Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic urticaria is a common condition that can be very disabling when severe. A variety of causes has been reported to induce urticaria, including food, infections, drugs and other factors. In more than 50% of cases of chronic urticaria, however, the cause remains unknown and cannot be ascribed to allergic, physical, environmental or other factors. Although an association between chronic idiopathic urticaria and malignancy has been occasionally reported, such an association remains controversial because it is difficult to demonstrate it is not just coincidental. Here we report the cases of four female patients with occult papillary carcinoma of the thyroid who developed chronic urticaria. In all of these cases, removal of the tumor led to prompt resolution of the urticarial lesions, thus suggesting a pathogenetic relationship between the two. This is the first report of papillary thyroid carcinomas associated with chronic urticaria and highlights how chronic urticaria may be an important cutaneous marker for patients with thyroid carcinoma.
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PMID:Chronic urticaria associated with thyroid carcinoma: report of 4 cases. 1758 8

Plant materials derived from the Aloe plant are used as cosmetic ingredients, including Aloe Andongensis Extract, Aloe Andongensis Leaf Juice, Aloe Arborescens Leaf Extract, Aloe Arborescens Leaf Juice, Aloe Arborescens Leaf Protoplasts, Aloe Barbadensis Flower Extract, Aloe Barbadensis Leaf, Aloe Barbadensis Leaf Extract, Aloe Barbadensis Leaf Juice, Aloe Barbadensis Leaf Polysaccharides, Aloe Barbadensis Leaf Water, Aloe Ferox Leaf Extract, Aloe Ferox Leaf Juice, and Aloe Ferox Leaf Juice Extract. These ingredients function primarily as skin-conditioning agents and are included in cosmetics only at low concentrations. The Aloe leaf consists of the pericyclic cells, found just below the plant's skin, and the inner central area of the leaf, i.e., the gel, which is used for cosmetic products. The pericyclic cells produce a bitter, yellow latex containing a number of anthraquinones, phototoxic compounds that are also gastrointestinal irritants responsible for cathartic effects. The gel contains polysaccharides, which can be acetylated, partially acetylated, or not acetylated. An industry established limit for anthraquinones in aloe-derived material for nonmedicinal use is 50 ppm or lower. Aloe-derived ingredients are used in a wide variety of cosmetic product types at concentrations of raw material that are 0.1% or less, although can be as high as 20%. The concentration of Aloe in the raw material also may vary from 100% to a low of 0.0005%. Oral administration of various anthraquinone components results in a rise in their blood concentrations, wide systemic distribution, accumulation in the liver and kidneys, and excretion in urine and feces; polysaccharide components are distributed systemically and metabolized into smaller molecules. aloe-derived material has fungicidal, antimicrobial, and antiviral activities, and has been effective in wound healing and infection treatment in animals. Aloe barbadensis (also known as Aloe vera)-derived ingredients were not toxic in acute oral studies using mice and rats. In parenteral studies, the LD(50) using mice was > 200 mg/kg, rats was > 50 mg/kg, and using dogs was > 50 mg/kg. In intravenous studies the LD(50) using mice was > 80 mg/kg, rats was > 15 mg/kg, and dogs was > 10 mg/kg. The 14-day no observed effect level (NOEL) for the Aloe polysaccharide, acemannan, in the diet of Sprague-Dawley rats, was 50,000 ppm or 4.1 to 4.6 g/kg day(-1). In a 3-month study using mice, Aloe vera (extracted in ethanol) given orally in drinking water at 100 mg/kg produced reproductive toxicity, inflammation, and mortality above that seen in control animals. Aloe vera extracted in methanol and given to mice at 100 mg/kg in drinking water for 3 months caused significant sperm damage compared to controls. Aloe barbadensis extracted with water and given to pregnant Charles Foster albino rats on gestational days (GDs) 0 through 9 was an abortifacient and produced skeletal abnormalities. Both negative and positive results were found in bacterial and mammalian cell genotoxicity assays using Aloe barbadensis-derived material, Aloe Ferox-derived material, and various anthraquinones derived from Aloe. Aloin (an anthraquinone) did not produce tumors when included in the feed of mice for 20 weeks, nor did aloin increase the incidence of colorectal tumors induced with 1,2-dimethylhydrazine. Aloe-emodin (an anthraquinone) given to mice in which tumor cells had been injected inhibited growth of malignant tumors. Other animal data also suggest that components of Aloe inhibit tumor growth and improve survival. Various in vitro assays also demonstrated anticarcinogenic activity of aloe-emodin. Diarrhea was the only adverse effect of note with the use of Aloe-derived ingredients to treat asthma, ischemic heart disease, diabetes, ulcers, skin disease, and cancer. Case reports include acute eczema, contact urticaria, and dermatitis in individuals who applied Aloe-derived ingredients topically. The Cosmetic Ingredient Review Expert Panel concluded that anthraquinone levels in the several Aloe Barbadensis extracts are well understood and can conform to the industry-established level of 50 ppm. Although the phototoxicity anthraquinone components of Aloe plants have been demonstrated, several clinical studies of preparations derived from Aloe barbadensis plants demonstrated no phototoxicity, confirming that the concentrations of anthraquinones in such preparations are too low to induce phototoxicity. The characterization of aloe-derived ingredients from other species is not clear. In the absence of well-characterized derivatives, biological studies of these materials are considered necessary. The studies needed are 28-day dermal toxicity studies on Aloe Andongensis Extract, Aloe Andongensis Leaf Juice, Aloe Arborescens Leaf Extract, Aloe Arborescens Leaf Juice, Aloe Ferox Leaf Extract, Aloe Ferox Leaf Juice, and Aloe Ferox Leaf Juice (ingredients should be tested at current use concentrations). In Aloe-derived ingredients used in cosmetics, regardless of species, anthraquinone levels should not exceed 50 ppm. The Cosmetic Ingredient Review Expert Panel advised the industry that the total polychlorobiphenyl (PCB)/pesticide contamination of any plant-derived cosmetic ingredient should be limited to not more than 40 ppm, with not more than 10 ppm for any specific residue and that limits were appropriate for the following impurities: arsenic (3 mg/kg maximum), heavy metals (20 mg/kg maximum), and lead (5 mg/kg maximum).
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PMID:Final report on the safety assessment of AloeAndongensis Extract, Aloe Andongensis Leaf Juice,aloe Arborescens Leaf Extract, Aloe Arborescens Leaf Juice, Aloe Arborescens Leaf Protoplasts, Aloe Barbadensis Flower Extract, Aloe Barbadensis Leaf, Aloe Barbadensis Leaf Extract, Aloe Barbadensis Leaf Juice,aloe Barbadensis Leaf Polysaccharides, Aloe Barbadensis Leaf Water, Aloe Ferox Leaf Extract, Aloe Ferox Leaf Juice, and Aloe Ferox Leaf Juice Extract. 1761 30

