Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
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HELLP syndrome continues to be a clinical entity of difficult diagnosis. Weinstein first defined it in 1982 giving the practicing obstetrician a sequence of useful initials (H = hemolysis; EL = elevated liver enzymes; LP = low platelets). Since then a lot has been written and it has become clear that the syndrome is a form of severe preeclampsia. The American College of Obstetrics and Gynecology does not include HELLP in the description of severe pre-eclampsia as such but does accept each of its components as being part of severe pre-eclampsia. The case presented deals with a 33 year old white female, admitted at 27 weeks gestation with nausea, epigastric pain resembling acute abdomen, nose bleeding and mild hypertension. The analysis revealed an abnormal liver profile with elevated GOT, GPT and LDH, heavy proteinuria (14.4 g/day), decreased platelet count (92000/mm3) and elevated total bilirubin. Pregnancy was terminated by cesarean section 24 hours after admission because the patient's condition was deteriorating. Obviously in pre-eclampsia/eclampsia there is a systematic injury to all tissues. Proof of this is the hypertension as a consequence of vascular spasm and proteinuria due to glomerular injury. In HELLP the sequence of events is probably altered; hepatic injury precedes vascular and renal injury of conventional preeclampsia. The syndrome results from many clinical and pathological symptoms derived from endothelial microvascular injury which determine a rapid platelet activation causing vascular spasm, platelet aggregation and further endothelial injury through a feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Massive proteinuria and HELLP syndrome]. 130 8

Vascular spasm has been considered to be an important component of the eclamptic state. If this abnormal vascular reactivity affects the coronary arteries in eclampsia, one might expect to find areas of myocardial contraction band necrosis, a lesion secondary to coronary reflow after periods of no flow. We reviewed the cardiac findings in the 34 patients with fatal eclampsia (hypertension, edema, proteinuria, and convulsions without evident cause) autopsied at The Johns Hopkins Hospital since 1899, and compared each with the next pregnant or puerperal nontoxemic autopsied patient. The eclamptic patients were 15-45 years old (average 27 years). Convulsions began antepartum in 21 patients, intrapartum in eight, and postpartum in five. The hearts weighed 200-407 g (average 312 g). One heart had rheumatic valvular disease and one had myocarditis. Histologic study of heart sections showed the presence of contraction band necrosis in 12 cases (35%). The control cases included two patients with rheumatic valvular disease, two with endocarditis, two with myocarditis, two with pericarditis, and one with leukemic infiltration. Only one control patient (3%) had contraction band necrosis (p less than 0.001). The frequent occurrence of myocardial contraction band necrosis suggests that coronary artery spasm may be common in patients who die with eclampsia.
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PMID:Morphologic evidence for coronary artery spasm in eclampsia. 719 18

Pre-eclampsia is a pregnancy-specific syndrome of unknown etiology, defined by clinical findings of elevated blood pressure combined with proteinuria and oedema. The decidual portion of the spiral arteries of women who later develop pre-eclampsia does not undergo the normal pregnancy-induced remodelling that converts these vessels to high volume-low resistance conduits. We have postulated that this failure leads to vascular spasm, restricted blood flow, placental ischaemia and the release of toxic substances that enter the maternal circulation, resulting in multi-organ disease. The complex and interwoven pathways of endocrine, paracrine and autocrine factors appear to result in a vicious cycle of endothelial cell dysfunction, which is expressed clinically as pre-eclampsia.
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PMID:New insights into the etiology of pre-eclampsia. 833 23

Hypertension in pregnancy is one of the main causes of maternal, fetal and newborn morbidity and mortality in civilised countries. Current recommendations of the European Society for Hypertension prefer definition of hypertension in pregnancy based on absolute values of blood pressure, i.e. systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. The most important task of classification of hypertension in pregnancy is to distinguish whether hypertension comes before pregnancy (the so called pre-existing hypertension) or whether it is a pregnancy-induced condition (the so called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within the first 20 weeks of pregnancy. Gestational hypertension is characterised with poor blood circulation in many body organs, higher value of blood pressure usually being just one of the characteristic features. Non-pharmacological treatment of hypertension must be considered in pregnant women with systolic blood pressure 140-150 mm Hg or diastolic blood pressure 90-99 mm Hg. Salt restriction is not recommended, as well as weight reduction in obese women. Systolic blood pressure > or = 170 mm Hg or diastolic blood pressure > or = 110 mm Hg in pregnant women must be considered serious condition necessitating hospitalisation. Pharmacological therapy should include labetalol i.v. or metyldopa or nifedipin administered orally. Intravenous administration of dihydralazine is no longer a therapy of choice, for its use is connected with increased occurrence of adverse effects. The threshold values for commencement of anti-hypertension therapy are systolic blood pressure 140 mm Hg or diastolic blood pressure 90 mm Hg in females with gestational hypertension without proteinuria or with pre-existing hypertension before commencement of 28th week of pregnancy. Drug administration to reduce hypertension is instituted after reaching the same threshold values in females with gestational hypertension and proteinuria or after occurrence of the symptoms any time during pregnancy, with the same threshold values of blood pressure in the case of pre-existing hypertension at the presence of accompanying diseases or organ malfunction and further in the case of pre-existing hypertension and gestational hypertension. In other cases drug treatment of hypertension is recommended at systolic blood pressure values of 150 mm Hg or diastolic blood pressure values of 95 mm Hg. Unless serious hypertension is involved, the drugs of choice include metyldope, labetalol, calcium channel blockers and beta-blockers. Calcium channel blockers are considered safe, unless administered concurrently with magnesium sulphate (risk of hypotension in the case of potential synergism). ACE inhibitors and angiotensine blockers II (AT1-blockers) are contraindicated in pregnancy. Treatment with diuretics is not substantiated, unless oliguria is present. I.v. magnesium sulphate is recommended for prevention of eclampsia and spasm treatment.
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PMID:[Hypertension in pregnancy]. 1672 58

Membranous nephropathy (MN) accompanying Neuromyelitis optica spectrum disorders (NMOSD) has rarely been described previously. We recently presented a 45-year-old Chinese male presenting with recurrent lower extremity pitting edema, or eyelid edema, proteinuria and hyperlipidemia. especially intractable hiccup and vomiting, painful tonic spasm (PTS) as the revealing symptom of a demyelinating disorder of central nervous system. The kindey biopsy specimen showed MN stage 2. Serological testing revealed antibodies AQP4, MRI head and spine revealed medulla oblongata and C1-C2 cervical vertebra lesions. Treatment with methylprednisolone, cyclophosphamide, azathioprine resulted in consistent clinical improvement.
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PMID:Membranous nephropathy with Neuromyelitis optica spectrum disorder. 2864 74