Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Remission followed prednisolone therapy in 9 out of 21 Nigerian children with the nephrotic syndrome who had highly selective proteinuria (CG/CA less than 15%). Of these, 5 patients have remained well off all treatment during a follow-up of nearly 5 years, 4 have relapsed more than once but have responded to further courses of prednisolone. 3 of 21 with less selective proteinuria also remitted but all relapsed and only one of these has responded again. The other two have relapsed and further courses of prednisolone have not totally abolished their proteinuria though they are asymptomatic and in good health. Toxicity (hypertension, sometimes with encephalopathy and infection) was commoner in the patients with less selective proteinuria treated with steroids than in those with highly selective proteinuria. 3 steroid-sensitive patients who had had repeated relapses became free from relapse off all treatment after a course of cyclophosphamide, given during steroid-maintained remission. All but 2 of the renal biopsies taken were regarded as abnormal. The lesions were less severe in those who responded than in those who did not. There is some evidence to suggest that Plasmodium malariae may be a cause of some of the steroid-sensitive disease, as well as the steroid-resistant.
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PMID:Differential protein clearances and response to treatment in Nigerian nephrotic children. 79 39

We have retrospectively evaluated 24 sepsis episodes caused by viridans streptococci in 23 neutropenic children during a 21 months period at the Pediatric Hematology Unit of St. Louis Hospital. The underlying malignancies included acute lymphoblastic leukemia, acute non lymphoblastic leukemia, aplastic anemia and solid tumor. In 17 children neutropenia, defined as a neutrophil count of less than 500 per cubic millimeter, was caused by cytotoxic chemotherapy. For 6 other children neutropenia was consequential to pretransplant treatment regimen for autologous bone marrow transplantation including cytotoxic chemotherapy and total body irradiation. All patients had a silicone rubber atrial catheter. In 9 patients sepsis was associated only with fever for less than 48 hours. In 5 other children fever was prolonged more than 72 hours in spite of specific antimicrobial therapy. No other organism was isolated. In 10 patients, however, the infectious syndrome was severe and the features included cardiac failure (7 patients), pneumonia (7 patients) resembling adult respiratory distress syndrome, encephalopathy (3 patients) without meningitis and proteinuria, 7 of these patients needed a management in a pediatric intensive care unit and 2 died in spite of adapted antibiotics. Streptococci were isolated in blood cultures in 23 children.
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PMID:[Frequency and severity of systemic infections caused by Streptococcus mitis and sanguis II in neutropenic children]. 278 Jan 2

A survey of 67 pregnancies in 51 professional women (physicians, psychologists, nurses, administrators, etc.) revealed the occurrence of symptoms of cognitive dysfunction such as forgetfulness, disorientation, confusion and reading difficulties in 28 pregnancies occurring in 21 women. These were unrelated to such factors as age of delivery, percentage weight gain, the baby's sex or birth weight, alcohol consumption, smoking, a history of migraine or allergy or other symptoms occurring during pregnancy such as sleepiness and lack of concentration, irritability, loss of interest in job or nightmares. Nor was there any correlation with hypertension, proteinuria, glycosuria, ketonuria, anemia, or morning sickness. Furthermore, these cognitive disturbances were not related to depression or sleep deprivation. Despite these symptoms, none of the women suffering from them were forced to interrupt their professional activities during pregnancy. The syndrome of benign encephalopathy of pregnancy should be recognized so that simple precautions can be taken to prevent any interference with professional or other activities. The etiology of the syndrome is unknown.
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PMID:Benign encephalopathy of pregnancy. Preliminary clinical observations. 395 58

The patients with severe and 10 with accelerated or malignant hypertension were treated with the angiotensin-converting enzyme inhibitor captopril. Captopril acutely reduced blood pressure in all patients except two who had suppressed plasma renin activity. Four patients with encephalopathy showed immediate improvement after the first dose. Two patients could be withdrawn from nitroprusside infusion upon administration of captopril. Nineteen of 20 patients have remained on captopril for 12-32 months. Blood pressure is controlled in 18 and improved in two. Eleven required addition of diuretic and one addition of clonidine. The maximal antihypertensive effect of captopril with or without diuretics was evident after 3 months of continuous therapy and was associated with elevated plasma renin levels, normal aldosterone excretion and preservation of renal function. Captopril was well-tolerated, but produced occasional rash, loss of taste and proteinuria. We conclude that captopril, alone or in combination with other drugs, is effective in both the acute and long-term management of severe and malignant hypertension.
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PMID:Acute and chronic treatment of severe and malignant hypertension with the oral angiotensin-converting enzyme inhibitor captopril. 616 12