All chemotherapy agents can cause hypersensitivity reactions, which have limited the used of critical drugs in very sick patients for fear of inducing a more severe reaction and possibly death. The choice of an alternative chemotherapy regimen is often limited by tumor sensitivity and, because of the increasing number of cancer survivors, exposure to multiple courses of the same or similar chemotherapy agents. Increased exposures lead to sensitization and to hypersensitivity reactions in an increasing patient population. The need to offer first line therapy after cancer recurrence has spurred the clinical development of rapid desensitizations, which allow patients to be treated with medications to which they have presented hypersensitivity reactions. Desensitization protocols are available to treat hypersensitivity reactions to most chemotherapy agents including taxenes, platinums, doxorubicin, monoclonal antibodies and others, by gradual re-introduction of small amounts of drug antigens up to full therapeutic doses. Candidate patients include those who present mild to severe type I hypersensitivity, mast cell/IgE dependent, reactions during the chemotherapy infusion or shortly after. Symptoms include pruritus, flushing, urticaria, angioedema, respiratory and gastrointestinal distress, changes in blood pressure including hypotension, and shock with anaphylaxis. Associated musculoskeletal symptoms and pain can be present in patients reacting to taxenes as in anaphylactoid reactions, in which mast cell/IgE mechanisms cannot be demonstrated. There is now strong evidence that anaphylactoid reactions are amendable to treatment with the same rapid desensitization protocols as for type I hypersensitivity reactions. Initial rapid desensitizations should only be performed in settings with one on one nurse-patient care and where resuscitation personnel and resources are readily available. Temporary tolerization is achieved in a few hours. After the first desensitization, standard protocols are available for safe, repeated desensitizations in outpatient settings with similar conditions, which not only provides flexibility, but allows patients to remain in clinical studies. Breakthrough symptoms are less severe than the initial hypersensitivity reaction in all series reviewed, and deaths have not been reported. The aim of this review is to familiarize the medical community with the type of hypersensitivity reactions amendable to rapid desensitization and to review protocols for chemotherapy desensitization that can be used for most chemotherapy agents. Few studies have measured the cancer response to the chemotherapy agents delivered through rapid desensitizations. One patient population in which 26 patients were desensitized to carboplatin and 16 to paclitaxel had similar rates of remission as for non-desensitized patients. Education of nurses, pharmacists, oncology and allergy specialists will lead to the universal use of rapid desensitization protocols for all cancer patients with hypersensitivity reactions to chemotherapy agents. Basic research is needed to uncover the cellular and molecular mechanisms underlying the temporary tolerization induced by rapid desensitization, so that pharmacological interventions can improve its safety and efficacy.
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PMID:Rapid desensitization of hypersensitivity reactions to chemotherapy agents. 1869 Sep 34

