Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venous thoracic outlet syndrome is caused by subclavian vein obstruction with or without thrombosis. The primary symptom is arm swelling, frequently accompanied by cyanosis, pain, and occasionally paresthesias. Venography is the only reliable diagnostic tool. Therapy has three goals: (1) remove the thrombus (in thrombotic cases), (2) remove the extrinsic compression, and in a minority of cases, (3) remove the intrinsic stenosis.
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PMID:Venous thoracic outlet syndrome. 1500 93

Ischemic steal secondary to a hemodialysis arteriovenous (AV) access occurs in approximately 10% of cases. The pathophysiological basis of this condition is a marked decrease or reversal of flow in the arterial segment distal to the AV fistula or AV graft, induced by the low resistance of the fistula outflow. Clinically it can manifest with either mild symptoms (coolness, paresthesia, and absence of distal pulses), or severe symptoms (rest pain, severe paresthesia, paralysis, cyanosis, and gangrene) immediately after construction of the AV access or later after its inception. Diagnosis is based on clinical manifestations, aided by the vascular laboratory and angiography. Mild cases can be observed closely, most of them will reverse in a few weeks. In order to prevent permanent sequela, severe cases require immediate intervention. Several surgical treatments have been used: access ligation, banding, elongation, distal arterial ligation, and distal revascularization-interval ligation. Best results, with maintenance of access function and reversal of symptoms, have been obtained with the distal revascularization-interval ligation procedure.
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PMID:Management of steal syndrome resulting from dialysis access. 1501 Nov 79

Maurice Raynaud first described the vasospasm of arterioles in 1862, and Raynaud's phenomenon is now felt to be common, affecting up to 20% of women of childbearing age. Raynaud's phenomenon has been reported to affect the nipples of breastfeeding mothers and is recognized by many lactation experts as a treatable cause of painful breastfeeding. In 1997, Lawlor-Smith and Lawlor-Smith reported 5 women with Raynaud's phenomenon associated with breastfeeding, but there are few other case reports, and none report the possible relationship between Raynaud's phenomenon of the nipple and previous breast surgery. We report 12 women who breastfed 14 infants, all of whom were seen in 1 pediatric practice and 1 lactation consultation center in San Francisco, California, within the past 3 years. Of the 12 women, 11 were seen between June 2002 and May 2003. All women suffered from extremely painful breastfeeding, with symptoms precipitated by cold temperatures and associated with blanching of the nipple followed by cyanosis and/or erythema. Poor positioning and poor attachment or latch may cause blanching of the nipple and pain during breastfeeding, but 10 of the 12 mothers were evaluated by experienced lactation consultations, who were sure that inappropriate breastfeeding techniques were not contributing factors. Because the breast pain associated with Raynaud's phenomenon is so severe and throbbing, it is often mistaken for Candida albicans infection. It is not unusual for mothers who have Raynaud's phenomenon of the nipple to be treated inappropriately and often repeatedly for C albicans infections with topical or systemic antifungal agents. Eight of our 12 mothers and their infants received multiple courses of antifungal therapy without relief before the diagnosis was made. To diagnose Raynaud's phenomenon accurately, additional symptoms such as precipitation by cold stimulus, occurrence of symptoms during pregnancy or when not breastfeeding, and biphasic or triphasic color changes must be present. All our mothers experienced precipitation of symptoms by cold stimuli and demonstrated biphasic or triphasic color changes, and 6 of the 12 experienced symptoms during pregnancy. Interestingly 3 of 12 mothers also reported a history of breast surgery, including 1 mother who had a fibroadenoma removed and 2 who had breast-reduction surgery. The association between breast surgery/implants and autoimmune disease, including Raynaud's phenomenon, has been discussed extensively, but the association of Raynaud's phenomenon of the nipple during breastfeeding has not been reported previously. Given the small numbers in the study, it is uncertain as to whether this may be a precipitating factor in developing Raynaud's phenomenon. Treatment options include methods to prevent or decrease cold exposure, avoidance of vasoconstrictive drugs/nicotine that could precipitate symptoms, and pharmacologic measures. There are reports in the lay press of the use of herbal medicines, aerobic exercise, and dietary supplements, but because most women with painful breastfeeding require immediate relief of the pain to continue breastfeeding successfully, it is important to offer a treatment plan that will alleviate the pain quickly. Nifedipine, a calcium channel blocker, has been used to treat Raynaud's phenomenon because of its vasodilatory effects. Very little of the medication can be demonstrated in breast milk and thus is safe to use in breastfeeding mothers. Of the 12 mothers in our series, 6 chose to use nifedipine, and all had prompt relief of pain. Only 1 mother developed side effects from nifedipine. Pediatricians and lactation consultants should be aware of this treatable cause of painful breastfeeding and should specifically question their patients, because most mothers will not provide this information to the breastfeeding consultant. Prompt treatment will allow mothers to continue to breastfeed pain free while avoiding unnecessary antifungal therapy.
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PMID:Raynaud's phenomenon of the nipple: a treatable cause of painful breastfeeding. 1506 Feb 68

