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)

Current strategy for the use of biochemical markers in the diagnosis of acute myocardial infarction is not yet uniform. New markers of myocardial damage have significantly altered the former viewpoints. The study included 41 patients with confirmed acute myocardial infarction (25 males and 16 females, age range 42-85 years). Control group comprised of 25 patients with chronic renal failure without signs of acute coronary event (n = 11) and patients with confirmed coronary artery disease (n = 14). The level and activity of CKMB (microgram/L and U/L), and the level of myoglobin and cTnl were determined. The results showed the sensitivity of CKMB (microgram/L) in the first six hours from the onset of pain to be statistically significantly higher than the sensitivity of cTnl, while myoglobin was confirmed to be the earliest marker. Determination of CKMB (U/L) activity should be abandoned since it was found to have the lowest sensitivity and specificity. Also, a combination of myoglobin and CKMB (microgram/L) showed a statistically significantly higher sensitivity and diagnostic efficacy but lower diagnostic specificity compared to the combination of myoglobin and cTnl.
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PMID:Clinical value of biochemical markers in the diagnosis of acute myocardial infarction. 1126 88

A 76-year-old woman, who had received hemodialysis due to chronic renal failure of unknown cause for two months, was admitted to our hospital. She was suffering from severe pain in the left thigh, rapidly progressive anemia and thrombocytopenia after receiving a contusion on her left thigh. Soon after admission, the patient died of shock. Autopsy revealed multiple myeloma(lamda type) with extramedullary plasmacytoma and systemic amyloidosis. In the kidney, there were typical tubular casts with multinucleated giant cells and interstitial fibrosis. More specific findings included an extramedullary plasmacytoma in the left iliopsoas muscle surrounded by a huge hematoma. Internal hemorrhage resulting from indirect contusion at this site was likely to have caused her shock. Since typical clinical findings of multiple myeloma, such as serum M protein and hypercalcemia, were not found in this case, it was difficult to make a diagnosis of multiple myeloma. In case of multiple myeloma, micro- or macroscopic extramedullary tumor formation is not rare, but there has been no report of a case with macroscopic tumor formed in skeletal muscle, exhibiting massive hemorrhage. We report here a case of multiple myeloma with an unusual clinical course.
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PMID:[A case of myeloma kidney complicated by extramedullary plasmacytoma with massive bleeding]. 1143 3

A difficult pain occurred in a man with chronic renal failure as a result of the underlying condition of calciphylaxis. In this condition, calcification of small and medium-sized arteries occurs, which may result in ischemia and gangrene. In general, the prognosis is poor, with mortality rates ranging from 23-63%. Pain associated with this condition has been previously reported. In this report, the pain occurred in the lower limbs and penis, and was associated with local necrosis. The pain was observed to be significantly worse on dialysis. A multiprofessional approach to care ultimately resulted in good symptom control.
J Pain Symptom Manage 2001 Jul
PMID:A case of difficult pain in a patient with chronic renal failure and calciphylaxis. 1151 4

Calciphylaxis is a rare, painful, necrotizing skin condition that occurs most frequently in patients with chronic renal failure who are receiving dialysis. These patients commonly have secondary hyperparathyroidism. Treatment involves a multidisciplinary approach. Surgical wound debridement, local wound care, pain control, and nutritional support are the primary care issues that must be addressed. The outcome is often poor, with the fatal outcome often resulting from sepsis.
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PMID:Calciphylaxis in the patient with chronic renal failure. 1183 81

A 73-year-old woman with chronic renal failure developed generalized muscular weakness and pain 6 days after the start of allopurinol treatment(200 mg/day). Routine laboratory tests revealed elevated levels of serum creatine kinase, and the patient was clinically diagnosed as rhabdomyolysis, due probably to severe myositis. A high level of serum oxipurinol, the chief active metabolite of allopurinol, was also revealed. The muscular weakness was relieved in seven weeks with intermittent hemodiafiltration.
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PMID:[A case of allopurinol-induced muscular damage in a chronic renal failure patient]. 1192 47

A 15-year-old boy with chronic renal failure secondary to Alport's syndrome underwent living-related renal transplantation from his 48-year-old father. His primary immunosuppressive regimen was composed of tacrolimus, mizolibine, and methylprednisolone. The postoperative course was satisfactory with one episode of mild acute rejection, treated successfully with methylprednisolone pulse therapy. Two months later, hypercalcemia (11.8-13.2 mg/dl) and hypophosphatemia (2.5-3.0 mg/dl) were noted without any bone symptoms. The serum intact-parathyroid hormone (PTH) and serum alkaline phosphatase levels were 240 pg/ml and 2483 IU/l, respectively. Ultrasound studies revealed enlargement of the two parathyroid glands. Under the diagnosis of tertiary hyperparathyroidism, he underwent percutaneous ethanol injection (PEIT) into the left parathyroid gland. Although levels of serum calcium and phosphorus returned to normal ranges and the intact PTH level decreased to 95 pg/ml with the three injections, another injection was needed to normalize recurrent hypercalcemia 2 months later. The patient experienced only transient mild dysphonia and local pain after PEIT. Although PEIT is believed less effective than parathyroidectomy, it has some advantages such as applicability to high-risk patients, repeatability of treatment, low incidence and severity of side effects.
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PMID:A case of post-transplant hyperparathyroidism treated with ethanol injection. 1195 72

