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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurotoxicological profile of actoprotector bromantane was studied on rats using S. Irwin's protocol of multi-test observation. The drug in doses of 30-300 mg/kg stimulated and in doses of 600-9,600 mg/kg suppressed behavioral activity. Spontaneous motor activity increased after single treatment with bromantane in doses of 30-300 mg/kg, did not change after treatment in doses of 600 mg/kg, and was inhibited after treatment in doses above 600 mg/kg. In doses of 300-600 mg/kg the drug reduced pain sensitivity threshold and in doses above 600 mg/kg elevated the pain threshold and tactile sensitivity and reaction to knock. Bromantane induced mydriasis in all studied doses; in doses above 10 g/kg the preparation induced blepharoptosis. In doses above 5 g/kg bromantane slightly increased respiration rate and depth (Kussmaul-like respiration). In some animals bromantane in high doses induced regurgitation, diarrhea, and polyuria. Rectal temperature decreased by 0.5-1 degrees C after virtually all doses. Behavioral effects of bromantane in doses of 30 and 600 mg/kg were associated with stimulation of the central dopamine and suppression of muscarinic and nicotinic cholinergic structures, n-cholinolytic effects of bromantane was more pronounced at a dose of 30 mg/kg than at a dose of 600 mg/kg.
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PMID:Toxic effect of single treatment with bromantane on neurological status of experimental animals. 1212 51

Aquaporins (AQP) are a family of at least ten homologous water transporting proteins in mammals that are expressed in many epithelial, endothelial and other tissues. Abnormalities in humans and mice lacking AQPs provide direct evidence for their physiological importance. Humans lacking AQP1 or AQP2 manifest polyuria with defective urinary concentrating ability and humans with mutations in MIP (AQP0) develop cataracts. Transgenic knockout mice lacking AQP1 or AQP3 are also remarkably polyuric, and knock-in mice expressing a mutant AQP2 have severe nephrogenic diabetes insipidus resulting in impaired neonatal survival. Other interesting phenotypes in AQP knockout mice include reduced pain sensation, reduced intraocular pressure, defective corneal fluid transport and impaired dietary fat processing (AQP1), dry skin (AQP3), protection from brain swelling and impaired hearing/vision (AQP4), and reduced fluid secretion by salivary and airway submucosal glands (AQP5). However, many phenotype studies were negative, such as normal airway/lung and skeletal muscle function despite AQP expression, indicating that tissue-specific aquaporin expression does not indicate physiological significance. The general paradigm from studies on transgenic mouse models of AQP deletion is that AQPs facilitate rapid near-isosmolar transepithelial fluid absorption / secretion, as well as rapid vectorial water movement driven by osmotic gradients. The transgenic mouse studies suggest that aquaporin inhibitors may have clinical indications as diuretics and in the treatment of cerebral edema, elevated intraocular pressure, and other conditions of abnormal fluid homeostasis.
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PMID:Physiological importance of aquaporin water channels. 1217 89

Pain in diabetes is a common debilitating condition for which pathophysiology remains poorly understood. To evaluate the underlying mechanisms, we used intravenous injection of streptozotocin to produce rapid (24-hour) onset of diabetes (blood glucose > 300 mg/dL and urine glucose > 2,000 mg/dL with polyuria). In this model, mechanical and thermal hyperalgesia and tactile allodynia are detectable by 48 hours after streptozotocin administration in the absence of ketonuria or physical debility. Treatment with insulin attenuated hyperglycemia and prevented the development of mechanical and thermal hyperalgesia. Direct application of streptozotocin to peripheral nerve did not produce hyperalgesia. We conclude that streptozotocin can induce pain independent of a general debility or direct toxic effect of streptozotocin on peripheral nerve and that elevated blood glucose may contribute to the enhanced nociception.
J Pain 2001 Jun
PMID:Rapid onset pain induced by intravenous streptozotocin in the rat. 1462 24

The skeleton is the most common organ to be affected by metastatic cancer. Hypercalcemia of malignancy (HM) affects 10 to 20% of patients with advanced cancer. HM causes a series of symptoms, constipation, nausea and vomiting, confusion and/or stupor, polyuria and polydipsia, bone pains, which decrease quality of life. The normalization of calcemia significantly improves all these symptoms. Despite that, HM remains largely underdiagnosed and undertreated. HM is an emergency. Treatment of HM includes rapid rehydration of isotonic saline and i.v. bisphosphonates. Complications from metastatic bone disease include pathological fracture, HM, spinal cord compression, bone marrow infiltration, pain, and reduced mobility. Treatment with bisphosphonates are effective to reduce these complications. They should be started when bone metastases are diagnosed and continue until it is no longer clinically relevant. The most currently used bisphosphonates were clodronate and pamidronate. The increase convenience of a 15 minutes infusion, the greater efficacy and longer duration of response makes zoledronate the standard of care for HM and metastatic bone disease.
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PMID:[Bisphosphonates in malignant hypercalcemia and bone pain]. 1509 27

