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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present a case report that the patient had symptoms suggesting pheochromocytoma, a large tumor (> 50 g) and a single minimally altered laboratorial test, exemplifying a diagnostic pitfall. A 31 y.o. male patient had two acute abdominal events, the last one accompanied by headache, arterial hypertension, facial flushing, perspiration and cutaneous pallor. In another admission, the patient had sustained arterial hypertension and cardiac arrhythmia. From laboratory analysis, the vanililmandelic acid was slightly modified. Scintigraphy disclosed a large adrenal mass suggesting pheochromocytoma. Histopathology confirmed this hypothesis. This report points out that patients with symptoms suggesting pheochromocytoma, even when plasma catecholamines and urinary metanephrines levels are normal, may harbor large tumors with a high catecholamines turnover or that had undergone hemorrhagic necrosis.
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PMID:[Slight hormonal alterations in a patient with a large pheochromocytoma]. 1662 87

This 48 year-old male presented with sudden right sided weakness and hypertension, and on CT was found to have a deep left hemispheric intracerebral hematoma. There were accompanying bilateral hypointensities in the occipital lobes, unchanged 1 day later, when expansion of the hematoma and uncal herniation resulted in death. The past medical history included liver transplantation followed by long term cyclosporin, features of thrombotic thrombocytopenic purpura (TTP) attributed to cyclosporin, type 1 diabetes mellitus and acute renal failure attributed to diabetic nephropathy. There was a 2-month history of hypertension poorly responsive to therapy. The occipital lobes at autopsy showed focal cortical hemorrhages with bilateral discoloration of white matter sparing subcortical zones. Microscopy showed white matter pallor with parenchymal cysts, enlarged perivascular spaces and focal acute hemorrhages consistent with edema secondary to acute hypertension. Cortical hemorrhages were associated with intravascular thrombi and fibrin exudates, as well as an accompanying microinfarct, attributed to TTP. The occipital pathology reflects the posterior leukoencephalopathy syndrome (PLS) combined with cortical lesions of TTP. PLS is usually diagnosed radiologically by occipital hypointensities, and is reversible, so that autopsy pathology is rarely examined. TTP may predispose to the development of the PLS in certain cases.
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PMID:48 year old male with sudden onset of right sided weakness. 1676 58

The typical symptoms and signs of neuroleptic malignant syndrome (NMS) consist of fever muscle rigidity (stiffness, myoclonus, rod-like), alterations of consciousness (confusion, agitation, aggression, or catatonia), autonomic nervous system disturbances (i.e., hypertension, tachycardia, tachypnea, profuse sweating, and urine incontinence), abnormal blood tests such as low serum electrolytes, elevated serum creatinine phosphokinase (CPK) level, and leukocytosis. Muscle rigidity is often associated with myonecrosis, myoglobinuria, and elevated serum CPK. The mortality among NMS cases is in the 10 to 70% range depending on the severity of the symptoms and time of therapeutic approach. Mandatory therapy should include removal of causative agents, correction of body fluid and electrolytes, administration of benzodiazepine, clonazepam and bromocriptine (dopamine agonist), proved life-saving medications. The authors reported herein six cases with unusual clinical features of NMS. Four of them had been on antipsychotic for a year before becoming anorexic, dehydrated, agitated, and violent with paranoid delusion. One instance with underlying delirium tremens developed NMS after receiving haloperidol (30 mg IV) in addition to diazepam (200 mg IV) within 24 hours. Another patient was found to suffer from severe NMS after receiving bupropion (Dopamine inhibitor antidepressant) 300 mg/day. All patients displayed cardinal signs and symptoms of NMS in addition to dehydration and pallor. They were treated in the psychiatric ward and recovered rapidly from NMS after receiving clonazepam and bromocriptine and removal of the offending agents.
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PMID:Neuroleptic malignant syndrome: a review and report of six cases. 1721 72

