only symptomatic treatment.


    Myasthenia Gravis – Diagnosis And Treatment

    Myasthenia gravis is an immunologically mediated disease in which antibodies are directed against the acetylcholine receptor, causing disturbances in the functionality of acetylcholine receptors and in neuromuscular transmission, leading to muscle fatigue. Muscle fatigue can become pseudo-paralytic, with transient paresis which improve at rest and anticholinesterase medication.

    There are two clinical forms, cephalic or superior form and generalized form. In most cases, the disease begins at the cephalic muscles, especially in the eye muscles, and for 15% of patients symptoms are limited to this level (ocular myasthenia). Bulbar muscles is then affected and generally within about three years disease spreads to other muscle groups.

    Myasthenia Gravis Diagnosis

    The clinical diagnosis of myasthenia gravis is not difficult in typical cases. It is easier in bulbar forms of the disease, when oculo-bulbar clinical signs are persistent. Beside this signs appear skeletal muscle fatigue, which is more pronounced in the second part of the day and is relieved by rest. An important step in diagnosis of myasthenia gravis is the evidence that fatigue is caused by effort. The key element in the diagnosis of myasthenia gravis is improvement of  deficits after administration of anticholinesterase medication.

    Edrophonium test

    In myasthenia gravis patients, the number of acethylcholine receptors at the neuromuscular joint is low, resulting a   decreased interaction between acethylcholine and its receptor. Acethylcoline is metabolized by an enzyme called acetylcholinesterase. Pharmacologic inhibition of acetylcholinesterase will increases the concentration acethylcoline, improving muscle contraction. Edrophonium is a short-acting anticholinergic that improves muscle fatigue in myasthenia gravis patients.

    For this test is needed a dose of 1 mg of a total dose of  10 mg of edrophonium solution, administered intravenously. If no response is noted,  is injected the rest of the dose (9 mg). Bradycardia may occur due to excessive cholinergic stimulation of the heart and for this reason this test should be combined with atropine.

    Myasthenia Gravis Diagnosis

    Myasthenia Gravis Diagnosis

    Edrophonium test has a low sensitivity in ocular form of myasthenia gravis and may present both false-positive and false-negative results. Other disease such as amyotrophic lateral sclerosis and cavernous sinus lesions may have a positive result at this test.

    Combination between edrophonium test, electromyography and ocular tonography increase the chance of diagnosis in ocular form of the disease.

    Anti-acetylcholine receptor antibodies

    Anti-acetylcholine receptor antibodies are useful in diagnosing myasthenia gravis . This antibodies are present in 90% of patients with generalized form of myasthenia gravis and in 50-70% of patients with ocular form of the disease MG.

    Other tests useful in myasthenia gravis diagnosis are represented by CT and MRI (especially in diagnosing thymus abnormalities), electromyography and ice pack testing (useful in diagnosing ocular form of the disease).

    Myasthenia Gravis Treatment

    Pharmacological therapy in myasthenia gravis include anticholinesterase medication and immunosuppressive therapy.

    Anticholinesterase Medication

    These drugs inhibit acetylcholinesterase, allowing  a longer interaction between acetylcholine and its receptor. The most used drugs in this class are:

    • Pyridostigmine (Mestinon) is the most commonly used, being considered first-line drug in the treatment of myasthenia gravis. Can be administered orally, has a long half-life time and reduced cholinergic side effects. Drug effects start at 15-30 minutes after administration, reach a maximum at 1-2 hours, and the effect lasts 3-5 hours. Most patients require 5-6 tablets per day.
    • Prostigmine or neostigmine has a long duration of action and can be administered both orally and intramuscularly at varying intervals, according to patient response. It has a shorter but stronger duration of action than mestinon and cholinergic side effects are more frequently.
    • Ambenomium chloride (Mytelase) is useful in generalized form of the disease. It is the most efficient drug used in resistant forms of myasthenia gravis to other anticholinergic drugs.
    Myasthenia Gravis Treatment

    Myasthenia Gravis Treatment

    Immunosuppressive therapy

    Immunosuppressive therapy is including corticosteroids and other immunosuppressive drugs.

