Homemade Skin Care Recipes
Much of the medical treatment of constipation is based on pharmacologic intervention using simple bulking agents and laxatives. The growing acceptance of the use of botulinum toxin in the treatment of anal fissure1 has highlighted the diverse clinical use of this agent, and has generated further interest in its use in patients with constipation from functional outlet obstruction.2 This chapter describes the background relating to the therapeutic use of botulinum toxin, its pharmacologic properties, and its use in patients with disordered defecation. We also describe other new pharmacologic agents used in the treatment of patients with chronic constipation such as serotonin (5-hydroxytryptamine) receptor agonists, colchicines, and neurotrophin-3 agonists.
Van Ermengem3 first noted that botulinum toxin, a potent neurotoxin, was produced by the gram-positive bacillus Clostridium botulinum. However, it was not until the discovery by Burgen et al4 in 1949 that the toxin blocked neuromuscular transmission that its potential as a therapeutic tool evolved. There are seven different types of known botulinum neurotoxin, labeled as type A to G. Although they share a similar chemical structure, the neurotoxin types are antigenically distinct, resulting in variations in their potency. For example, types C and D cause disease in animals (avian botulism), whereas types A, B, E, and F can affect humans, with type A resulting in the most severe clinical effects.5 The mechanism of action of botulinum toxin of blocking neurotransmitter release at the cholinergic nerve terminals is thought to take place in three steps. The toxin first binds to receptors on the unmyelinated presynaptic membrane of the neuron, prior to internaliza-tion into the cell by...
Botulism as a neuroparalytic intoxication was recognised at least a century ago as often being derived from eating sausage (Latin, botulus). The producing organism is a strictly anaerobic, Gram-positive, spore-forming bacillus and is widely distributed in soils and, fresh water and marine sediments. The organism is particularly prevalent in marine and freshwater sediments where there is considerable land drainage from rivers and little water movement, e.g. the Baltic and coasts of Scandinavia, and some areas of the Great Lakes in North America. Although all strains of clostridia capable of producing the neurotoxin were originally called Cl. botulinum, it is now recognised that certain strains of other clostridia may be capable of producing the toxin, e.g. Cl. butyricum, Cl. barati. There are four distinct phenotypic groups recognised within this taxon (designated groups I-IV) (see Table 15.1), plus two other groups, Cl. butyricum and Cl. baratii. For food microbiologists only the...
There are no sufficiently selective indicator media for the detection of the organism. There have been immunofluorescence methods developed for detection of the main groups of Cl. botulinum.22,23 However, reliance is generally placed on growth of the organism in a food enrichment culture at 25-30 C for 5-10 days and detection of toxin. In most cases, vacuum-packaging the food sample, perhaps with adjustment of pH and addition of ca 10 w w of freshly steamed and cooled cooked meat broth for additional nutrients, is sufficient. Botulinum toxin is detected by intra-peritoneal injection of mice with filter-sterilised cultures or food extracts and observation of typical neuroparalytic symptoms over a period of up to 3 days. Toxin can be neutralised by boiling for 10 minutes, the usual negative control for toxin tests, or with specific antiserum. Several authors have devised immunologically based assays, e.g. radio-immunoassays (RIA), enzyme-linked immunosorbent assays (ELISA see, e.g.,...
People who are most likely to be sunburned and who are most at risk for sun-induced skin cancer are those with fair skin, blue eyes, and red or blond hair, although anyone who spends time outdoors is at risk. The more sun exposure you receive, the more your skin is damaged. Certain medications such as the antibiotic tetracycline, some diuretics (water pills), some tranquilizers, birth control pills, and over-the-counter antihistamines make the skin more sensitive to the sun, increasing the likelihood of being sunburned. You are at risk for sunburn even on cloudy days clouds do not block sunlight they merely scatter the sun's rays. There are a number of simple steps you can take to protect yourself from the harmful rays of the sun. Try to plan outdoor activities for early in the morning or late in the afternoon so you can avoid being in the sun between 10 00 am and 3 00 pm, when the sun's rays are strongest. When you are out in the sun, use a sunscreen with a sun protection factor...
Clostridial neurotoxins (seven related types, classified as A to G) are arguably the most potent toxic substances known to man. Most relevant as the agents causing disease in humans are toxins produced by Clostridium botulinum, C. butyricum, and C. barati. All of these Gram-positive, spore-forming anaerobic bacteria are found in soils and marine sediments throughout the world. In addition, C. botulinum can be found in household dust, on the surfaces of foods, and even in honey, whose ingestion is considered a strong risk factor for the disease. Infection with C. botu-linum results in three epidemiologic forms of botulism Botulinum toxin poisoning due to food ingestion is comparatively rare ( 1000 annual cases worldwide 30 cases in the U.S.). The same is true for the other forms of disease. For this reason, population-wide immunization is not considered practical. As a result, the largely unprotected population constitutes an attractive target for a bioterrorist assault based on the...
There is little commonality in the scientific methods, processes, and formulations required for the wide variety of cosmetics and toiletries in the market. Products range from preparations for hair, oral, and skin care to lipsticks, nail polishes and extenders, deodorants, body powders and aerosols, to quasi-pharmaceutical over-the-counter products such as antiperspirants, dandruff shampoos, antimicrobial soaps, and acne and sun screen products.
There are three main trading blocks, the United States, Europe, and Japan. Obviously globalization as an integrated free-trade network cannot work if each block classifies and regulates skin care products differently. Unfortunately, no international consensus currently exists, inevitably sparking disputes and trade practices that may place some producers at a grave disadvantage. Japanese authorities have created their own laws in response to the problem that many skin care products are neither pure drugs nor pure cosmetics in the traditional sense, but mixtures of the two. The category we call cosmeceuticals they call quasidrugs (5). They allow cosmetics to include pharmacologically active ingredients, provided that the medicinal effects are mild and the products have been demonstrated to be safe. The legal wording leaves a lot of room for ambiguities and ad hoc interpretations that some perceive as a trade restraint.
The distinction between warts and plantar calluses is sometimes difficult and is important because the latter can be treated with keratolytics and debridement alone and do not require the more destructive therapies used on verrucae. The difference can be determined by paring the lesion down with a scalpel blade. Warts will show a single or sometimes multiple cores that interrupt normal skin lines. They also exhibit dark red or black speckles, which are the thrombosed ends of the feeder vessels. Calloses show neither of these changes.
The epidermis responds to chronic trauma with increased cell proliferation and increased keratin production (Fig. 9). The characteristic morphologic features of lichenification include palpable thickness of the skin compared to nearby normal skin accentuation of the normal cross-hatched skin markings and the presence of lichen-type scale. Lichenification is especially characteristic in the chronic lesions of atopic dermatitis and neuro-dermatitis. It is particularly marked in the variant of these two diseases known as lichen simplex chronicus. Color is surprisingly hard to describe accurately. This is partly due to the lack of absolute color standards and partly due to the confounding effect that the patient's normal skin color has on lesional color. One must also discount the color contributed by secondary characteristics such as scale or crust. This can usually be accomplished by looking at the peripheral edge of a lesion, since both scale and crust are often less prominent in this...
Elicit a history of skin problems, the length of time skin disorders have existed, daily routine skin care, and current medications. Ask the patient about exposure to sunlight in particular, establish long-term patterns of exposure to sunlight, either at work or in recreational activities, and determine what form of sun protection the patient has customarily used. Record the patient's history of scars, vaccination sites, and burns. Establish a patient history of exposure to radiation or arsenic be sure to ask about the patient's occupational history to discover if he or she has been at risk of ingesting arsenic at an industrial site. PHYSICAL EXAMINATION. Observe the color, texture, turgor, and pigmentation of the patient's skin for deviations from normal skin parameters. Note in detail any lesions, nodules, or plaques.