Brown tumor is a focal lesion of the bone caused by primary or, less commonly, secondary or tertiary hyperparathyroidism (HPT). While the mandible is the most frequently involved bone in the head and neck region, atypical involvement of the cranium in the area of the sphenoid sinus is exceedingly rare. In the literature, a unique case of brown tumor of the sphenoid sinus was reported in a patient with primary HPT. We present a case of sphenoid sinus and occipital bone brown tumor associated with primary HPT. A 47-yr-old woman presented a 2-yr history of headaches, dizziness, diffuse body and articular pain, fatigue, and a 6-month history of intermittent nausea and vomiting, polydipsia, and polyuria. Magnetic resonance imaging (MRI) demonstrated an expansive mass lesion in the sphenoid sinus with erosion of the sellar floor and medial wall of the right orbit, and expansion in the medulla of bone. Examination of biopsy specimens obtained from sphenoid sinus mass confirmed the diagnosis of brown tumor. The biochemical laboratory studies showed elevation of parathyroid hormone and confirmed the diagnosis of primary HPT. Excision of a parathyroid adenoma affected the metabolic status into normalizing. At the follow-up of 12 months postoperatively, the size of sphenoid sinus brown tumor decreased and the mass of occipital bone disappeared. In conclusion, this is a first report of primary HPT masquerading as a destructive fibrous sphenoid sinus brown tumor associated with a mass lesion of occipital bone and hypercalcemia in the literature.
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PMID:Sphenoid sinus brown tumor, a mass lesion of occipital bone and hypercalcemia: an unusual presentation of primary hyperparathyroidism. 1523 58

We report a case of multisystem Langerhans cell histiocytosis (LCH) with lung, bone and pituitary involvement. A 20-year-old man developed thirst, polydipsia and polyuria in 1983. He had right femur pain from 1988 and osseous LCH was diagnosed based on the operated specimen in 1989. From July 1990, he had right chest pain on coughing and dyspnea and was admitted in November 1990. LCH involving the lungs was diagnosed by CT images and diabetes insipidus was also detected. Steroid therapy was started from 1991, but he discontinued it in 1998. Though he stopped smoking, his clinical symptoms worsened and he experienced bilateral pneumothoraces in 2002 and since then he has been receiving home oxygen therapy. Pulmonary LCH is thought to have a good prognosis, but in recent studies, its survival rate appears low. We report a case of multisystem LCH with lung deterioration over about 15 years.
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PMID:[A case of multisystem Langerhans' cell histiocytosis with lung deterioration over 15 years]. 1684 15

The number of newly diagnosed cases of multiple myeloma in the Czech Republic is about 3-4 per 100 000 persons per year. In the higher age groups, the incidence increases. Multiple myeloma is an illness that reacts well to treatment which can result in periods of remission lasting for years. Some of the patients are even able to return to work. A pre-requisite for successful treatment is early diagnosis and this is usually in the hands of first line physicians. This is the reason why the Czech Myeloma Group, in conjunction with neurologists, orthopedicians and radio diagnosticians has issued the following recommendations for first line physicians containing a more detailed description of the symptoms and the diagnostic pitfalls of the disease. This disease reminds a chameleon for the variety of its symptoms. For the sake of clarification, we shall divide multiple myeloma symptoms into five points, each of which is reason enough to warrant an examination to confirm or rule out a malignant cause of health problems (a negative result does not automatically mean exclusion). If any of the recommended examinations results positive, the diagnostic process must be continued, in which case a general practitioner refers the patient to a specialist health centre. Observing these recommendations should minimize the number of cases of late diagnosis. 1. Bone destruction symptoms. - Unexplained backache for more than one month in any part of spine even without nerve root irritability or without pain in other part of skeleton (ribs, hips, or long bones). - Pain at the beginning of myeloma disease is very similar to benigne common discopathy, however the intensity of backache is decreasing within one months in benigne disease. In the case of malignant process the intensity of bone pain is steadily increasing. - Immediate imaging and laboratory investigation are indicated by resting and night pain in spinal column or in any part of skeleton. - Backache with the sign of spinal cord or nerve compression should be sent for immediate X Ray, and focussed CT/MRI followed by acute surgery if needed. - Osteoporosis especially in men and premenopausal women. 2. Features of changed immunity or bone marrow function. Persistent and recurrent infection, typical is normochromic anaemia, with leucopenia and trombocytopenia. 3. Raised erythrocyte sedimentation rate even increase concentration of total plasma protein. 4. Impaired renal function. Increased level of creatinin or proteinuria, nephrotic syndrome with bilateral legs oedema. 5. Hypercalcemia with typical clinical symptoms (polyuria with dehydratation, constipation, nausea, low level conscience, coma). Every one from these points has to be reason for general medical doctor to start battery of tests: -X-ray of bones focused to painful area (mandatory before physiotherapy, local anaesthesia or other empiric therapy). If plain X-ray does not elucidate pain and symptoms are lasting more than one month, please consider all circumstances and results from laboratory investigation. This patient needs referral to the centre with MRI/CT facilities (CT or MRI is necessary investigation in case of nerve root or spine compression). -Investigation of erythrocyte sedimantion rate (high level of sedimentation of erythrocyte can indicate multiple myeloma). -Full blood count. -Basic biochemical investigation serum and urine: serum urea, creatinin, ionts including calcium, total protein, and albumin CRP (high concentration of total protein indicates myeloma, low level of albumin indicates general pathological process, similary increased concentration of fibrinogen, impaired renal function indicates myeloma kidney, however hypercalcemia is typical for highly aggressive myeloma). -Quantitative screening for IgG, IgM and IgA in serum (isolated raised level one of immunoglobulin with decreased level of the others indicates myeloma). -Common electrophoresis of serum is able to detect monoclonal immunoglobulin level at few gramm concentration. If all the laboratory investigation are in normal level the possibility that the current problems are multiple myeloma origine is smaller, but it does not exclude one of rare variant--non secretory myeloma (undifferentiated plasmocyt lost characteristic feature to produce monoclonal immunoglobulin). If any of tests indicate the possibility of myeloma, patient require urgent specialist referral to department with possibility to make diagnosis of malignant myeloma.
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PMID:[Recommendations for early identification of damage to the skeleton by malignant processes, and for early diagnosis of multiple myeloma]. 1817 27