    • Corticosteroids are part of the common treatment for myasthenia gravis, considering the autoimmune nature of the disease. Are used especially in the ocular form of the disease and in unresponsive  bulbar and generalized forms. At the beginning of the treatment, corticosteroids are worsening the symptoms over a period of 10-14 days. It was observed that under treatment with corticosteroids, areas of thymic hyperplasia have disappeared or their number has reduced.
    • Other immunosuppressants. Are effective in unresponsive cases to corticosteroids, in unresponsive cases to other therapies or in cases that did not have a favorable response after thymectomy (surgical removal of the thymus). The most common drugs are: azathioprine, cyclophosphamide, 6-mercaptopurine and cyclosporine.


    Plasmapheresis is useful in myasthenia gravis especially in resistant forms, in preoperative preparation for thymectomy, in unimproved cases after surgery and in myasthenic crisis. Clinical improvements are temporary, for a period of 4-6 weeks.

    Surgical Treatment

    Thymectomy, surgical removal of the thymus is considered the most effective method of treatment in myasthenia gravis. Patients with thymoma present a more pronounced muscular fatigue. Although thymoma metastases rarely, by local invasion may give serious complications. Pure ocular form of myasthenia gravis is not usually an indication for thymectomy. After thymectomy, approximately 80% of patients are asymptomatic under medication or achieve complete remission in 5 years after thymectomy.


    Male Contraceptive Gel

    New preliminary findings show promise in the field of male contraceptives, through the use of a new contraceptive gel. If further studies establish that the gel is effective, male patients will have an alternative to condoms and vasectomy. The first studies show that the topical application of the new gel decreases the number of sperm cells but does not completely eliminate them. This means that the risk of pregnancy is only reduced, not excluded.

    The gel, called Nestorone, is a combination of synthetic progestin and testosterone. This is the first time that this combination has been used under the form of a topically applicable gel. Prior studies included the use of the combination as a patch or even in an injectable form.

    According to Dr. Christina Wang, the lead author of the study, and her fellow co-researchers, supplementary testing is needed before the new gel can be available for the large public.  Dr. Joseph Alukal from the NYU Langone Medical Center believes that most men will be more than interested in using the new contraceptive method, as most men are worried about unexpected and unwanted pregnancy. Dr. Alukal is not part of the research team.

    The current research has been presented in Houston, at the annual meeting of the Endocrine Society. The gel was tested on two different locations. The testosterone component was applied on the arm whilst the progestin component was applied on the abdomen. Both gels were applied on a daily basis over a six month period. 56 male patients participated in the study. The study used three types of gels: two of the gels contained testosterone and different doses of synthetic progestin whilst the third gel contained testosterone in a combination with placebo gel.

    Male Contraceptive Gel

    Male Contraceptive Gel

    According to the Mayo Clinic’s website, the normal concentration of sperm cells per millimeter is above 15 million. 89 percent of the patients who received the gels containing both active components have shown a sperm count of under 1 million per millimeter whilst only 23 percent of the patients using the gel containing placebo have shown the same modification. 78 percent of the patients using the gel containing the active combination have shown a complete decrease of sperm cells per millimeter, compared to only 23 percent of the patients using the gel containing placebo. Dr. Christina Wang explained that the combination of testosterone and synthetic progestin inactivates the hormones that control the production of sperm cells.

    There are currently no known long-term side effects, other than a moderate acne, seen in 21 percent of the participants. Dr. Wang speculates that a decrease in the amount of testosterone in the gel might reduce this side effect. Dr. Alukal questions the reversibility of the effects.

    Alongside further testing of the drug, Dr. Wang has planned early phase testing that will involve the use of dimethandrolone – a male hormone with higher potential than testosterone.

    For the time being, the only available contraceptive methods for male patients are condoms and the vasectomy surgical procedure.