Autosomal dominant polycystic kidney disease (ADPKD) has aroused great interest these last years, especially after the discovery of the genes responsible for this disease. It remains a frequent cause of chronic renal failure (CRF). In this work we report the results of a multi-centre retrospective study. The data relates to 41 centres of nephrology and dialysis in Morocco, 308 Moroccan families and 420 observations. We have tried to determine the frequency of this pathology in Morocco, its complications and difficulties in taking care of it. The average age of the discovery of ADPKD was 46 +/- 3 years and the sex ratio was of 1.08. The ADPKD frequency among Moroccans who undergo dialysis was 6.5%. Pain was the most frequent symptom which revealed the disease (21%); while renal failure at different stages was found in 17% of the patients and high blood pressure (HBP) in 11%. The clinic diagnosis was confirmed by echography in 95% of cases. The association with a hepatic cysts was found in 17.8% of the cases. In addition, to HBR and urinary tract infection, the complications were largely dominated by renal chronic failure and the difficulties in taking care of it because of economic problems. Through this the authors discuss and report the profile and the prognostics of this infection in our society, with a special focus on the evolution of the renal function, the delay in the diagnosis and the management.
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PMID:[Autosomal dominant polycystic kidney disease (ADPKD). in Morocco. Multicenter study about 308 families]. 1201 54

Renal transplantation from a living donor is now considered the best treatment for chronic renal failure. We reviewed the operative complications in 38 living related donor nephrectomies performed at our institution over the past 14 years. The mean age of our donors was 30 years old with age range between 18 and 58 years old and female predominance (55.2%). These swabs were realized by a posterolateral lumbar lombotomy with resection of the 11 third. The left kidney was removed in 34 donors (90%), surgical complications were noted in 39.4% of the cases: one case of wound of inferior vena cava (2.6%), one case of release of the renal artery clamp (2.6%), four cases of pleural grap (10.5%), one case of pneumothorax (2.6%), one case of pleurisy (2.6%), three cases of urinary infection (7.8%), three cases of parietal infection (7.8%) and one case of patient pain at the level of the wound (2.6%). There were no mortalities. We conclude that the morbidity of living donor nephrectomy is negligible compared with the advantages for the recipient.
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PMID:[Surgical complications of nephrectomy in living donors]. 1205 87

Although colchicine induced myopathy has been described in patients with chronic renal failure, colchicine induced myopathy with myotonia has been reported very rarely. A 49-year-old man with chronic renal failure was hospitalised for investigation of fatigue, malaise and severe pain in all extremities. He was on colchicine therapy for 5 months. Neurological examination showed mildly decreased sensation in a distal symmetric pattern in lower extremities, moderate proximal limb weakness, hyporeflexia and severe myalgia on palpation. No clinical evidence of myotonia was present. Laboratory studies showed elevated creatine phosphokinase (CK), lactic dehydrogenase (LDH), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Electromyographic (EMG) findings were compatible with myopathy and abundant, widespread myotonic discharges were determined. Muscle biopsy was consistent with vacuolar myopathy. After withdrawal of colchicine, CK, LDH, AST and ALT levels were normalised and the symptoms were disappeared gradually. In conclusion, the detection of myopathic motor unit potentials with myotonic discharges on EMG in patients on colchicine therapy is an important finding and it is possible to suggest that this clue may lead to the invasive procedure of muscle biopsy unnecessary.
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PMID:Colchicine-induced myopathy with myotonia in a patient with chronic renal failure. 1295 45

Fabry disease is a hereditary metabolic disease, with an X-linked transmission, that is due to the deficit of alpha-galactosidase A, a lysosomal enzyme. The enzyme deficiency is responsible for an accumulation of neutral glycosphingolipids in the organism with a consequent disease of overload that is responsible for pain, dermatological, renal, cardiac, gastro-intestinal, cochlear and neurological manifestations. Fabry disease starts during childhood but the diagnosis is often made too late. An early diagnosis is nevertheless essential in order to commence a treatment before the occurrence of morbid cardio or cerebro-vascular accidents, or the development of end-stage chronic renal failure. Some phenotypic variants of Fabry disease are probably under-diagnosed among patients with so-called idiopathic hypertrophic cardiomyopathy on haemodialysis. Treatment by substitution of the enzyme with a recombinant alpha-galactosidase has been recently validated in breakthrough controlled clinical trials. Substitutive enzyme treatment represents a major therapeutic development. At the same time, it raises numerous questions such as the ideal age for initiation of treatment, the dose and the optimal frequency of enzyme administration, the reversibility of certain histopathological lesions and the determination of the best markers for the assessment and follow-up of the efficacy of treatment. Monitoring of the plasma levels of the enzyme substrate and the antibody titre seem to be essential. The documentation of short-term clinical benefits could require the use of sophisticated investigation methods such as the study of the myocardial function by tissue Doppler imaging.
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PMID:[Fabry disease in 2004]. 1501 73


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