In published reports of naphazoline ingestion, clinical effects are hypertension, bradycardia, pallor, diaphoresis, and respiratory distress. We report three cases of acute pulmonary edema after the intentional ingestion of naphazoline-containing antiseptic first aid liquid. These cases presented with altered mental status, hypertension, bradycardia, and diaphoresis. Chest x-ray on admission revealed acute pulmonary edema. Two cases required mechanical ventilation. All of these clinical effects resolved within 24 hours and the patients were discharged with no sequelae. Since naphazoline stimulates the peripheral alpha-2 adrenergic receptor, we speculate that intense vasoconstriction may have elevated cardiac afterload and left atrial-ventricular blood volume and caused acute pulmonary edema.
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PMID:Acute pulmonary edema associated with naphazoline ingestion. 1785 65

We report a case of a 17-year-old adolescent male with Takotsubo-like cardiomyopathy in the setting of pheochromocytoma who presented with hematemesis, hypertension, and pallor. Takotsubo-like cardiomyopathy is rarely reported in the pediatric population, and this is the first report in the pediatric literature of Takotsubo-like cardiomyopathy associated with both pheochromocytoma and an elongated course of the left anterior descending coronary artery.
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PMID:Takotsubo-like cardiomyopathy in a 17-year-old male with a pheochromocytoma. 1870 53

The treacherous and deceptive nature of pheochromocytoma makes it crucial to detect and treat it promptly; otherwise it will almost certainly be fatal from cardiovascular complications or metastases. Hypertension occurring in patients with pheochromocytomas is sustained in about 50% and paroxysmal in the remainder; however, many patients remain normotensive. Hypertension attacks may be precipitated by physical activity, postural changes, anxiety, certain foods or wine, some drugs, operative procedures, etc. Cardinal manifestations are paroxysmal hypertension, headache, palpitations +/- tachycardia, inappropriate sweating; anxiety, tremulousness, pallor (rarely flushing), chest and abdominal pains; nausea and vomiting often occur. Hypercatecholaminemia manifestations are more common and pronounced when paroxysmal hypertension occurs, but persons with familial pheochromocytoma may be asymptomatic. Protean manifestations of pheochromocytoma may simulate many conditions, some of which may have elevated plasma and urine catecholamines and their metabolites. Baro-reflex failure, postural tachycardia syndrome, sleep apnea, carcinoid, renal failure, and pseudopheochromocytoma may be diagnostic challenges. The history, physical examination, biochemical testing (after eliminating interfering drugs, when possible) for plasma and urinary metanephrines can usually establish or exclude presence of pheochromocytomas. Occasionally a clonidine suppression test is needed to differentiate neurogenic from pheochromocytic hypertension. Manifestations suggesting hypercatecholaminemia without hypertension are highly atypical of pheochromocytoma. Pheochromocytoma may present as panic attacks, pre-eclampsia, cardiomyopathy, infection with fever and leucocytosis, diabetes, migraine, shock, Cushing's syndrome, multiple organ failure with lactic acidosis, neurological manifestations, transitory electrocardiogram abnormalities, constipation, intestinal obstruction, visual impairment, convulsions, etc. The key to diagnosis is always to think of pheochromocytoma in the differential diagnosis of hypertension.
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PMID:The protean manifestations of pheochromocytoma. 1924 99