     Peripartum Cardiomyopathy

    Researchers at Beth Israel Deaconess Medical Center (BIDMC) have made new discoveries regarding peripartum cardiomyopathy. The researchers found that there is a critical connection between this disease and preeclampsia or pregnancy hypertension. Peripartum cardiomyopathy is a form of left ventricular systolic dysfunction that occurs in the last month of pregnancy or during the first 5 months postpartum. The incidence of this disease varies from 1/3000 to 1/10000, but this disease can go unnoticed due to the volume overload in the last period of pregnancy. Peripartum cardiomyopathy etiology  is incomplete  elucidated. It seems that some inflammatory factors, nutritional factors, and or infectious factors are involved. The role of  immune response during pregnancy has been also questioned, which is also implied in the occurence of  preeclampsia (gestational hypertension).

    Pregnancy Hypertension

    Pregnancy Hypertension

    Symptoms of peripartum cardiomyopathy are due the decreased heart pump function (dyspnea, tachycardia, leg edema, cough, palpitations, thromboembolic events). Most women recover spontaneously, but in some cases it progresses to heart failure requiring transplantation. Complications in later stages may lead to death by congestive heart failure, systemic embolism, ventricular tachyarrhythmias. It should be noted that recurrence of cardiomyopathy is possible in later pregnacies. Also, the prognosis is worse if the recovery of ventricular function was not complete.

    Senior author Zoltan Arany, MD, PhD, investigator year the Cardiovascular Institute at BIDMC and Assistant Professor of Medicine at Harvard Medical School, noted that before this condition could not be fully understood considering that it occurs in healthy women . ” The majority of women who develop this condition are otherwise healthy, even active,” said Dr.Arany. In addition, stressors that can affect the health of pregnant women are predominant in the first trimester, and not in the last when it occurs this  form of  cardiomyopathy .

    Researchers found that peripartum dilated cardiomyopathy is actually a vascular disease. The discovery was made in collaboration with Several members of BIDMC’s Department of Obstetrics and Gynecology, led by co-first author Sarosh Rana, MD. Researchers found that peripartum dilated cardiomyopathy is caused by excess anti-angiogenic signaling. They also have found that an important role is played by high expression of SFLT1, a factor involved in the development of preeclampsia, during late pregnancy. In addition, it was also found that women diagnosed with peripartum cardiomyopathy had increased levels of anti-angiogenic factors in their blood.

    Now researchers are trying to determine why some pregnant women manage well with increasing levels of anti-angiogenic factors, characteristic of the last period of pregnancy, and others do not. They also hope to find a cure for this disease.


    Diets Rich In Beta-Carotene A Potential Health Risk

    Researchers at Ohio State University have found that diets rich in beta-carotene can have negative effects. Beta-carotene is actually a red-orange antioxidant pigment that is found in abundance in fruits and vegetables. This antioxidant is called provitamin A because it is converted in the body into vitamin A,  which has many roles, such as in vision, skin integrity, immunity etc. After its absorbtion in the gut, beta-carotene is clived into two molecules of vitamin A. However, when the body has enough vitamin A, the formation of new molecules is inhibited. So there are mechanisms that prevent hypervitaminosis A. In addition, excess carotene is stored in fatty tissues of the body. It should be noted that excess beta-carotene also cause orange discoloration of the skin which is reversible. Beta-carotene is cleaved in two modes, symmetric and asymmetric. When cleaved symmetrically it forms two molecules of retinal that are then converted into retinol (vitamin A) and retinoic acid. Asymmetric cleavage of beta-carotene  leads to the formation of two asymmetric products, apocarotenal. Asymmetric cleavage causes a decrease in retinoic acid.

    Scientists believe that too much beta-carotene can lead to negative health effects. This finding may explain the result of an earlier trial in which patients with supplementation of beta-carotene developed lung cancer. Then it was found that beta-carotene supplementation in smokers increases the risk of lung cancer.
    Even if final research conclusions are not yet available scientists recommend moderate consumption of beta -carotene. What researchers now aim to see is if these substances that act as antivitamin A are determined by environmental factors. It seems that these drugs block the action of vitamin A  and disrupt the whole metabolism.