Botulism is a serious neurotoxic disorder that is caused by the gram-positive, spore-forming bacterium Clostridium botulinum, which is found in soil and in the gastrointestinal (GI) tract of birds, fish, and mammals. Although it is usually harmless in the spore state, the organism flourishes in warm anaerobic environments, causing germination with bacterial multiplication and toxin production. Botulism occurs when the bacterium is ingested into the GI tract or enters through an open wound. Once ingested or embedded, the bacterium enters the vascular system. Toxins act at the neuromuscular junction by impairing the release of the neurotransmitter acetylcholine from the presynaptic membrane. Loss of acetylcholine causes paralysis of voluntary and involuntary muscles.
Whether paradoxical contraction of the pub-orectalis muscle during defecation is a cause of constipation or a coincidental finding is unclear. A study by Jorge et al15 evaluated 112 constipated patients with EMG and defecography. One third of these patients displayed findings consistent with paradoxical puborectalis contraction as measured by these techniques. However, the correlation between EMG and defecography was poor 33 of patients displaying findings of anismus on defecography had a normal EMG, and 30 of patients with an EMG suggesting anismus had normal defecography. Treatments directed at inhibiting contraction of the pub-orectalis muscle, such as injection of botulinum toxin or division of the puborectalis muscle, have yielded mixed results.
Clostridium botulinum 18.104.22.168.1 Sub-unit bacterial toxins. To this group belong the toxins produced by Clostridium botulinum. C. botulinum are motile, Gram-positive rod-shaped spore-forming anaerobic bacteria. C. botulinum is not one species, but a group of bacteria which are all capable of producing neurotoxins. Biochemically, C. botulinum is very similar to Clostridium sporogenes and Cl. novii. However, the latter do not produce toxins and are therefore not relevant here. According to the toxin they produce, there are eight types of C. botulinum A, B, C1, C2, D, E, F, and G. After an incubation period of 12 to 72 hours, symptoms may start with nausea and vomiting, followed by tiredness, headache, muscular paralysis, double vision, and respiratory problems, often with fatal results. The duration of botulism is 1 to 10 days, mortality is relatively high (30 to 65 ). In most foods, botulinum spores are of no consequence unless they are able to germinate and produce the toxin. The...
Close to 20 different collagen molecules have been identified and characterized. Type I collagen makes up over 90 of the collagen in the body and is the dominant type in mature wounds. Type III collagen is also a key in early wound healing, composing up to a third of all wound collagen during the granulation tissue of the fibroblastic phase, before being replaced during the remodeling phase to restore the normal 4 1 ratio between types I and III collagen that exist in normal skin and mature wounds.
A reduction of the effective intercellular lipid barrier properties can lead to deficiencies ranging from dry skin (depletion of lipids owing to excessive use of detergents), to hyperproliferation and abnormal scaling. Causes include essential fatty acid deficiency, abnormal intercellular deposition of various lipids, accumulation of
(2) On unusual occasions,bullous eruptions or vesiculobullous lesions, unassociated with LE skin lesions, occur in patients with SLE (Bacman et al. 2004, Camisa and Sharma 1983, Gammon et al. 1985, Hall et al. 1982, Olansky et al. 1982, Penneys and Wiley 1979). These lesions predominantly involve flexural or extensor skin (Fig. 6.19), the upper trunk, and the supraclavicular regions, but the face and the mucosal membranes are also predilection sites. The bullae arise on erythematous or normal skin, tend to be tense, and may approach the size of blisters in
TREATMENT The most affective treatment currently available is chemodenervation with botulinum toxin. The latter blocks neuromuscular transmission by inhibiting release of acetyl choline at peripheral nerve endings. Onset is usually within three to five days, and the duration of effect is typically about three months. For the 4 to 5 of patients who do not respond to botulinum toxin type A (Botox ) or who develop resistance to it, botulinum toxin type B (Myobloc ) is also available, and generally works well in most cases. When chemodenervation fails to give adequate results pharmacological agents such as benzodiazepines or anticholinergic agents can be added. For those who do not obtain satisfactory control of spasms on these regimens, surgical myectomy with removal of orbicularis muscle from the upper eyelids combined with brow fixation, will usually produce acceptable results.
Roughness and scaling are visible features of clinically dry skin in patients with atopic dermatitis (3). Closer examination of these areas by scanning electron microscopy shows that the surface morphology is changed from a regular pattern to a coarser one, with broad, irregularly running furrows and loss of minor furrows (3). Likewise, in xerosis, increasing derangement of minor furrows and later also of major furrows can be observed (23). A more coarse and irregular skin surface pattern with larger squares is also found in recessive X-linked ichthyosis (24). Using instrumental evaluation of the skin topography the influence of moisturizers on the skin structure has been addressed (25,28-33). The roughness parameters and the distance between furrows peaks can describe changes in the hydration status (28-35). Dry skin tends to have a larger number of high peaks and a larger distance between the peaks than normal skin (33,34). Hydration of normal skin has been reported both to decrease...
Content and organization of these intercellular barrier lipids have broad implications for the permeability barrier function (36,83-85,125,126). The lipid compo- sition of the SC is highly variable among individuals, depending on a number of factors (Table 4). In dry skin and in skin exposed to organic solvents, the lipid
A lack of water may be too simple an explanation for all types of problems covered by the term dry skin, such as redness, scaling, roughness, itching, and a feeling of discomfort. Rather than just aiming at a general increase in the water content, the abnormal epidermis should probably be treated according to the underlying pathogenesis. The possibilities to correct or prevent abnormalities in the skin by different treatments may also help to explain the differences in preference for different moisturizers among individuals. This opens up new possibilities for further improvement in the treatment of different dry skin disorders.
Bland cleansers and moisturizers are continued for 48 h or until all post-peel irritation subsides. Patients are then able to resume the use of their topical skin care regimen including topical bleaching agents, acne medications, and or retinoids. Post-peel adverse reactions such as excessive desquamation and irritation are treated with low to high potency topical steroids. Topical steroids are extremely effective in resolving post-peel inflammation and mitigating the complication of post-inflammatory hy-perpigmentation. In the author's experience, any residual post-inflammatory hyperpigmen-tation resolves with use of topical hydro qui-none formulations following salicylic acid peeling.
Lesions evolve according to a characteristic time course. Fresh lesions first present as small, round, well-defined, slightly raised erythemas with dull surfaces that soon become rough to the touch and scaly. Scales are adherent and are often attached to the hair follicles ( carpet tack phenomenon). Follicular orifices are first widened with keratotic plugs and may then disappear completely there is a gradual loss of hair in the lesions, leading to irreversible scarring alopecia. Lesions spread slowly and regress at the centers, which become smooth and sunken. Intermediate lesions become elevated and indurated at variable degrees and develop atrophy and loss of normal skin texture in their centers. At the periphery, rests of the active lesion remain as ring-like, arcuate, or polycyclic scaly erythemas that continue to spread. Old (burnt-out) lesions may be disfiguring they are large, with irregular borders, sharply demarcated, depigmented (porcelain white in dark skin), hairless,...
Always take into account patient safety, and weigh it against the possibility of the patient's further increase in intracranial pressure. Implement measures to limit the effects of immobility, such as skin care, range-of-motion exercises, and a turning and positioning schedule. Note the effect of position changes on intracranial pressure, and space activities as necessary.
Neurologic manifestations Botulinum tox-inbw, OP pesticides , thallium, scombrotoxin, ciguatoxin, tetrodotoxin, brevitoxin, saxitoxin, domoic acid, mushroom toxins, post-Campylo-bacter Guillain-Barre syndrome. Systemic illness Listeria monocytogenes, Brucella spp.bw Trichinella spiralis, Toxoplasma gondii, Vibrio vulnificus, hepatitis A virus.