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.
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PMID:Acute fatty liver of pregnancy: the hepatologist's view. 805 22

We describe 11 cases of Systemic Lupus Erythematosus (SLE) with pediatric onset (10 females and 1 male). Mean age at onset was 10.9 years (range 3 to 16 years). Initial manifestations: cutaneous involvement in 7 cases, articular symptoms in 7 cases, renal involvement in 5 cases (proteinuria and/or microhematuria, or renal failure), pancytopenia in 3 cases. In 3 cases the onset of the disease was extremely sudden and severe: one patient had an intestinal infarct following mesenteric thrombosis associated with glomerulonephritis; another started with encephalopathy (deep coma, stage III); a third patient presented renal failure due to acute glomerulonephritis. At diagnosis all patients received systemic steroid therapy with the exception of one who had only a cutaneous involvement. The course of the disease is described. We underline that, in our series, it was rare for organs and systems, apart from the central nervous system, to be involved in exacerbations after initial onset of the disease. Six patients are presently asymptomatic or have only minor cutaneous and/or articular manifestations which are well controlled with low-dose cortisone therapy. Laboratory indices did not return to normal in any of the patients. In fact, in our series the disease doesn't appear to reach a complete remission, even many years after onset and no patient seems to be able to withdrawal the therapy at all. Our data confirm, according to other Authors, that the course of LES with paediatric onset is more severe than in adults.
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PMID:[Systemic lupus erythematosus: description of a pediatric series]. 868 1

Mitochondrial encephalomyopathy is a hereditary syndrome showing impairment of muscle and the central nervous system. In this disorder, the following three syndromes have been identified on the basis of characteristic symptoms: Kearns-Sayre syndrome (KSS), mitochondrial encephalomyopathy with lactic acidosis, and stroke-like episodes (MELAS), and myotonic epilepsy with ragged-red fibers (MERRF). In this report, we describe a case of mitochondrial encephalomyopathy with renal disease. A 25-year-old man was referred to our hospital in May, 1992 for evaluation of long-standing proteinuria. He had a small stature, exotropia and no pretibial edema. No mental retardation was observed. Urinary protein excretion was 2.0 g/day and urine sugar was negative. Laboratory examination revealed a serum urea nitrogen 19 mg/dl, and a creatinine value of 1.5 mg/dl. Creatinine clearance was 45.8 ml/min. His serum and spinal fluid lactate value were elevated. Biopsied muscle showed an absence of ragged-red fibers, and the presence of an A-to-G point mutation at nucleotide pari 3243 in the mitochondrial tRNA(Leu(UUR)) in peripheral blood leucocytes. He was thought to have MELAS. On the renal biopsy specimens, light microscopic examinations showed minor glomerular abnormalities with two glomerular collapses and tubulo-interstitial damage. Electron microscopic examinations showed partial thickening of the glomerular basement membrane. We report here this rare case of MELAS with renal disease, and also review seventeen cases of mitochondrial encephalopathy associated with renal disease. The existence of a relationship between mitochondrial disorder and renal damage remains obscure.
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PMID:[A case of mitochondrial encephalomyopathy (MELAS)]. 871 14

Eclampsia is a rare condition peculiar to pregnant and puerperal women, characterized by clinical pre-eclampsia (hypertension, proteinuria, edema) and generalized seizures. Three cases of eclamptic encephalopathy are reported: CT and MRI demonstrated transient abnormalities in the cortical and subcortical regions of the posterior areas of the brain - namely, parieto-occipital lobes - associated with occasional involvement of basal ganglia and/or brainstem. Pathogenesis is still unclear. Strict similarity with the pathological findings characterizing hypertensive encephalopathy suggests that a focal impairment in cerebral autoregulation may be the cause of vasodilation and fluid extravasation leading to hydrostatic edema; selective involvement of posterior areas could be explained by their lesser degree of adrenergic innervation supporting circulatory autoregulation mechanisms.
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PMID:Eclamptic encephalopathy: imaging and pathogenetic considerations. 940 96