    Harrison and colleagues, Robert Curley, professor of medicinal chemistry and pharmacognosy, and Steven Schwartz, professor of food science and technology, Both at Ohio State, have created synthetic molecules that mimic derivatives of beta-carotene. Of the 11 synthetic molecules created, 5 functioned as inhibitors of vitamin A. They found that these molecules do not activate retinoic acid receptors, as does vitamin A, but rather inhibit them. Therefore, these molecules act as antagonists of vitamin A. Previous studies have suggested that pollution and smoking can lead to increased production of these compounds. Earl Harrison, Dean’s Distinguished Professor of Human Nutrition at Ohio State and lead author of the study, said that these components are found in food and can represent the negative side of beta-carotene. He added that more studies are needed to certify the clear origin of these substances.


    Teen Brain Networks Associated With Drug Abuse

    Researchers at the University of Vermont have discovered why some teens are more likely to use drugs and alcohol than their peers of the same age. The study was recently published in the journal Nature Neuroscience. Using a functional MRI, researchers were able to identify the brain networks associated with such behaviors. According to the researchers, a diminished activity in these networks is correlated with an impulsive behavior. It seems that there are some differences between the various networks of the prefrontal cortex that makes young people having deviant behavior (for alcohol, drugs, etc.).

    Teen Drugs

    The study results, which implied 1896 14-year-olds,  suggests that such  behaviors are caused by peculiarities of the brain. In other words, susceptibility to drugs and alcohol is driven by activity in brain networks responsible for this behaviour. A teenager prone to drug use will be tempted at some point to try these substances. Dr.Garavan, who served as the principal investigator of the Irish component of this large European research project, called IMAGEN, said: “The differences in tissue networks seem to precede drug use. ” He added that testing low activity of these circuits in the brain may serve as a marker for potential drug use.

    Also, researchers found the brain circuitry responsible for ADHD. ADHD, attention deficit hyperactivity disorder, is a disorder of growth that occurs more frequently in boys. Studies have shown that ADHD is in most cases genetic in nature. Moreover,  children with ADHD  may have language delay and are more prone to depression or anxiety. It was also found that children with ADHD have a lower volume of brain (especially with greater reduction prefrontal cortex of the left). Because the association of ADHD with antisocial personality disorder, lately has been much discussion of a possible organic connection between ADHD and drug use. Association was done because both behaviors have a common pattern, namely impulsiveness. But researchers have found that networks involved  in ADHD are different from those involved in drugs abuse.

    Teens involved in the study were asked to perform a repetitive task, namely to press a specific button on a keyboard. Those with better inhibitory control could perform this task faster. In this way the researchers identified seven networks in which impulses have been inhibited and 6 networks in which pulses were not inhibited. Dr. Garavani cautions that these two behavioral disorders, drug abuse and ADHD, have the two different regions of the brain substrate. He added theta addiction is a major health problem in western world.



    According to a study published in the American Journal of Human Genetics, psoriasis is caused by rare mutations of the CARD14 gene. The discovery was made by researchers at Washington University School of Medicine in St.. Louis. Psoriasis, affects approximately 3-5% of the population and is a chronic dermatological disease manifested most frequently by erythematous plaques, well-defined and covered by scales. Until recently the cause was not known, but there several triggers have been incriminated , such as trauma, certain drugs or infections, like streptococcic throat infection . It is important to note that psoriasis is inherited in families and that it usually appears during childhood. In addition to skin manifestations, sometimes the condition is accompanied by pruritus and pain. Psoriasis has a significant aesthetic impact. Treatment consists of emollients, vitamin D analogues, retinoids, corticosteroids, phototherapy. In severe cases, when psoriasis is manifested by painful arthritis, the patient may receive methotrexate or immunosuppressive agents.

    Plaque Psoriasis

    Plaque Psoriasis

    In terms of histopathology, psoriasis is characterized by a proliferation of epidermal keratinocytes combined with dermal inflammation . Normally, skin cells have a turn over period of 28 days (they grow and mature gradually ov