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http://www.drmarylupo.com/ Rosacea is sometimes called 'adult acne', but it's not. Over 14million Americans have Rosacea. For most, Rosacea is an embarrassing cyclical condition, coming and going.

Debulking is the surgical removal of part of a malignant tumour which cannot be completely excised, so as to enhance the effectiveness of radiation or chemotherapy. It is used only in specific malignancies, as generally partial removal of a tumor is not considered a worthwhile intervention. Ovarian carcinoma and some types of brain tumor are debulked prior to commencing radio- or chemotherapy. It may also be used in the case of slow growth tumors to shift tumor cells from phase of cell cycle to replicative pool.

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Shy bladder syndrome is a type of phobia in which the sufferers are unable to urinate in the presence of other people such as in a public restroom.

In other words, shy bladder is the fear of not being able to urinate without complete privacy.

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While there is no way for certain to know how many people suffer from paruresis, surveys done over the last several decades indicate that the numbers could range from less than one percent to more than 25 percent of Americans.

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La palmitoiletanolamide (PeaVera, PeaPure, Palmidrol, Achille e altri PEA prodotti rappresenta una rivoluzione nel trattamento del dolore. Si tratta di un efficace analgesico naturale, senza effetti collaterali. La sua azione è stata documentata in molte centinaia di articoli scientifici. Il suo meccanismo è stato scoperto dalla professoressa Rita Levi Montalcini, premio Nobel per la medicina.

Qui è disponibile una breve introduzione su questa sostanza particolare. (Qui Informazioni per i medici) PEA è disponibile in Italia dal 2007 ed è stata classificata dal Ministero della Salute italiano come alimento dietetico per fini medici speciali.

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A stroke is a "brain attack". It can happen to anyone at any time. It occurs when blood flow to an area of brain is cut off. When this happens, brain cells are deprived of oxygen and begin to die. When brain cells die during a stroke, abilities controlled by that area of the brain such as memory and muscle control are lost. How a person is affected by their stroke depends on where the stroke occurs in the brain and how much the brain is damaged. For example, someone who had a small stroke may only have minor problems such as temporary weakness of an arm or leg. People who have larger strokes may be permanently paralyzed on one side of their body or lose their ability to speak. Some people recover completely from strokes, but more than 2/3 of survivors will have some type of disability.

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Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

Severe combined immunodeficiency (SCID) is a life-threatening syndrome of recurrent infections, diarrhea, dermatitis, and failure to thrive. It is the prototype of the primary immunodeficiency diseases and is caused by numerous molecular defects that lead to severe compromise in the number and function of T cells, B cells, and occasionally natural killer (NK) cells. Clinically, most patients present before age 3 months. Without intervention, SCID usually results in severe infection and death in children by age 2 years. A committee of experts, initially sponsored by the World Health Organization (WHO), meets every 2 years with the goal to classify the group of primary immunodeficiency diseases according to current understanding of the pathways that become defective in the immune system.[1] Eight classification groups have been determined, with SCID being one of the best studied. Over the past few decades, the diverse molecular genetic causes of SCID have been identified with progress from studies of the immune system.[2] SCID is considered a pediatric emergency because survival depends on expeditious stem cell reconstitution, usually by bone marrow transplantation (BMT). Appropriate diagnosis is essential because instituting proper treatment is lifesaving. Despite the heterogeneity in the pathogenesis of immune defects, common cutaneous manifestations and typical infections can provide clinical clues in diagnosing this pediatric emergency.[3] Skin manifestations were prevalent in primary immunodeficiency disorders studied in 128 pediatric patients in Kuwait; skin infections were the most prevalent findings, seen in 39 patients (30%), followed by dermatitis in 24 (19%).[4] Skin infections were significantly more prevalent in those with congenital defects in phagocyte number, function, or both, as well as in those with well-defined immunodeficiencies. Dermatitis was evident in all patients with hyper–immunoglobulin (Ig) E syndrome and Wiskott-Aldrich syndrome.[4] Erythroderma of infancy with diffuse alopecia was seen exclusively in patients with SCID disorders, and telangiectasia in patients with ataxia telangiectasia; and partial albinism with silvery gray hair was associated with Chediak-Higashi syndrome. With the advances in BMT and gene therapy, patients now have a better likelihood of developing a functional immune system in a previously lethal genetic disease. However, once an infant develops serious infections, intervention is rarely successful.

A salivary gland stone -- also called salivary duct stone -- is a calcified structure that may form inside a salivary gland or duct. It can block the flow of saliva into the mouth. The majority of stones affect the submandibular glands located at the floor of the mouth. Less commonly, the stones affect the parotid glands, located on the inside of the cheeks, or the sublingual glands, which are under the tongue. Many people with the condition have multiple stones. Salivary Gland Stone Causes and Symptoms Salivary stones form when chemicals in the saliva accumulate in the duct or gland. They mostly contain calcium. The exact cause is not known. But factors contributing to less saliva production and/or thickened saliva may be risk factors for salivary stones. These factors include: dehydration, poor eating, and use of certain medications (such as antihistamines), blood pressure drugs, psychiatric drugs, and bladder control drugs. Trauma to the salivary glands may also raise the risk for salivary stones. The stones cause no symptoms as they form, but if they reach a size that blocks the duct, saliva backs up into the gland, causing pain and swelling. You may feel the pain off and on, and it may get progressively worse. Inflammation and infection within the affected gland may follow. Salivary Gland Stones Diagnosis and Treatments If you have symptoms of a salivary gland stone, your doctor will first check for stones with a physical exam. Sometimes tests may also be ordered, such as X-ray, CT scan, or ultrasound.

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