Treatment for patients with these deformities involves the use of special training and facial exercises, as well as the judicial use of repeated Botox injections to paralyze unwanted facial muscle function. Most of these patients are unhappy with results of this type, but many physicians dismiss the problem as inconsequential and recommend neither thorough examination nor prompt surgical treatment at a time when surgery could prevent a bad result. It is human nature that patients wish to avoid or delay surgery until they are convinced that it is necessary. They are commonly advised to wait several weeks by a well-meaning relative, friend, or neighbor who made a good spontaneous recovery without treatment 71 will. The problem is that 29 of all patients with untreated acute facial palsy will have not be so fortunate.1 Table 41-1 presents an algorithm for evaluating such cases of acute facial palsy.
PA Norris and coworkers reported in vivo sequential expression of CAMs in UVB-induced erythema compared with intracutaneous injection of purified protein derivative (PPD). E-selectin expression on endothelial cells was seen after 6h in both reactions, with a prolonged expression (1 week) in the PPD reaction. PPD but not UVB induced basal keratinocyte ICAM-1 expression and VCAM-1 expression on stellate-shaped cells in the upper dermis, first seen at 24 h (Norris et al. 1991). In PLE, similar findings regarding CAM expression were found as after PPD injection, but keratinocyte ICAM-1 expression was strong already after 5 h, and VCAM-1 was expressed on perivascular cells (Norris et al. 1992). UVA irradiation in vivo on healthy skin increased endothelial ICAM-1 after 24 h, whereas ICAM-1 expression on cultured keratinocytes decreased after UVA but increased on cultured fibroblasts 6-48 h after irradiation. These authors also reported constitutive keratinocyte ICAM-1 expression (Treina et...
The patient with myxedema is generally weak and therefore progressively immobile. Hypothyroidism exposes the patient to the risk of skin breakdown. One goal is to increase the patient's mobility while accommodating her or his extreme weakness with frequent rest periods. Provide meticulous skin care.
TREATMENT Botulinum toxin has become the primary treatment of choice for oromandibular dystonia and essential blepharospasm. More than 90 of patients obtain some relieve of spasms that can last for an average of three months. One to two unit injections of botulinum toxin type A (Botox or Dysport ) are placed into the involved facial muscles. For patients who become refractory to type A, toxin type B (Myobloc ) can offer some benefit. Complications of botulinum toxin when used in the mid and lower face include bruising, mouth droop, chewing and speaking problems, and dry mouth. Pharmacologic therapy may be useful as an adjunct but is rarely useful as a primary treatment modality. About 20 to 30 of patients will report some benefit from one drug or another. The most important drugs are Clonazepam (Klonopin), trihexyphenidyl (Artane), and baclofen (Lioresal). Unlike blepharospasm, there is no good surgical procedure for oromandibular dystonia.
In Drosophila, as in other organisms, the small GTPase Rac1 (Ras-related C3 botulinum toxin substrate) may function as a major target of the CDM family (Kiyokawa et al., 1998a, 1998b Nolan et al., 1998 Albert et al., 2000 Reddien and Horvitz, 2000 Gumienny et al., 2001). Rac1 is a member
Skin eruptions may be more common in primary infections (6). The rash may be present in different ways, including flushing of the face, neck, or chest during the febrile period an erythematous or maculopapular rash after the third or fourth day a confluent petechial rash with round pale areas of normal skin or a combination of these. Less frequent than rash but not rare are mild hemorrhagic manifestations, such as petechiae, epistaxis, gingival hemorrhage, gastrointestinal hemorrhage, and microscopic hematuria. Hemorrhage is more commonly associated with a platelet count below 50,000 mm3, although hemorrhage does not necessarily occur with a low platelet count (7). The tourniquet test, a method for the assessment of capillary fragility or platelet function, may be positive in more than one-third of patients with dengue fever. To perform the tourniquet test, the blood pressure cuff is inflated to a point midway between the systolic and diastolic blood pressures and maintained for 5...
Vehicle penetrates normal skin 50-fold faster than follicle-free skin. Retention also 20 to 30-fold higher in normal skin Particle size dependency of follicular penetration, optimum 5 im Greater concentrations of hydrocortisone and testosterone observed in epidermis and dermis of normal skin, particularly at the depth of sebaceous glands, compared with follicle-free skin. In vivo effect less pronounced than in vitro Flux and absorption of caffeine, niflumic acid, and p-aminobenzoate threefold slower in follicle-free skin Particle size dependency of follicular
Nonsolar lentigines These are macules of medium to dark-brown pigmentation that retain normal skin markings over their surface. Even when confluent, their size rarely exceeds 5 mm. They may be clinically indistinguishable from a junctional nevus. They are generally darker, sharper, and more regular than ephelides (see Photo 5). Solar lentigines These are macules of light- to medium-brown pigmentation tht retain normal skin markings over their surface. Color is often uneven, and the margins are irregular and fuzzy. Size varies from 0.5 to 1 cm or more (see Photo 6).
Defining Characteristics (Specify vomiting, diarrhea, excessive renal excretion, dry skin and mucous membranes, weight loss, decreased urinary output, altered intake, sunken fontanels in infant, decrease of tears and saliva, sunken soft eyeballs, nasogastric suction, fistula.)
Botulinum toxin The new pharmacologic approaches described in this chapter aim to benefit patients with chronic constipation by improving either gastrointestinal motility or evacuatory function. Better appreciation of the complex role of pelvic floor muscles in defecation has led to the relatively novel use of botulinum toxin in patients with obstructed defecation. Initial results, although encouraging, are inconclusive, with larger, randomized studies now needed. It would also help to have a more accurate method of assessing the biologic activity (effective therapeutic dose) of botulinum toxin use.
Injection of botulinum toxin can be quite helpful for patients who develop hyperkinesis following reinnervation (e.g., after XII to VII cross-innervation). It may also be helpful for patients who have severe synkinesis that results in excessive facial twitches. The toxin is injected into the orbicularis oculi muscle for eyelid spasms and into the zygomaticus major muscle for midfacial spasms. EMG may be helpful in localizing the muscle for injection. An initial dose of 5 to 10 U can be injected into the orbicularis oculi and 10 to 20 U into the zygomaticus and then repeated if necessary to achieve the desired results. The duration of effect lasts approximately 3 months, and patients will require repeated injection.
Basal transepidermal water loss, skin thickness, skin blood flow and skin colour in relation to sodium-lauryl-sulphate-induced irritation in normal skin. Contact Derm 1991 25 108-114. 162. Loden M. Urea-containing moisturizers influence barrier properties of normal skin. Arch Dermatol Res 1996 288 103-107.
Skin lesions fragile, flaccid vesicle or bulla filled with clear fluid, arising on normal skin or on an erythematous base large erosions with lateral spread of blisters Vegetating (vegetans) variant lesions in skin folds form vegetating plaques with excessive granulation tissue and crusting occur more frequently in intertriginous areas and on scalp and face
Several sources of advice are available to the food industry. Leatherhead Food Research Association has operated a Botulinum Laboratory for many years and offers member companies advice and challenge-testing facilities for assessing the botulinal safety of food products. Leatherhead Food RA also markets Food MicroModel, a computer-based set of predictive models for the growth and death of all the major foodborne pathogens, including Cl. botulinum and Cl. perfrin-gens. LFRA Library has several books on Cl. botulinum and other food-poisoning organisms, and the Information Group at Leatherhead Food RA can also access the scientific literature on all aspects of food poisoning, and provide information on the current situation or conduct literature searches on specific items. Campden and Chorleywood Food Research Association (CCFRA) also has similar facilities for work with clostridia. Much of the recent research on heat resistance of the spores of psychrotrophic strain of Cl. botulinum and...
