Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of correlating the L/S ratio in the amniotic fluid with fetal lung maturity has been substantiated in normal pregnancies. In gestations complicated by fetomaternal diseases, however, the assay is less reliable. This study involves 555 pregnancies in which there was a significant maternal, fetal, or placental disorder. The L/S ratio was related to fetal respiratory maturity as measured by Dubowitz criteria and the occurrence of RDS. The results show that pre-eclampsia, chronic hypertension, diabetes (Class D, E, F), significant cardiovascular disease, severe hemoglobinopathies, various congenital anomalies, chronic placental insufficiency, and prolonged ruptured membranes accelerated the L/S ration. Conversely, mild diabetes (Class B, C), intrinsic renal disease, hepatitis, collagen disease, hydrops fetalis, syphilis, and toxoplasmosis were associated with a delay in the L/S ratio. A significant increase in erroneous responses was noted in these patients when the L/S ratio was correlated to infant maturity and to the incidence of RDS. Possible mechanisms for these findings are discussed.
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PMID:The lecithin/sphingomyelin ratio in cases associated with fetomaternal disease. 57 73

Thirty consecutive patients with severe scleritis or episcleritis were admitted as in-patients to the Medical Ophthalmology Unit and assessed for systemic disease. There were seventeen women and thirteen men. The mean age was 53 with a median of 57 (range 23-83). Eighteen of the patients had scleritis: eleven of these had evidence of connective tissue disease and three of them had temporal arteritis. Twelve patients had episcleritis: six of them had a collagen disease and one of them developed temporal arteritis. This high incidence of temporal arteritis in association with scleritis has not been previously reported. It is important to diagnose and treat overt temporal arteritis early with parenteral steroids so that ischaemic papillopathy can be avoided. A higher incidence of collagen diseases than previously described is reported in episcleritis. It is thought that this is secondary to selection since patients with the usual self-limiting episcleritis are not normally referred for further in-patient investigation. In no patient was more than one significant diagnosis made. There was no significant medical illness in only 11% of patients with scleritis and 33% of patients with episcleritis. The majority of the non-collagen diseases (e.g. hypertension) were not previously recognized. In none of the patients with temporal arteritis was the diagnosis made before admission. It is concluded that full examination and investigation for underlying disease is indicated in both scleritis and severe episcleritis.
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PMID:Scleritis and temporal arteritis. 101 96

A 22-year old unmarried healthy woman was admitted to the Swedish department with low fever, tiredness, SR 75 mm, positive uricult, but no urinary tract symptoms. Urinary tract infection was suspected and treatment was started with norfloxacin. Nevertheless, the urine culture proved to be negative. A few weeks later she had increasing trouble with stiff knee and shoulder joints and the left foot became swollen. The subfebrile status continued, and tonsillitis was suspected and diagnosed. V-penicillin and cefaklor treatment was applied. She was transferred to the infectious diseases ware, where fever was confirmed with leukocytosis (19 x 1 billion/1), C-reactive protein at 66 (normal value 10) mcg/ml, pronounced blood pressure increase (160/130 mm Hg), anemic signs, and pathological liver status with increased transaminases (ASAT 6.3-10.4 and ALAT 8.,8-16 ukat/1). ALP increased slightly to 6 ukat/1. The symptoms of weight loss indisposition, and muscles and joints aches, especially in foot ache continued. Collagen disease was suspected, and she was transferred to the internal medicine department. She regularly had tachycardia and high blood pressure. She had to use crutches for mobility because of the pain. S-albumin was 32 (normal 36- 50) g/l and S-hepatoglobin was 2.7 (normal value .4-1.8) g.l. Various others tests were normal. Ulnaris neuropathy was suspected on the left hand. Intensive blood pressure reducing combination treatment was started with 200 mg x 1 of metoprolol, 10 mg x 2 nifedipin, and 20 mg x 1 enalapril. The Desolett oral contraceptive (containing 30 mcg of ethinyl estradiol and 150 mcg of desogestrel) she had been taking for a few months were discontinued. Quick improvement of clinical and laboratory parameters followed. SR and leukocytosis became normal. The values of ALP, ASAT, and ALAT became normal some days later. She was discharged shortly thereafter, and blood pressure medication was gradually discontinued. In the 1940s there were reports about the hepatotoxic effects of synthetic estrogens followed by carbohydrate, lipid, and protein metabolism alterations. Jaundice has also been reported, and the Swedes have an ethnic susceptibility to it. The global incidence rate is 1/10.000 vs. 1/100 and 1/4000 in Sweden induced by high-dose OCs containing more than 50 mcg ethinyl estradiol, but with low-dose OCs this rate is much lower. Both estrogens and gestagens can increase blood pressure. A 1969 study reported that 22 young women developed arthritis, arthralgia, and myalgia after taking pills for 3- 12 months. Rheumatic symptoms were also recorded with pill use. Thus, it is very likely that OCs were responsible for the patient's symptoms, especially since her status rapidly improved after discontinuing them.
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PMID:[Were the severe adverse effects on several organs and the marked blood pressure increase caused by oral contraceptives?]. 182 62