Phaeochromocytomas are rare neuroendocrine tumours secreting high levels of catecholamines, able to exert serious metabolic and cardiovascular effects. The serious and potentially lethal cardiovascular complications of these tumours are due to the potent effects of secreted catecholamines, especially noradrenaline, the main transmitter released from sympathetic nerve terminals. Hypertension, tachycardia, pallor, headache and anxiety, usually dominate the clinical presentation. Occasionally, patients with predominantly epinephrine-secreting tumours present hypotension or even shock. Other cardiovascular complications of pheochromocytoma include ischaemic heart disease, acute myocardial infarction, cardiac arrhythmias, heart failure due to toxic cardiomyopathy, or pulmonary edema. Catecholamines have been shown to influence the extracellular matrix with collagen deposition and subsequent fibrosis in the arterial wall and in the myocardium. These morphofunctional changes of the myocardium and of arterial wall can be emphasized by ultrasound imaging. Indeed, ultrasound imaging of the myocardium and arterial wall not only identifies wall thickness but also contains information on texture that may be revealed by acoustic tissue characterization. The latter can be quantified through videodensitometric analysis of echographic images or through ultrasonic integrated backscatter signal analysis. This paper reviews cardiovascular complications in patients with pheochromocytoma and utility of the new ultrasound technique as backscatter signal. It is useful for evaluating preclinical pathological morphofunctional changes of the myocardium and arterial wall, characterized by increased collagen content in pheochromocytoma patients. The recognition of early catecholamine-induced alterations in patients with pheochromocytoma, is important to prevent at least morbidity and mortality, before surgical treatment.
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PMID:Cardiovascular complications in patients with pheochromocytoma: a mini-review. 2058 Jan 87

A 13-year-old female presented with complaints of headache, vomiting, diplopia and progressive blurring of vision developing sequentially over 1 month. Examination revealed marked pallor and bilateral lateral rectus palsy with a visual acuity of 6/12 and 6/36 in the left and the right eye, respectively. Fundus examination showed late stage papilloedema in both eyes. Investigation for anaemia revealed severe iron deficiency. MRI of the brain was normal. The cerebrospinal fluid opening pressure was markedly raised at 320 mm of water but fluid analysis did not reveal any abnormality. Thus, a diagnosis of iron deficiency anaemia with idiopathic intracranial hypertension was made. The patient responded dramatically to intravenous iron treatment. Physicians must be aware of this rare presentation of the common problem of iron deficiency, the rapid correction of which plays an instrumental role in salvaging the patient's vision and preventing a recurrence of disease.
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PMID:Iron deficiency masquerading as idiopathic intracranial hypertension. 2168 48

Although acute glomerulonephritis is a rare complication of Plasmodium falciparum malaria, it has not been reported in connection with Plasmodium vivax. We report a case of complicated P. vivax malaria presenting as acute glomerulonephritis. A three-year-old boy presented with high grade fever, a seven-day history of the progressive swelling of his body and a one-day history of vomiting. An examination revealed hypertension (>95th percentile), pallor and hepatosplenomegaly. Investigations showed a platelet count 80,000/mm(3) with haematuria [20-30 red blood cells/high power field with more than 80% dysmorphic red blood cells]. A peripheral smear showed the presence of trophozoites of P. vivax. The patient was diagnosed as having P. vivax causing acute glomerulonephritis and was treated successfully with antimalarials and enalapril. With the changing epidemiological pattern of malaria, especially in endemic areas, unusual complications such as acute glomerulonephritis may sometimes present in cases of P. vivax malaria.
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PMID:Plasmodium vivax presenting as acute glomerulonephritis in a 3-year-old child. 2229 Jan 13

The phenomenon of erythrocyte sickling observed in sickle cell anaemia is responsible for ischaemia and tissue infarction compromising several organs and systems including the mouth and face. This brief paper reports the case of a 17- year-old female with a complicated sickle cell anaemia, hypertension and paraplegia (after an ischaemic stroke at the age of six years). Oral examination revealed the absence of tooth 12, fractures of teeth 11, 21 and 22 (from trauma), active caries lesions in the enamel of teeth 36, 37 and 46, mucosal pallor, and a smooth tongue. Oral radiographs revealed bone rarefaction and trabecular bone coarsening. Dental surgeons and physicians should be aware of the general and oral abnormalities that can be present in individuals with sickle cell anaemia to allow for preventive measures and implementation of effective treatment options.
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PMID:Oral considerations in the management of sickle cell disease: a case report. 2297 72


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