Side Effects GI N&V, diarrhea, peptic ulcer activation, abdominal pain. Dermatologic Flushing, warm feeling, skin rash, pruritus, dry skin, itching and tingling feeling, keratosis nigricans. Other Hypotension, headache, macular cystoid edema, amblyopia. NOTE Megadoses are accompanied by serious toxicity including the symptoms listed in the preceding as well as liver damage, hyperglycemia, hyperuricemia, arrhythmias, tachycardia, and dermatoses.
Frequent use causes a yellow discoloration to skin, catheter, and clothes Soaking for 5 min with the disinfectant is required during transfer set replacement May cause skin irritation and reaction Very dry skin results from exposure to povidone-iodine Growth of Pseudomonas sp. was observed in an opened multi-dispensed bottle of povidone-iodine 31 Povidone-iodine does not kill viruses such as HIV or Hepatitis May cause sclerosing encapsulating peritonitis 28 More costly
Two basic functional types of T helper (Th) cells can be distinguished. Th1 clones secrete mainly IL-2 and IFN-gamma. They are involved in cell-mediated inflammatory functions, e.g., the induction of delayed type hypersensitivity. Th2 clones produce IL-4, IL-5, IL-6, IL-10, and IL-13 (51,52) and stimulate IgE antibody by IL-4 and IL-13, activate eosinophils by IL-5 (53). In addition, they inhibit macrophages, antigen presenting cells, and T helper 1 (Th1) T-cells by IL-10 (54). The phenotype of the malignant T-cell clone patients with Sezary syndrome is consistent with peripheral T memory cells. Their cytokine transcription and secretion is comparable to human T helper 2 (Th2) cells with IL-5, IL-10, and IL-13. Attempts to reveal Th1 and 2 profiles in skin biopsies of CTCL patients revealed conflicting results. Saed et al. (55) demonstrated the presence of IL-2 and IFN-gamma, but no IL-4, IL-5, or IL-10 in the epidermis of MF by RT-PCR and concluded that MF exhibits a Th1 cytokine...
(Wilson and Nicoll, 2001) shows essentially the same results as those in cultures. In addition, DSI is not affected by postsynaptically-applied botulinum toxin (Wilson and Nicoll, 2001), suggesting that vesicular release is not involved in DSI. In cerebellar slices, it has been demonstrated that DSI of Purkinje cells is completely occluded by WIN55,212-2-induced suppression of inhibitory transmission, blocked by CB1 antagonists and deficient in CB1-knockout mice (Kreitzer and Regehr, 2001a Diana et al., 2002 Yoshida et al., 2002). Involvement of endocannabinoids in DSI has also been reported in other regions of the CNS including the basal ganglia (Wallmichrath and Szabo, 2002) and the neocortex (Trettel and Levine, 2003 Trettel et al., 2004). These findings strongly suggest that endocannabinoids mediate DSI widely in the CNS.
Although many autoantigens targeted in SLE are redistributed in cells dying by apop-tosis, only ribonucleoprotein complexes containing La SSB, Ro SSA, Sm, and U1-70 kDa have been implicated in the pathogenesis of experimental photo-induced epidermal damage. It has been proposed that a pathologic immune response develops in patients with lupus against one or more of the photoproducts found in normal skin after UV irradiation, raising the possibility that these ribonucleoprotein complexes themselves (unlike other autoantigens) might be lupus chromophores. It is also possible that photoproducts that present in normal skin after UV irradiation might be metabolized abnormally in patients with lupus owing to genetic polymorphisms, predisposing to an exaggerated autoimmune response against these photo-products. The resulting immune response is directed against the UVB-induced complexes and subsequently spreads to individual component molecules (RNA and protein), generating an autoamplifying...
Malignant melanomas may arise de novo, that is, in apparently normal skin or in association with a pre-existing melanocytic nevus. When malignant melanomas arise de novo, they begin as a small, lightly pigmented macule that in time is characterized by asymmetry, scalloped borders, poor circumscription, and variations in color of predominantly tan to brown (Fig. 1A). Some such macular lesions become patches that are increasingly asymmetrical, poorly circumscribed, and varied in color (Fig. 1B). Other macular lesions of melanoma eventually become papular or nodular. Some other macular lesions may simply enlarge to become patches, others plaques, and still others combinations of papules or nodules upon patches or plaques (Figs. 2A-C 3A and B). Some nodules and tumors ulcerate. Some melanomas may undergo partial or complete regression (Fig. 4). The clinical features of malignant melanomas just described apply to malignant melanomas at all anatomic sites of the skin and mucous membranes.
The surgeon will ask whether you have any chronic diseases or conditions, such as high blood pressure or a blood clotting disorder, that could cause problems during surgery or affect the healing process. People with diabetes, chronic heart or lung disease, or poor circulation also have a higher risk of surgical complications. Tell the surgeon if you take any medication (prescription or nonprescription) or vitamins. Some drugs, such as aspirin, and some vitamins, such as vitamin E, can interfere with blood clotting. Also tell the doctor if you smoke. Smoking inhibits blood flow and can affect the way your skin heals after surgery.
In patients with chronic constipation and pelvic floor dysfunction, injecting botulinum toxin into the puborectalis muscle weakens or paralyzes the overactive muscle and causes straightening of the anorectal angle to allow easier defecation. It was first used in patients with obstructed defecation in 1988 by Hallan and colleagues.13 In their study, seven patients with obstructed defecation diagnosed using electromyographic (EMG) studies and dynamic proctography, received botulinum toxin injection to the puborectalis muscle. Taking an empirical dose of 3 ng botulinum toxin (approximately equivalent to 60 U of Botox), four patients derived benefit from the treatment. This finding was based on symptom questionnaires as well as a reduction in the maximum squeeze pressure on anorectal manometry and an increase in the anorectal angle on posttreatment proctography analysis. However, of the remaining three patients, one did not derive any benefit, and two suffered from symptoms of...
Deceleration of linear growth is an important sign that is helpful in the early recognition of this disease. Affected children are relatively overweight for their height, although they are rarely obese. If hypothyroidism is severe and longstanding, immature facies and immature body proportion (increased upper lower body ratio) may be noted with delay in dental and skeletal maturation. The children have cold intolerance, dry skin and dry hair texture. In patients with severe long-standing hypothyroidism, muscular pseudohypertrophy gives a Herculean appearance called Kocher-Debre-Semelaign syndrome 23 .
Eczemas Asteatotic dry skin, contact, seborrheic Infections Candidiasis, herpes zoster, onychomycosis, scabies Photodamage Actinic elastosis, colloid milium, Favre-Racouchot syndrome, freckling, photoaging (wrinkling, solar lentigo), poikiloderma of Civatte Premalignant Actinic keratosis, Bowen disease Malignancies BCC, lentigo maligna melanoma, MF, SCC Ulcerations leg, pressure decubitus Other Cutaneous horn, pruritus
Allergic contact dermatitis is a skin condition that occurs when your skin comes into contact with allergens, substances to which you are allergic but that are harmless to most people. This condition is not triggered by harsh soaps or acids, for example, because these substances are irritants that will produce a rash on anyone's skin, given enough exposure. To diagnose allergic contact dermatitis and to determine its cause, your doctor will examine your rash and ask questions about the materials you use at home and at work. He or she may perform a patch test, in which small amounts of suspected allergens are applied to your skin for a couple of days. If an area of skin becomes inflamed, that substance may be an allergen for you.