Hypertension in pregnancy is defined by a systolic blood pressure > or = 140 mm Hg and a diastolic blood pressure of > or = 90 mm Hg or by a rise in blood pressure of systolic > or = 30 mm Hg and diastolic > or = 15 mm Hg. High blood pressures are found in 5-10% of all pregnancies. The outcome of pregnancy is influenced by the fact whether there occurs a proteinuria in addition to hypertension. While the prognosis of an isolated hypotension is good, the combination of hypertension and proteinuria leading to preeclampsia is the primary cause of maternal death in many countries and is responsible for 20-25% of perinatal mortality. A simple classification divides between chronic hypertension, preeclampsia, preeclampsia superimposed on chronic hypertension and transient hypertension. With chronic hypertension pregnancy outcome is determined by a preexisting nephropathy and the occurrence of a superimposed preeclampsia. Preeclampsia and superimposed preeclampsia are pregnancy induced multiorganic diseases, endangering both the mother and the fetus. Transient hypertension is a benign pathology, which occurs toward the end of pregnancy usually on the basis of a latent essential hypertension, which is laid open through pregnancy. While a severe chronic hypertension in pregnancy must be treated to prevent a hypertensive maternal encephalopathy, a less severe chronic hypertension should not be treated as the risk of a superimposed preeclampsia and the maternal and fetal outcome cannot be influenced by antihypertensive therapy. The incidence of preeclampsia is 3-5% in nulliparae and 0.5% in multiparae. Preeclampsia is a severe and dangerous pathology with an unknown etiology. Pregnancy termination is the only causal therapy. At present it is still recommended to terminate a severe preeclampsia after stabilizing the mother, irrespective of gestational age. In less severe preeclampsia occurring before 32 weeks of gestation, termination of pregnancy can be postponed under intensive monitoring and a prophylaxis with magnesium sulfate in order to accelerate the fetal lung maturation with glucocorticoids. A conservative management in the case of a HELLP-syndrome (Haemolyis, Elevated Liver enzymes, Low Platelets), which is a very severe form of preeclampsia, is not recommended because it hasn't been validated in prospective controlled studies. The most dangerous complication of preeclampsia is eclampsia, which is defined by general tonic-clonic convulsions before or after birth. The most effective prophylaxis of eclamptic attacks is the intravenous therapy with magnesium sulfate. A primary prohylaxis for preeclampsia doesn't exist. Treatment with low-dose aspirin in high-risk patients, i.e. after a severe preeclampsia, in cases of chronic hypertension, in cases of nephropathy and in cases with antiphospholipid-syndrome++ can be recommended. The prophylactic use of low-dose heparin, which has lead to a significant decreased incidence of preeclampsia in retrospective analysis, is now the object of a randomized, controlled trial in our hospital. All women who suffered from a preeclampsia should have a check-up after 3-6 months. Preexisting pathologies are found in up to 40% of patients, mostly in multiparae, i.e. chronic hypertension, nephropathy, endocrine pathologies, anomalies of blood coagulation and antiphospolipid-syndrome.
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PMID:[Hypertensive disorders in pregnancy]. 1054 28

In this work, patients having type 2 diabetes mellitus and diabetic mothers were tested for the presence of mitochondrial DNA point mutation A3243G. This mutation is associated with the MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes), diabetes and deafness. Twenty-two diabetic persons were screened. DNA was isolated from peripheral blood lymphocytes and from swabs of oral mucosa. The mitochondrial DNA point mutation A3243G was detected using PCR-RFLP test. The mutation was detected in oral mucosal DNA of two patients (but not from lymphocyte DNA). One patient was a man with hearing and visual impairments and proteinuria; the other was a woman having proteinuria but no hearing impairment. The mutation was not detectable in oral mucosal DNA from the control persons: 20 diabetic patients having diabetic fathers and 22 healthy, nondiabetic volunteers. The incidence of mitochondrial DNA point mutation A3243G in this study of Croatian diabetic patients is in line with data in the literature.
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PMID:A pilot study of mitochondrial DNA point mutation A3243G in a sample of Croatian patients having type 2 diabetes mellitus associated with maternal inheritance. 1566 Feb 1


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