Dysfunction of the NF1 gene coding a RAS GAP is the major cause of neurofibromatosis type 1 (NF1), whereas neurofibromatosis type 2 (NF2) is caused primarily by dysfunction of the NF2 gene product called merlin that inhibits directly PAK1, an oncogenic Rac/CDC42-dependent Ser/Thr kinase. It was demonstrated previously that PAK1 is essential for the growth of both NF1 and NF2 tumors. Thus, several anti-PAK1 drugs, including FK228 and CEP-1347, are being developed for the treatment of NF tumors. However, so far no effective NF therapeutic is available on the market. Since propolis, a very safe healthcare product from bee hives, contains anticancer ingredients called CAPE (caffeic acid phenethyl ester) or ARC (artepillin C), depending on the source, both of which block the oncogenic PAK1 signaling pathways, its potential therapeutic effect on NF tumors was explored in vivo. Here it is demonstrated that Bio 30, a CAPE-rich water-miscible extract of New Zealand (NZ) propolis suppressed completely the growth of a human NF1 cancer called MPNST (malignant peripheral nerve sheath tumor) and caused an almost complete regression of human NF2 tumor (Schwannoma), both grafted in nude mice. Although CAPE alone has never been used clinically, due to its poor bioavailability/water-solubility, Bio 30 contains plenty of lipids which solubilize CAPE, and also includes several other anticancer ingredients that seem to act synergistically with CAPE. Thus, it would be worth testing clinically to see if Bio 30 and other CAPE-rich propolis are useful for the treatment of NF patients.
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PMID:CAPE (caffeic acid phenethyl ester)-based propolis extract (Bio 30) suppresses the growth of human neurofibromatosis (NF) tumor xenografts in mice. 1872 24