Puborectalis muscle, lack of perineal descent, a lack of straightening of the rectoanal angle, and poor opening of the anal canal.37 Definition of specific measurement criteria (anorectal angle change, perineal descent) would be misleading due to the wide range of normal results.38 During the exam, the patient may strain numerous times and evacuate only a small amount of contrast with each attempt or fail to empty any contrast at all. Straining against the pelvic floor or a non-opening anal canal can accentuate the anterior bowing of a rectocele or cause posterior rectal bowing. Once diagnosed, dyskinetic puborectalis is usually treated with biofeedback and bowel management. Patients who fail conservative treatment have been offered botulinum toxin injections into the puborectalis muscle with limited success.39 Several studies have shown that neither electromyography nor cinedefecography is ideal relative to either specificity or sensitivity in the diagnosis of paradoxical...
The aging of skin provides an important model for biological gerontology. The connective tissue of the dermis is readily accessible for studies from individuals of all ages. Generally a small punch biopsy is sufficient to supply cultures of fibroblasts, keratinocytes, or sections for histology. Such studies demonstrate pronounced changes in histology with age, alterations that share many features with similar changes occurring in other tissues in the body.2 These observations suggest that the study of aging skin could yield important clues to the pathogenesis of other age-related connective tissue disorders, and perhaps, aging in general. Skin, however, is unique it its exposure to relatively high levels of ultraviolet radiation. Therefore, a distinction is usually drawn between those changes in the skin attributed to long-term exposure to solar radiation (actinic skin damage) and those independent of such extrinsic causes (intrinsic skin aging). Much of this discussion will focus on...
A variety of spots or growths can appear on the surface of your skin especially as you get older but most are harmless and do not require treatment. The most common noncancerous skin growths are actinic (or solar) keratoses, cherry angiomas, skin tags, age spots (also called sun spots or liver spots), moles, seborrheic keratoses, and warts. Treatment is usually not necessary unless you want to improve the appearance of your skin. You can purchase a nonprescription skin-bleaching cream at your local pharmacy to help fade the spots. There are a number of treatments available for age spots, including laser treatment to break up the pigment (color) in the spots, prescription skin creams, freezing with liquid nitrogen, or a chemical skin peel that uses a mild acid to remove the top layer of skin.
Anismus, also termed pelvic floor dyssyner-gia, spastic pelvic floor syndrome, paradoxical puborectalis contraction, and nonrelaxing pub-orectalis syndrome, accounts for an estimated 50 of patients with symptoms of chronic constipation.6 Rome II diagnostic criteria for a diagnosis of pelvic floor dyssynergia are specified in Table 13.2.3 This disorder of unknown etiology is characterized by failure of the puborectalis muscle to relax during defecation. Invasive surgical therapy or injection of botulinum neurotoxin7 are associated with an unacceptable incidence of incontinence. In 1993, Enck's8 critical review found that biofeedback has become widely accepted as the treatment of choice for anismus.
The histology of a keratoacanthoma is very similar to that of a well-differentiated squamous cell carcinoma of the skin. KAs commonly contain squamous cells with atypical mitosis, individual cell keratinization, and other histologic signs of malignancy. The microscopic differentiation is dependent on both the cellular detail and the low-power configuration of the lesion. At each margin, a narrow spur of dermal connective tissue separates the normal epidermis from the lesion at the transitional junction between the normal and proliferating cells. For this reason, marginal punch biopsy is not adequate to distinguish between the two. Excisional biopsy or an incisional biopsy that contains a cross-section of the lesion into the adjacent normal skin is needed.
Dry Skin and Moisturizers Chemistry and Function, edited by Marie Loden and Howard I. Maibach 27. Dry Skin and Moisturizers Chemistry and Function, Second Edition, edited by Marie Loden and Howard I. Maibach 29. Sensitive Skin Syndrome, edited by Enzo Berardesca, Joachim W. Fluhr, and Howard I. Maibach
Whether one is pro or con, the term cosmeceutical has permanently entered the vocabulary of skin care science. For some, the term has been transformed into a marketing tool, touting the benefits of skin care products. Others see it as a provocation for unwanted, costly, regulatory actions. The most benign view is that the category is superfluous and has no raison d'etre. Cosmeceuticals seem to have a certain semantic resonance, as witnessed by similar sounding neologisms for example, neutraceuticals (foods with health benefits) and neoceuticals (over-the-counter drugs with cosmetic effects).
Assess the patient for signs of dehydration such as tachycardia, altered level of consciousness, dry skin with poor turgor, dry mucous membranes, weight loss, and weak peripheral pulses. Check for postural hypotension that is, a drop in systolic blood pressure greater than 15 mm Hg when the patient is moved from a lying to a sitting or standing position.
New insights about the function of the skin, as well as the development of new products for skin care, make it necessary to question or redefine the definitions of cosmetics and drugs. Moreover, in the United States, Europe, and Japan, different definitions of cosmetics are used. The definition of a drug is more or less equivocal on these countries. According to the Food, Drug, and Cosmetic (FDC) Act, a drug is defined as an article intended for use in the diagnosis, mitigation, treatment, or prevention of disease or intended to affect the structure or any function of the body.
Establish accurately the time of onset of the problem. If it is a chronic disorder, document the frequency and duration of individual attacks, exacerbations, or recurrent episodes. Many skin problems have a fairly characteristic age of onset, gender preference, and duration. Recurrences may follow recognizable fixed patterns, which will aid in diagnosis.
Among the wide-ranging environmental factors affecting human life, ultraviolet (UV) irradiation can be regarded as one of the most significant. Although UV light has an essential impact on terrestrial and aquatic ecology and is a fundamental necessity for the life of humans, animals, and plants, mid-wavelength UVB (290-320 nm) in particular can also exert hazardous effects on health. UV radiation not only plays an instrumental role in the development of skin cancer but also has profound effects on local and systemic inflammatory responses. While studying the biological effects of UVB irradiation, it has become evident that UV exposure can significantly compromise the immune system. The implications of the immunosuppres-sive properties of UV irradiation are manifold because UVB-induced immunosup-pression not only is responsible for the inhibition of protective cell-mediated immunity but also contributes to the initiation, development, and perpetuation of several skin disorders (Fisher...
Used as superficial chemical peeling agents, the pH of these solutions ranges from 0.08 to 2.75. Peeling solutions with a pH below 2 have dem-2 onstrated the potential to induce crusting and necrosis, which has not been seen with the partially neutralized solutions with a pH above 2 4 . The higher concentration acid (70 ) created more tissue damage than the lower concentration (50 ) compared to solutions with free acid. An increase of transmembrane permeability coefficient is observed with a decrease in pH, providing a possible explanation for the effectiveness of glycolic acid in skin treatment.
Glycolic acid has been recognized as an important adjunctive therapy in a variety of conditions including photodamage, acne, rosacea, striae albae pseudofolliculitis barbae, hyper-pigmentation disorders, actinic keratoses, fine wrinkles, lentigines, melasma and seborrheic keratoses 5 . Moreover, it can reduce UV-in-duced skin tumor development and it has been proposed as a therapeutic modality against skin exfoliative conditions such as ichthyosis, xeroderma and psoriasis. In post-menopausal women a cream containing 0.01 estradiol and 15 glycolic acid, applied to one side of the face for 6 months, induces a significant improvement in reversing markers (rete peg pattern, epidermal thickness) of skin aging 6 . Glycolic acid chemical peels are an effective treatment for all types of acne, inducing rapid improvement and restoration of normal-looking skin. In these patients glycolic acid is more widely used than Jessner's solution, considering the equal treatment effect but a reduced...