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.
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PMID:[Electrolyte and acid-base balance disorders in advanced chronic kidney disease]. 1901 44

Brucellosis which is a endemic in Turkey, is a systemic infection which can affect any organ or system in the body. Since signs and symptoms of brucellosis resemble many other diseases, misdiagnosis and related increase in morbidity rate, are common. In this report, a case of brucellosis complicated with endocarditis, pyelonephritis, sacroileitis and thyroiditis, was presented. The case was a 32-years-old female patient in whom the diagnosis of brucellosis was delayed by 12 months since it was not taken into consideration during the clinical follow-up of the patient in various clinical centers. The patient was admitted to our center with the complaints of fever, headache, back pain, night sweats, fatigue, loss of appetite, weight loss, dysuria and polyuria. The patient had a history of consumption of raw milk and dairy products. Positive Brucella tube agglutination test (1/1280) and isolation of Brucella spp. in blood cultures led to the diagnosis of brucellosis. Sacroileitis was diagnosed upon pain on right hip joint movements, pain and restriction at the same joint in FABER test. The detection of vegetation during echocardiography, cardiac murmur during physical examination and the determination of increased ESR and CRP levels led to the diagnosis of endocarditis. Abdominal ultrasonography and urinalysis results (hematuria, proteinuria and pyuria) revealed pyelonephritis and increased free T3 and T4, decreased TSH and positive anti-thyroid autoantibodies (anti-TG, anti-TPO) revealed thyroiditis. Treatment was started with combination of rifampisin (1 x 600 mg/day) and doxycycline (2 x 100 mg/day). After the diagnosis of endocarditis, trimethoprim-sulfamethoxazole (3 x 960 mg/day) and streptomycin (1 x 1 g/day) were added to the treatment. Valve replacement surgery was planned, however, the patient didn't accept surgical intervention and antimicrobial treatment continued with streptomycin for 21 days and other antibiotics for six months. The patient exhibited significant improvement after the medical treatment. Although sacroileitis is a frequent complication of brucellosis, endocarditis, thyroiditis and pyelonephritis are among the rare complications. In cases of brucellosis with multiorgan involvement including endocarditis, successful results may be achieved by aggressive antimicrobial treatment. In endemic areas, brucellosis should always be taken into consideration in patients with fever of unknown origin and multisystem involvement.
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PMID:[A case of brucellosis complicated with endocarditis, pyelonephritis, sacroileitis and thyroiditis]. 1933 91

This article is a shortened version of the clinical guideline for lower urinary tract symptoms (LUTS), which has been developed in Japan for symptomatic men aged 50 years and over irrespective of presumed diagnoses. The guideline was formed on the PubMed database between 1995 and 2007 and other relevant sources. The causes of male LUTS are diverse and attributable to diseases/dysfunctions of the lower urinary tract, prostate, nervous system, and other organ systems, with benign prostatic hyperplasia, bladder dysfunction, polyuria, and their combination being most common. The mandatory assessment should comprise medical history, physical examination, urinalysis, and measurement of serum prostate-specific antigen. Symptom and quality of life questionnaires, bladder diary, residual urine measurement, urine cytology, urine culture, measurement of serum creatinine, and urinary tract ultrasonography would be optional tests. The Core Lower Urinary Tract Symptom Score Questionnaire may be useful in quickly capturing important symptoms. Severe symptoms, pain symptoms, and other clinical problems would indicate urological referral. One should be careful not to overlook underlying diseases such as infection or malignancy. The treatment should be initiated with conservative therapy and/or medicine such as alpha(1)-blockers. Treatment with anticholinergic agents should be reserved only for urologists, considering the risk of urinary retention. The present guideline should help urologists and especially non-urologists treat men with LUTS.
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PMID:Clinical guideline for male lower urinary tract symptoms. 1981 47


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