NEW DENOMINATIONS: With the arrival of new therapeutic strategies requiring rapid intervention, acute coronary syndromes required classification on earlier data than the Q-wave or MB creatinine kinase. In a patient with anginal pain and depending on the electrocardiogram, we now distinguish syndromes with or without ST segment elevation. REGARDING ANTIPLATELET DRUGS: Aspirin is used in all cases, as well as clopidogrel. Anti PG IIb-IIIa agents are set aside only for the forms at risk, when an angioplasty is envisaged in the short term. ANTICOAGULANTS: Enoxaparin has demonstrated its superiority over unfractionated heparin. In general, the biological controls are not indispensables; they can however be used in certain cases (notably elderly patients). OTHER TREATMENTS: These are beta-blockers (first dose via the intravenous route in the case of persisting pain, then relay to the oral route), calcium-channel blockers (diltiazem, verapamil) when beta-blockers are contraindicated, nitrate derivatives with demonstrated antalgic effect but not to be used if an extension to the right ventricle or low blood pressure is suspected, nasal oxygen in the case of cyanosis or respiratory distress, enzyme conversion inhibitors if hypertension persists, and repeated intravenous injections of morphine in the case of persisting intense pain. CORONARY REVASCULARISATION: In all the patients considered at high risk, coronary revascularisation is recommended within the first 24 hours, when technically possible.
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PMID:[Acute coronary syndromes without ST segment elevation]. 1522 96

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Fifty injuries by stingrays are annually examined in the New Caledonia hospital. The injuries occur most often in the lower extremity, rare puncture injuries to the thorax or abdomen can cause death. The wound is associated with envenomation. The pain is intense with oedema, cyanosis, erythema often followed by tissue necrosis. In many cases, the management of stingray wounds is inadequate and the gravity often not well appreciated. Localized morbidity and prolonged healing may occur without an effective surgical management. Wound exploration and debridement are particularly indicated after first-aid measures, such as immersion in hot water. The characteristics, treatment and prevention are discussed in connection with two cases.
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PMID:[Surgical management of stingray injuries. About two clinical cases]. 1535 63

Cholesterol crystal embolization (cholesterol embolism, cholesterol embolic disease) is a multiorgan disease, which is a severe iatrogenic complication from an invasive vascular procedure, such as manipulation of the aorta during angiography or vascular surgery, and after anticoagulant and fibrinolytic therapy. The diagnosis is made postmortem in two-thirds of cases. Cholesterol crystal embolism is an increasing and still underdiagnosed disease. Pathognomonic is the constellation of acral pain, nonhealing ulcerations and necrosis, livedo racemosa with intact peripheral arterial pulses and sudden onset of renal failure and arterial hypertension. Biopsy of the affected organs is essential for diagnosis. We report the case of a 66-year-old man who following coronary arteriography with PTCA and implantation of stents developed acral necrosis and cyanosis, livedo racemosa and acute irreversible renal failure.
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PMID:[Cholesterol embolism syndrome after coronary angiography]. 1559

Popliteal artery entrapment syndrome (PAES) is an uncommon pathological entity, caused by segmental popliteal artery compression by the surrounding myofascial structures. Clinical symptoms may appear acutely, with temporary ischaemic attacks, or chronically, with concerned calf claudicatio intermittens and for 30% are bilateral. Diagnosis, besides being based on clinical objectivity (acute and deep pain to the struck limb, mainly during active plantar hyperextension) and history-taking (subject-age and lack of atherosclerosis), is based on ultrasonographic (eco-color Doppler of the aortic-iliac-femural-popliteal trunks, tensiometric Doppler), angio-RM, angio-CT scan and dynamic angiographic exams. Treatment, essentially, is surgical by simple freeing of the popliteal artery from surrounding myofascial structures or by autologous vein (saphenous v.) interposition grafting and patching, or bypass without vessel resection. About clinical case reported by the authors, 44-years female with left calf acute pain symptoms, cold skin by the thermo-touch, hypo-paraesthesia with fifth toe cyanosis and walking inability, surgical treatment, because of precox diagnosis, consisted of simple cut of myofibrous shoot starting from medial head of the left gastrocnemious muscle and compressing popliteal artery, with clinical chart complete resolution.
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PMID:[Early diagnosis importance for a correct surgical treatment of PAES (popliteal artery entrapment syndrome)]. 1596 Mar 45

Candida albicans (CA) antigen immunotherapy for recalcitrant warts is a novel treatment that has had much success in the recent past. Although several side effects are well documented in the literature, we report a new adverse reaction to CA antigen immunotherapy for verruca vulgaris of the distal fingertip. Our patient received an intradermal injection of CA antigen solution into periungual warts located on the distal left thumb and distal subungual area of the left index finger. Within 24 hours, the patient reported pain, edema, and a purple hue to only the index finger. Incision of the finger demonstrated no hematoma or compartment syndrome. Although the etiology is unknown, we believe the condition was most likely due to edema and vascular compromise secondary to a vigorous delayed-type hypersensitivity reaction, possibly leading to cyanosis of the distal index finger. We report this case to make physicians who use intralesional CA antigen aware of a new possible complication at this anatomic location.
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PMID:The painful purple digit: an alarming complication of Candida albicans antigen treatment of recalcitrant warts. 1653 37

In both superficial and deep femoral artery involvement, where angioplasty of the former is not suitable or feasible, angioplasty of the latter seems to be the method of choice and is a less invasive and efficient treatment particularly for limb threatening ischemia, an appropriate obstruction morphology provided. The authors describe a case of a 73-year-old man, with a rest pain of the foot and intermittent cyanosis of the toe, who underwent stent placement with transluminal angioplasty for severe stenosis in the deep femoral artery with the occluded superficial femoral and popliteal artery. The patient's ankle brachial index was remarkably increased from 0.25 to 0.61, and the preoperative symptoms were improved.
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PMID:Stent placement for severe stenosis in the deep femoral artery with the occluded superficial femoral and popliteal arteries. 1599 24


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