In this chapter, the natural toxins are divided into endogenous toxins of plant origin and contaminants of natural origin. Endogenous toxins of plant origin comprise many different types of substances. There is no simple way of classifying this group of toxic food components. The way they are dealt with here is based on a classification according to common functional groups (toxic phenolic substances, cyanogenic glycosides, and glucosinolates), the physiological action (acetylcholinesterase inhibitors), and the type of toxic effect induced (biogenic amines and central stimulants). Toxins in food can also be contaminants of natural origin. There are three important sources of this group of natural toxins. First, raw materials of plant origin may be mixed with toxic non-nutritive plant species, e.g., cereals have been reported to be contaminated by pyrrolizidine alkaloids. Secondly, raw materials of animal origin, mainly fish and milk, can also be contaminated if the animal has ingested...
Use of bland cleansers and moisturizers is essential. Recommended moisturizing agents include Cetaphil, SBR-Lipocream, or Aquaphor. Peeling related to Jessner's usually resolves in 2-7 days. Patients can resume the use of general skin care products after peeling subsides. Makeup can be worn to camouflage peeling. Excessive peeling, erythema, or irritation postpeel can be treated with low or mid- to high-potency steroids for 5-7 days. Use of such agents should be based on the extent of irritation and inflammation.
Elucidation of the molecular action of the Clostridial neurotoxins provided important evidence of the essential function of SNARE proteins in neurotransmission (see Burgoyne and Morgan, 2003). Tetanus toxin and the seven types of botulinum toxin are heterodimers, each containing a heavy chain (H) that targets the toxin to a particular neuronal type, and a light chain (L) that is a metalloproteinase. After entry into the cytoplasm, these endoproteinases specifically cleave VAMP (tetanus toxin or botulinum toxins B,D,F and G), SNAP-25 (botulinum toxins A and E) or syntaxin 1 (botulinum toxin C). Even in neuroendocrine cells, which have no receptors for the H-chains, exocytosis is blocked if the toxins are introduced into the cytoplasm, for example by permeabilization of the plasma membrane. In some cell types exocytosis is resistant to Clostridial toxins through the expression of toxin-resistant SNARE isoforms What do we know about the molecular mechanisms of vesicular release in...
Dry skin is characteristic of relatively severe kidney failure, but is not particularly distressing as a symptom. Itching, however, is a common and sometimes very distressing symptom. It doesn't usually appear until loss of kidney function is severe (about 80 percent). Its cause is also unknown. Our study, summarized at the end of the chapter, suggests that both
TREATMENT Anticonvulsants, such as carbamazepine, may be helpful in some cases, as are the short-acting benzodiazepines. But these are useful in only about one-fourth of cases with mild symptoms. The most effective treatment currently available is chemodenervation with botulinum toxin. The latter blocks neuromuscular transmission by preventing degranulation of acetylcholine at peripheral cholinergic nerve endings. The duration of effect is typically three to four months. Complications include transient ptosis, mouth droop, and other muscle weaknesses. Microvascular decompression of the seventh nerve root where it exits the brain stem is an effective surgical treatment in most cases, with about 70 to 89 of cases showing complete relief of spasms. Potential complications include hearing impairment and CSF leak, and the mortality rate is reported at 0.3 to 0.6 . Monitoring of abnormal muscle response intraoperatively may enhance the final result.
Lash loss is also associated with infiltrative lesions such as sarcoidosis, lymphoma, and cutaneous neoplasms. Inflammatory processes including severe blepharitis can cause lashes to fall out, and chronic infections with the mite Demodex folliculorum, found in 10 to 15 of normal individuals, can also be associated with madarosis. Loss of lashes and facial hair has been reported as a complication of botulinum toxin for oromandibular dystonia, but this is exceedingly uncommon. Iodine plaque brachytherapy and external beam irradiation for choroidal tumors is a known cause of madarosis. Loss of lashes is a common finding in leprosy and ichthyosis. In some cases the loss of lashes can be factitious or idiopathic.
Pepper and citric acid play special roles as synergists. Citric acid potentiates the antibacterial effects of other spices, because low pH disrupts bacterial cell membranes (Sherman and Billing, 1999). Black pepper comes from Piper nigrum, an exclusively tropical plant which has several useful properties. For example, the compound piperine inhibits the ubiquitous, deadly bacterium Clostridium botulinum. Black pepper is also a 'bioavailability enhancer,' meaning that it acts synergistically to increase the rate at which cells, including microorganisms, absorb phytotoxins (Sherman and Billing, 1999). Khan and Balick (2001) note that tamarind increased bioavailabilty of other drugs, including, I presume, herbal.
Ness, drowsiness, fatigue, hallucinations, insomnia, lethargy, mental changes, memory loss, strange dreams. GI Diarrhea, ischemic colitis, nausea, mesenteric arterial thrombosis, vomiting. Hematologic Agranulocytosis, thrombocytopenia. Allergic Fever, sore throat, respiratory distress, rash, pharyngitis, laryngos-pasm, anaphylaxis. Skin Pruritus, rash, increased skin pigmentation, sweating, dry skin, alopecia, skin irritation, psoriasis. Ophthalmic Dry, burning eyes. GU Dysuria, impotence, nocturia. Other Hypoglycemia or hyperglycemia. Respiratory Bronchospasm, dyspnea, wheezing. Drug Interactions See also Drug Interactions for Beta-Adrenergic Blocking Agents and Antihypertensive Agents.
Botulinum-type toxins inhibit the release of acetylcholine neurotransmitters at both nicotinic (motor) and muscarinic (cholinergic autonomic) receptors, resulting in deficiencies of neurotransmitters at the synapses (presynaptic inhibition). Symmetrical, descending, and progressive flaccid muscle paralysis extending from neck to arms and legs is a CHARACTERISTIC NEUROLOGICAL SYMPTOM of botulinum intoxication Possible respiratory failure due to the collapse of weak oropha-ryngeal musculature Early administration of trivalent equine botulinum antitoxin is essential as soon diagnosis is made one vial (10 ml) of antitoxin IV for adult and pediatric administration Experimental pentavalent toxoid of C. botulinum toxin A,B,C, and D types is available but its efficacy is unknown despite administration to several thousand volunteers and high-risk personnel serum antitoxin levels produced in humans correspond to protective levels exhibited in animal studies Administer vaccine to individuals and...
Although highly popularized by the press, ricin is not an effective biological weapon. Its toxicity, while high, is nearly 1000-fold less than that of botulinum and a very large amount would be required to produce the effects expected of an effective biological warfare agent. Its potential as a destabilizing agent and as a weapon against specific targets remains high because of its ready availability and multiple dissemination modes. Aerosol exposure, injection, or ingestion as food or drink may all lead to a lethal outcome.
Nitrates and nitrites are used to preserve meats. For example, they contribute to the prevention of growth of Clostridium botulinum, the bacterium that produces the well-known highly potent botulinum toxin. The adverse effects after intake of nitrates and nitrites are methemoglobinemia and carcinogenesis, the latter resulting from the formation of nitrosamines.
After the tape mask removal the exudate is cleaned by sterile saline. Spot peeling and re-taping may be done if the skin looks under-peeled, particularly in areas with severe wrinkling. It is usually accompanied by a short-duration burning sensation. The tape is left for an additional 4-6 h and then removed by the patient. We cover the face with bismuth subgalate antiseptic powder for 7 days (Fig. 8.10). Other options include occlusive moisturizers, antibiotic ointments, and biosynthetic occlusive dressings such as Meshed Omiderm.
Reactive hyperpigmentation can occur after any depth of chemical peels. Usually lighter complexions have a lower risk for hyperpig-mentation, but genetic factors play an important role, and sometimes light patients with dark genes will hyperpigment unexpectedly. Therefore, we recommend introducing bleaching preparation 2-3 weeks after the peel in all patients and continuing until erythema fades. Demarcation lines can be avoided if the boundaries of the peeling area are hidden under the mandibular line and feathered gradually to the normal skin (Fig. 8.16). Medium-depth neck peel is required in patients with blotchy pigmentation of the neck and in those with no clear mandibular line. Accentuation of the pigment in previously existing intradermal nevi is common and should be recognized when it occurs to avoid any unnecessary alarm of a changing mole .