A case of polyarteritis nodosa (PN) in childhood involving various organs such as the gastrointestinal tract, skin, CNS, kidneys and liver with hypogammaglobulinemia is reported. This 6 month old girl was admitted to our hospital with vomiting, diarrhea, bloody stools with mucous and weight loss. For the past 5 months she had these abdominal symptoms. She was diagnosed as having PN of the Kussmaul-Maier variety on the grounds of the biopsy of skin lesion where a necrotizing vasculitis was found. Prednisolone and methylprednisolone pulse treatment were not effective in suppressing the progress of the disease. At the age of 1 year 7 month a combination therapy of prednisolone and immunosuppressants (cyclophosphamide) was started and this was found to be effective. She was discharged when she was 2 year and 2 month. The dosage of prednisolone was tapered as the activity of the PN decreased and she did well with a maintainance dosage of 9.5 mg/day. At 3 year 6 month of age she suddenly developed hypertension (the plasma renin activity was found to be 16.6 ng/m/hr. and the aldosterone 220 ng/dl). CNS involvement such as spinal cord dysfunction, left sided convulsions, cerebral hemorrhage developed 5 months later. Methylprednisolone pulse therapy was performed 3 times and 2 mg/kg/day of prednisolone was administered. In spite of this therapy she passed away with a massive cerebral hemorrhage at the age of 4 year 8 month. Unfortunately an autopsy was not performed. Results of the immunological tests proved that the hypogammaglobulinemia was a common variable immunodeficiency (CVI). It has been reported that primary immuno-deficiency syndrome is often associated with collagen disease and auto-immune disease. This lack of the defense mechanism against the virus or extra antigen could be related to the onset of collagen and auto-immune disease. As the correlation between CVI and PN has not been clarified this case is of interest as concerns the cause of PN.
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PMID:[A case of hypogammaglobulinemia associated with polyarteritis nodosa presenting a variety of symptoms in childhood]. 197 16

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

Captopril, an inhibitor of the conversion enzyme, is a medication with a known efficacy in the treatment of arterial hypertension and congestive cardiac insufficiency. Its side-effects are few. Among them, agranulocytosis is a severe complication, all the more severe and frequent as it occurs in patients with chronic renal insufficiency, collagen disease, or patient treated with medication having a leucopenic potential. Our case reports an agranulocytosis secondary to captopril in a patient with cardiac insufficiency presenting none of these aggravating factors. The mechanism of agranulocytosis secondary to captopril remains currently debatable, but does not seem, in the present case, to be dose related. Thus, a captopril prescription must comply with certain rules; decrease of the dosage in case of renal insufficiency, usual precautions in patients with collagene diseases. The association to a medication with leucopenic potential is to be avoided. Hematologic monitoring will be adapted to each particular case.
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PMID:[Agranulocytosis caused by captopril]. 354 68