The nature of the biological relationships between cancers and allergies has intrigued researchers and health care providers for five decades. Three hypotheses have been proposed: antigenic stimulation predicts positive associations between cancers and allergies (i.e., allergy sufferers are more likely to get cancer), whereas immunosurveillance and prophylaxis predict inverse associations (i.e., allergy sufferers are less likely to get cancer). Immunosurveillance predicts inverse associations for cancers of all tissues and organ systems, and prophylaxis predicts inverse associations specifically for cancers of tissues and organ systems that interface with the external environment. To comparatively evaluate these hypotheses, we comprehensively reviewed the literature on cancer and allergies. We located 148 papers published from 1955 through 2006 that reported results of 463 studies of relationships between patients' histories of 11 specific allergies and cancers of 19 tissues and organ systems, and 183 studies of patients' histories of multiple allergies in relation to various types/sites of cancers. Analyses of these studies revealed that (1) frequencies of positive, inverse, and null allergy-cancer associations differed considerably among cancers of different tissues and organ systems; (2) more than twice as many studies reported inverse allergy-cancer associations as reported positive associations; (3) inverse associations were particularly common for cancers of the mouth and throat, brain glia, colon and rectum, pancreas, skin, and cervix but (4) particularly rare for cancers of the breast, prostate, and brain meninges, and for myeloma, non-Hodgkin's lymphoma, and myelocytic leukemia; (5) lung cancer was positively associated with asthma but inversely associated with other allergies; (6) inverse associations with allergies were more than twice as common for cancers of nine tissues and organ systems that interface with the external environment compared to cancers of nine tissues and organ systems that do not interface with the external environment; and (7) eczema, hives, and allergies to animal dander and food were most frequently inversely associated with cancers of tissues that interface with the external environment. Taken together, these results are more consistent with the prophylaxis hypothesis than the two alternatives. IgE is a widespread and ancient immunoglobulin isotype in mammals, occurring among all known marsupials, monotremes, and eutherians. The IgE system and its associated allergy symptoms may serve a common protective function: the rapid expulsion of pathogens, dangerous natural toxins, and other carcinogenic antigens before they can trigger malignant neoplasia in exposed tissues.
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PMID:Allergies: their role in cancer prevention. 1914 35

Reported herein is an autopsy case of mast cell leukemia, a rare form of systemic mastocytosis, complicated with portal hypertension. A 52-year-old woman presented with urticaria-like skin symptoms, anemia, and thrombocytopenia. Atypical mast cells (CD2+, CD25+, CD117+) with toluidine blue metachromasia were found in the peripheral blood and on bone marrow aspiration smears. Chemotherapy with cytosine arabinoside and idarubicin was ineffective and the patient died of multi-organ failure with rapidly progressing hepatosplenomegaly and large-volume ascites 3 months after admission. At autopsy the bone marrow, spleen, liver, and lymph nodes were extensively infiltrated by atypical tumor cells with occasional bi- or multi-lobated nuclei. They were positive for mast cell tryptase and possessed an activating mutation of the c-kitgene (D816V). Ascites (2200 mL) and non-ruptured esophageal varices with submucosal hemorrhage indicated the presence of severe portal hypertension. Although there was no evidence of liver cirrhosis, the hepatic sinusoids were clogged with tumor cells, with a tendency to be more severe in the perivenular areas, and the lumens of central veins were obliterated by tumor cell infiltration. The present case demonstrates that non-cirrhotic portal hypertension due to blocking of sinusoidal and venous flow could be a serious complication in mast cell leukemia.
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PMID:Mast cell leukemia with rapidly progressing portal hypertension. 1988 34

We present a case of cholangiocellular carcinoma accompanied with moderate blood eosinophilia. A 65-year-old man was admitted to our hospital because of widely spread skin eruption like urticaria with severe itching. Laboratory findings on admission showed leukocytosis (WBC 10,600/mm3) with moderate eosinophilia (eosinophils 3,678/mm3). Stool examination for ova and parasites was negative. Bone marrow aspiration revealed almost normal appearance. Chest X-ray was normal. Abdominal CT scan revealed a hepatic tumor (6.8 cm in diameter) in the left hepatic lobe. Needle biopsy of the hepatic tumor revealed an adenocarcinoma. We performed left hepatectomy with lymph node dissection without a bile duct reconstruction. The tumor was mass forming type accompanied with intra bile ductal growth in macroscopically. Pathological diagnosis was cholangiocellular carcinoma. After removal of the hepatic tumor, peripheral blood eosinophil counts fell down and cutaneous lesion disappeared immediately. Since the surgery, the patient had no sign of recurrence for 4 years.
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PMID:[A case of cholangiocellular carcinoma accompanied with peripheral blood eosinophilia which improved by removal of the hepatic tumor]. 2122 18