Agent Clostridium botulinum (marine). Toxin Botulinum toxin, exclusively Type E, in decomposing marine mammals and seafood. Botulinum toxins include Types A-G, but Types A, B, and E (saltwater toxin) cause most human botulism cases. LD50 (IV in mice) 0.0026 mcg kg. Mechanism Clostridial contamination of raw or improperly preserved seafood with exclusive production of botulinum toxin Type E on skin, in tissues, and muscle, particularly near gut. Vectors All home-canned salt- or freshwater seafood, raw seafood, raw marine mammals, especially dolphin, seal, whale-muktuk (raw whale skin and underlying pink blubber). Incubation 10 minutes before eating notify state public health authority and CDC (for release provision of human botulinum antitoxin).
All shellfish, 300 finfish species, and marine mammals can cause poisoning with potent biological toxins and increased CFRs ranging from 1-62 . Example botulinum toxin (botox) is 1, palytoxin is 2, TTX and saxitoxin are 5 among the living world's most potent biological toxins.
TREATMENT When removal is desired, complete surgical excision including the cyst wall is the treatment of choice. Pulsed dye laser ablation has been reported to give good results after multiple treatment sessions. Botulinum toxin has been suggested as an alternative therapeutic option because of its effect on reducing sweat production. Alfadley A, Al Aboud KA, Tulba A, Mourad MM. Multiple eccrine hidrocystomas of the face. Int J Dermatol 2002 40 125-129. Blugerman G, Schavelzon D, D'Angelo S. Multiple eccrine hidrocystomas a new therapeutic option with botulinum toxin. Dermatol Surg 2003 29 557-559.
Pruritis aggravated by heat, sweat, or wool often leads to chronic rubbing and as a result, the eyelid skin becomes violaceous early on and hyperpigmented with time. Coalescent papules, fissures, and fine scaling may occur. If the condition becomes chronic, thickening and accentuation of normal skin lines (lichenification) can occur on the periocular skin, and scaling plaques occur predominantly on the upper eyelids. With time eversion or stenosis of the lacrimal puncta may occur and frank ectropion may be seen in severe cases. Loss of eyelashes can occur. Darkening of periorbital skin suggests the diagnosis of atopy and is frequently of cosmetic concern to patients. Secondary staphylococcal infection or colonization of the eczematous skin is common leading to chronic anterior blepharitis. Associated ocular changes include keratoconjunctivitis, chemosis, sympblepharon, corneal pannus, Tranta's dots, anterior and posterior subcapsular cataracts, and keratoconus.
INTRODUCTION Keloids represent exuberant scar formation resulting from proliferation of dermal tissue following skin injury. Mechanisms for keloid formation represent abnormal wound healing and include alterations in growth factors, collagen turnover, tension alignment, and genetic and immunologic contributions. Keloids differ from hypertrophic scars in that they spread beyond the initial site of injury. Because they tend to be invasive into the surrounding normal skin both clinically and histologically, with prolongation of the proliferative phase of wound repair they have been described as incomplete tumors. Although any body area can be affected, keloids commonly develop on the face, neck, chest, shoulders, and back. Keloids on the eyelid skin are relatively rare, even in patients who are prone to keloid formation. These scars tend to occur with greater frequency in patients with darker skin tones, but patients of any skin type can develop this exuberant clinical response.
Hyperpigmentation Although postinflammatory hyperpig-mentation may occur in any patient undergoing skin resurfacing procedures, the risk may be lessened by pretreating the skin with a bleaching agent. We pretreat our patients, especially those with type III skin or greater, with a combination of 8 hydro-quinone, 1 hydrocortisone, and 0.05 retinoic acid for up to 4 weeks before they undergo laser resurfacing. By following this preoperative protocol, patients with Fitzpatrick type III or IV skin can undergo laser resurfacing with a reduced risk of postoperative hyperpigmentation. We have also treated patients with type V and VI skin with some success. These patients, however, usually develop transient hyperpigmentation and require prolonged skin care with bleaching agents. Rarely, hyperpigmentation may persist for longer than 6 months. Superficial TCA peels will correct this condition.
The author has observed cases of postin-flammatory hyperpigmentation even with low concentrations of superficial peeling agents. Hence, cautious titration is appropriate in darker skin types. Glycolic acid peels are titrated from 20-35 , 50 , and finally 70 . Similar titration methods are used for salicylic acid and TCA. Salicylic acid peels should be titrated from 20 to 30 . Despite the use of higher concentrations of TCA in some studies 12,13 , it is best to initiate TCA peeling in dark skin with low concentrations (i.e., 10-15 ). Post-peel care includes the use of bland cleansers and emollients until irritation and peeling subsides. The patient then resumes the use of topical skin care products and bleaching agents. Post-peel reactions such as excessive erythema, desquamation, and irritation are treated with low- to
Sunscreens have been developed to prevent the short- and long-term damaging effects of UV irradiation. However, the sun protective factor (SPF), which is defined as the ratio of the minimal erythema dose (MED) of sun-protected skin divided by the MED erythema of non-sun-protected skin, gives only a quantitative level of protection against sunburn and edema. Therefore, there is an ongoing debate on the potency of sunscreens to protect against many other deleterious biological UV effects such as photoimmunosuppression, skin aging, or skin cancer. Recent efforts have been directed toward determining the end points of sunscreen efficacy, such as immune protection factor (IPF), mutation protection factor (MPF), and protection against photocarcinogenesis (Gil and Kim 2000). Although standardized phototest procedures are available and can be used as tools to evaluate the protective effects of sunscreens toward UV induction of LE lesions, studies addressing this important topic are lacking....
May closely resemble ecthyma gangrenosum. As in bacterial ecthyma gangrenosum, cutaneous lesions due to opportunistic fungi may be a manifestation of hematogenous dissemination with secondary seeding of the skin. Alternatively, they may represent primary invasive infection, which may then disseminate. Gastrointestinal and respiratory tracts and skin are common portals of entry for disseminated infections. Invasive infections of the skin may occur in previously normal skin, but are more likely to occur in areas that have had a disrupted barrier, such as sites of vascular access, venipuncture, burns, or surgical procedures.
Special Concerns Use with caution, if at all, during lactation. Give a lower initial dose in liver impairment. Safety and efficacy have not been determined in children less than 2 years of age. Side Effects Most commonly, headache, somnolence, fatigue, and dry mouth. GI Altered salivation, gastritis, dyspepsia, stomatitis, tooth ache, thirst, altered taste, flatulence. CNS Hypoesthesia, hyperkinesia, migraine, anxiety, depression, agitation, paroniria, amnesia, impaired concentration. Ophthalmologic Altered lacrimation, conjunctivitis, blurred vision, eye pain, blepharo-spasm. Respiratory Upper respiratory infection, epistaxis, pharyngitis, dyspnea, coughing, rhinitis, sinusitis, sneezing, bronchitis, bronchospasm, hemoptysis, laryngitis. Body as a whole Asthenia, increased sweating, flushing, malaise, rigors, fever, dry skin, aggravated allergy, pruritus, purpura. Musculoskeletal Back chest pain, leg cramps, arthralgia, myalgia. GU Breast pain, menorrha-gia, dysmenorrhea, vaginitis....
The number of LCs is decreased in lesional skin of patients with LE compared with their nonlesional or perilesional skin, other inflammatory skin diseases, or normal skin (Bos et al. 1986, Shiohara et al. 1988, Sontheimer and Bergstresser 1982, Wollenberg et al. 2002). In another study, LCs were found to be reduced only in atrophic areas of the lesions (Mori et al. 1994). In perilesional epidermis, the numbers of CD1a+ and HLA-DR+ DCs are similar or identical to those in normal skin of healthy individuals (Mori et al. 1994).