The 6 cases reported here constitute, with 5 previously published cases, a special nosological entity tentatively called "acute benign cerebral angiopathy" by the authors. These 11 cases have in common certain radiological and clinical features. Arteriography shows segmental, multifocal and assymetrical stenoses involving the cerebral arteries between Willis' circle and the terminal arterioles and looking like "strings of sausages". The lesions disappear within one month and present the radiological characteristics of arteritis of medium caliber vessels. The clinical symptoms are suggestive of meningeal haemorrhage or acute cerebromeningeal oedema, with acute repetitive attacks of severe headache and agitation with obnubilation; epileptic seizures and transient neurological deficit may occur. True meningeal haemorrhage confirmed by lumbar puncture is seen in nearly one half of the cases; it seems to be due to alterations in the blood-brain barrier induced by the angiopathy. Intracerebral haematoma may develop, but the disease is usually benign and regresses spontaneously in a few days. None of the usual causes of cerebral arteritis (intra-cranial infection, collagen disease, allergic or toxic angitis) has been found. Pseudo-arteritis (notably spasm of ruptured arterial aneurysms) has been excluded. No aetiological factor common to the 11 cases reported has been elicited, although 6 of the patients had recently given birth and our 6 patients had benign virus infection before or during the clinical manifestations of the disease. In the authors' opinion, the most rewarding line of research would be the role of short acute attacks of arterial hypertension.
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PMID:[Acute benign cerebral angiopathy. 6 cases]. 622 47

Among 23 patients with Sharp's disease, 14 initially had only polyarthritis, Raynaud's syndrome and anti-ribonucleoprotein antibodies. During a mean 5.6 years (range: 1-7 years) follow-up these 14 patients, 2 cases of pericarditis, 1 case of trigeminal neuralgia, 2 cases of nephropathy and 1 case of pulmonary arterial hypertension were observed. The 9 remaining patients had symptoms of multiple collagen disease. They were followed up for a mean of 4.3 years (range: 3-7 years) and 3 developed pericarditis. We discuss the prognostic significance of anti-DNA antibodies (7 cases) and low serum complement (3 cases) which, when combined, seem to be associated with severe visceral lesions.
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PMID:[Evolutive aspects of Sharp's mixed connective tissue disease. 23 cases (author's transl)]. 697 52

To clarify the etiology of atherosclerosis in collagen disease, the prevalence and quality of coronary arterial lesions was examined histopathologically. The materials consisted of 68 autopsy cases, including 10 of rheumatoid arthritis (RA), 28 of systemic lupus erythematosus (SLE), 8 of progressive systemic sclerosis (PSS), 5 of dermatomyositis (DM) and 17 of miscellaneous collagen disease (MD). As a control group (C), 9 age-matched cases of hematologic disorders were chosen. In order to conduct systematic research on coronary arteries, tissue blocks were taken, according to the method proposed by the "Vascular Lesion of Collagen Disease Research Committee" in Japan. To estimate the narrowing of the coronary arterial lumen quantitatively, the coronary stenosis index (CSI), which was the sum of the grade of three main coronary arterial narrowing scores, were used. Significant coronary stenosis (more than 75% occlusion of the lumen) was observed in 8 cases of SLE, one of PSS, 2 of DM and 4 of MD. Stenosis was due to atherosclerosis except in 3 cases of MD. The degree of stenosis expressed by the CSI was higher in MD, SLE and DM than in C (p less than 0.05). Atherosclerotic lesions in collagen disease tended to have a higher population of cellular components than did those in C. There were no statistical correlations between the CSI and some risk factors (age, hypertension, hypercholesterolemia and long-term corticosteroid administration). In the 12 cases with significant stenosis due to atherosclerosis, only 4 patients received corticosteroid hormone for more than one year. Active vasculitis with prominent inflammatory cell infiltration was observed in 2 cases of RA, 3 of SLE and 9 of MD. In cases of vasculitis in SLE examined by the serial section method, luminal narrowing caused by intimal fibrocellular proliferation seemed to have a close relationship with inflammatory cell infiltration in the media and the adventitia. It was concluded that prolonged stimulation of the injured intima by the common risk factors played an important role in the acceleration of coronary atherosclerosis and this intimal change should be reconsidered as a preceding lesion of coronary atherosclerosis.
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PMID:Atherosclerosis of the coronary arteries in collagen disease and allied disorders, with special reference to vasculitis as a preceding lesion of coronary atherosclerosis. 713 12

Mixed connective tissue disease (MCTD) uncommonly develops stroke, although collagen disease is an important condition for stroke. A nonhypertensive woman with MCTD developed massive putaminal hemorrhage. No obvious predisposing factors were revealed by clinical and pathologic examination. MCTD may contribute to the development of brain hemorrhage by some mechanism other than hypertension.
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PMID:Brain hemorrhage in mixed connective tissue disease. A case report. 797 12


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