New treatments are required for rituximab-refractory follicular lymphoma (FL). In the present study, patients with rituximab-refractory FL received 8 weekly infusions of ofatumumab (CD20 mAb; dose 1, 300 mg and doses 2-8, 500 or 1000 mg; N = 116). The median age of these patients was 61 years, 47% had high-risk Follicular Lymphoma International Prognostic Index scores, 65% were chemotherapy-refractory, and the median number of prior therapies was 4. The overall response rate was 13% and 10% for the 500-mg and 1000-mg arms, respectively. Among 27 patients refractory to rituximab monotherapy, the overall response rate was 22%. The median progression-free survival was 5.8 months. Forty-six percent of patients demonstrated tumor reduction 3 months after therapy initiation, and the median progression-free survival for these patients was 9.1 months. The most common adverse events included infections, rash, urticaria, fatigue, and pruritus. Three patients experienced grade 3 infusion-related reactions, none of which were considered serious events. Grade 3-4 neutropenia, leukopenia, anemia, and thrombocytopenia occurred in a subset of patients. Ofatumumab was well tolerated and modestly active in this heavily pretreated, rituximab-refractory population and is therefore now being studied in less refractory FL and in combination with other agents in various B-cell neoplasms. The present study was registered at www.clinicaltrials.gov as NCT00394836.
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PMID:Ofatumumab monotherapy in rituximab-refractory follicular lymphoma: results from a multicenter study. 2238 54

Octreotide is widely used as medical therapy for acromegaly. It is known to markedly reduce growth hormone levels, improve symptoms and reduce tumor size. Common side effects include gastrointestinal symptoms, hepatobiliary disorders, dizziness, headaches, bradycardia, hyperglycemia or hypoglycemia and thyroid dysfunction. Although urticaria, allergy/hypersensitivity reactions and anaphylaxis have been noted as possible adverse reactions, there is a lack of data showing a causal relationship between octreotide and hypersensitivity reactions and there is no information on management when continued use of this medication is essential. We now report a case of a 60 year old male with acromegaly who had presented with a cutaneous hypersensitivity reaction to octreotide. In addition he failed treatment with surgery, radiation, and dopamine agonist and could no longer afford to continue treatment with pegvisomant. The patient underwent desensitization treatment for his octreotide allergy and was able to resume treatment without any further side effects. We believe this case represents the first report of successful desensitization treatment for octreotide allergy in an acromegalic patient.
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PMID:Desensitization treatment for hypersensitivity reaction to octreotide in an acromegalic patient. 2261 55

Paul Ehrlich, a German scientist, discovered what is known as the mast cell in the late 1800's, which has proven to be an important player in the immune system of vertebrates. Mast cells are ubiquitous throughout the tissues of the human body and play numerous roles, both beneficial and destructive. We know they are important in our army of immunity warrior cells, which defend us against viruses, bacteria and parasitic invaders. They are also very well known for the havoc they wreak, causing uncomfortable symptoms due to their release of histamine and other mediators which cause the all too familiar itching, sneezing, urticaria and rhinorrhea of allergic responses. Mast cell activities are diverse and include painful inflammatory reactions in autoimmune conditions such as rheumatoid arthritis. In the gastrointestinal system, mast cells are implicated in diverse actions such as increased gastric acid secretion, polyp formation and uncomfortable conditions such as Irritable Bowel Syndrome. The role of immunology and mast cells in these areas is intriguing but less well understood than their role in allergic responses. Because mast cells have been implicated in both physiologic as well as pathogenic processes, they have been the subjects of avid study. Review of the current literature on mast cell biology reveals that there are many studies of their presence within the tumor microenvironment and evidence, which supports mast cell influence on tumor angiogenesis, tumor invasion, and immune suppression. The studies reviewed in this article concentrate largely on mast cells in human GI malignancies. This review also provides background information regarding mast cells, such as their origination, their location within the body, how they are activated and how they function as mediators.
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PMID:Mast cells, disease and gastrointestinal cancer: A comprehensive review of recent findings. 2294 44


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