Glycolic acid peels are well tolerated in darker skinned racial-ethnic groups (Figs. 13.3a, b and 13.4a, b). Side effects are substantially minimized when concentrations are gradually titrated from the lower concentrations of 20-35 to the full-strength 70 peel. Glycolic acid peels are most advantageous when treating darker skin types with sensitive skin.
SCF has been shown to be expressed on stromal cells as a membrane-bound protein, and its expression can be induced by fibrogenic growth factors such as PDGF (Hiragun et al., 1998). It has also been shown to be expressed on keratinocytes as a membrane-bound protein in normal skin. However, in the skin of patients with mastocytosis, an increased amount of soluble SCF
In addition, luteinizing hormone-releasing hormone antagonists that inhibit the pituitary-gonadal axis, and vitamin D3 analogs that target receptors in the bladder are also in development. Botulinum A toxin (Botox) has also been explored in patients who were poor candidates for surgery. In a recent study of 10 patients with BPH and AUR, all patients given 200 U Botox injections into the transition zone of the prostate showed improvements in PVR, Qmax, and prostate volume, which were maintained during the 12-month follow-up period.55 Other areas being explored include de-sensitization of C-fibers, which are involved in nociception (pain perception), using intravesical resiniferatoxin solution56 and the effects of beta-radiation on key growth factors, including TGF 1 and bFGF. It is thought that betarays may shrink the hyperplastic cells and reawaken apoptosis.57
When the experimental data are of poor quality, or are ambiguous, there is a danger of overinterpretation this often leads to a part of the model being wrong. One fairly recent example concerns the binding of a peptide to botulinum neurotoxin B light chain (BoNT B). A model of this protein, complexed with a 38-residue peptide of its natural substrate synaptobrevin II, was reported at 2.0 A resolution in the year 2000 (PDB entry 1f83). It was proposed that the binding of the peptide revealed how the full-length synaptobrevin II binds to the protein and is catalyzed. However, questions were raised about the validity of the peptide's binding as the average B-factors of its atoms were over four times the average for the rest of the structure - see Figure 3a.17 Furthermore, very few of its residues were in favorable regions of the Ramachandran plot and a re-examination of the electron density maps showed there was actually little evidence for the peptide being in the proposed binding site....
Figure 3 An example of overinterpretation of data. (a) A model of neurotoxin type B from Clostridium botulinum (BoNT B) in complex with a 38-residue peptide of its natural substrate synaptobrevin II, PDB entry 1f83. The model is colored by B-factor (blue lowest, via orange, to green highest), showing that the peptide, with its greens and oranges, has considerably higher B-factors than the rest of the protein - which is largely blue. This strongly hints at the peptide being poorly defined at this location. (b) A model of the related botulinum neurotoxin type A, PDB entry 1e1 h. The model consists of two molecules, one colored green and the other, off the screen, colored gray. The green molecule is shown in the same orientation as the model in a. The protein is self-cleaving. The red loops - one from the green molecule and the other from the gray one - are where the cleavage has occurred. The breaks in the loops can be clearly seen. This model strongly suggests that the location of the...
Four signs of infection erythema, pain, swelling, and warmth imprecise margins of infection areas of edema and erythema blending into the surrounding normal skin systemic symptoms (e.g. fever, malaise) signs of lymphangitis with red lines extending proximal from the area of inflammation regional lymphadenopathy crepitus with anaerobic organisms
Resorcinol is used in hairdressing as a modifier (or a coupler) of the PPD group of dyes. It is the least frequent sensitizer in hairdressers. It is also used in resins, in skin treatment mixtures, and for tanning. Severe cases of dermatitis due to resorcinol contained in wart preparations have been reported.
It covers your body tissues and internal organs and protects them from injury and infection. Skin is made up of two layers a thin outer layer called the epidermis and a thicker inner layer called the dermis. Under the dermis is a layer of fat called subcutaneous tissue. The outer part of the epidermis is made up of dead cells and keratin (a tough, fibrous type of protein), which form a protective covering. These dead cells are constantly shed and then replaced by new cells. The inner part of the epidermis is made up of living cells that divide rapidly to produce those new cells. Certain cells in the epidermis produce the pigment known as melanin, which protects your skin and determines your skin color. The dermis is made up of connective tissue and contains structures such as hair follicles, sweat glands, sebaceous glands (which produce an oily substance called sebum), blood vessels, lymph vessels (which carry lymph into and out of the lymph glands),...
No quantitative differences in melanocytes are seen in various ethnic groups, melanocytes of darker-skinned individuals produce greater quantities of melanin and demonstrate exaggerated responses to cutaneous injury. This translates clinically to an increased susceptibility to irritation and to a greater risk of further pigment alteration in darker-skinned individuals. To decrease the potential risk of exacerbation of hyperpigmentation, the authors' protocol in darker skin types include pre-treatment for 2-4 weeks with bleaching agents such as hy-droquinone 4 cream. If indicated, higher concentrations of hydroquinone (5-10 ) can be compounded. In addition, tretinoin is discontinued 1-2 weeks prior to the series of chemical peels performed at 2- to 4-week intervals 18 . In addition, retinoids can be eliminated from the topical skin care regimen used between peeling procedures.
Most people have dry skin at some point, but people with atopic eczema have periodic eruptions of red, scaly patches of skin. In adolescents and young adults the patches usually appear inside the elbows and behind the knees and at the ankles and wrists in children they appear on the face and neck. But the eruptions can occur anywhere on the body and may not follow a pattern. The itching produced by the eruptions can be severe and prolonged. People who have atopic eczema seem to have easily irritated skin, so anything that dries or irritates the skin may trigger a flare-up. They are often sensitive to low levels of humidity, and their skin condition may worsen in the winter. If this is true for you, try to bathe no more than once a day, avoid using very hot water, and use the mildest soap you can find. After bathing, pat your skin dry do not rub it. Immediately apply a moisturizing lotion or oil to your skin, before it has completely dried. Avoid dressing in clothes made of rough or...
Photodynamic therapy is based on the photo-oxidative effects (i.e., generation of oxygen radicals) creating by illuminating porphyrins and their derivates that have accumulated in tumor cells after topical application. The tumor-selective effect of PDT is due to the preferential uptake of aminolevulinic acid (ALA) into tumor cells. The ratio of uptake of ALA between tumor and normal skin in CTCL is 5 1 (11). The most widely used photosensitizer for topical PDT is delta-ALA. Its uptake results in accumulation of protoporphyrin IX (PpIX) that exerts in vitro toxic effects on both, T- and B-lymphocytes during PDT (12). Photodynamic therapy is capable of inhibiting proliferation of transformed T-cells, in a manner similar to PUVA (13).
To diagnose athlete's foot, your doctor will examine the affected areas of your skin and may remove a small sample of skin to examine under a microscope. The doctor will prescribe an antifungal cream to be applied to your skin. If the athlete's foot is severe, he or she may prescribe oral antifungal medication. You will need to use all of the antifungal medication prescribed even if your skin looks and feels better to be sure that the infection has been completely eliminated.
Erythema, worsening of psoriasis, skin pain, irritation, rash, desquamation, contact dermatitis, skin inflammation, fissuring, bleeding, dry skin, localized edema, skin discoloration. Drug Interactions T Risk of photo-sensitivity when used with fluoro-quinolones, phenothiazines, sulfon-amides, tetracyclines, thiazides.
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Think Clean and Green to Flawless Skin
Lets accept the fact: many of us are skin conscious. As much as possible, we wanted to have a fresh, good looking skin. However, many of us failed to recognize that simple steps are the best ways to attain it.