Cases reported • Hypertension, Malignant

1/29. Posterior leukoencephalopathy syndrome may not be reversible.

The association of an acute reversible encephalopathy with transient occipital lobe abnormalities on imaging studies is well known. This condition has been called reversible posterior leukoencephalopathy syndrome. The clinical presentation usually includes seizures, headache, altered mental status, and blindness, often associated with hypertension and immunosuppressants. The authors discuss a two-year-old male with down syndrome who presented 2 months after allogeneic bone marrow transplantation with severe oculogyric crisis, without other complaints. The patient was being treated for hypertension and was receiving cyclosporine for prophylaxis of graft-vs-host disease. A computed tomography scan of the head revealed marked bilateral lucencies mainly involving the white matter of the occipital lobes, with a few foci of punctate hemorrhage. The condition improved when cyclosporine was discontinued, but an area of leukomalacia was identified on follow-up magnetic resonance imaging. To the authors' knowledge, oculogyric crisis as a presentation of reversible posterior leukoencephalopathy has not been previously described. Recognizing this association is important, because patients receiving cyclosporine are often receiving other medications that can potentially cause dystonic eye movements, possibly leading to a delay in diagnosis and treatment, which can result in an irreversible neurologic deficit.

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2/29. Reversible brain lesions in childhood hypertension.

Posterior leukoencephalopathy syndrome is characterized by an acute, usually reversible, encephalopathy with transient occipital lobe abnormalities detected on MRI that occur mostly in association with acute hypertension. The clinical presentation includes seizures, headache, altered mental status and blindness. Disturbed autoregulation of cerebral blood flow and endothelial injury are central to the pathogenesis of this disorder. Prompt control of hypertension results in rapid and complete neurological recovery. In this report we discuss the cases of two children with acute onset hypertension of different aetiologies that presented with the characteristic features of posterior leukoencephalopathy syndrome. CONCLUSION: Early recognition of this readily treatable condition may obviate the need for extensive and invasive investigations. Despite the alarming lesions on the MRI, prompt control of hypertension carries a uniformly favourable prognosis.

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3/29. Wilms' tumor, the hyponatremic/hypertension syndrome, and an elevated atrial natriuretic factor.

hyponatremia and malignant hypertension are rare manifestations of Wilms' tumor. hyponatremia associated with malignant hypertension of any cause is not explained. We present a patient with hyponatremia, malignant hypertension, Wilms' tumor, and an elevated atrial natriuretic factor (ANF). We believe the elevated ANF caused the hyponatremia.

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4/29. Malignant hypertension and cerebral haemorrhage in Seckel syndrome.

Seckel syndrome is an autosomal recessive condition with severe short stature and facial and neurological anomalies. Intracranial haemorrhage, due to rupture of a cerebral aneurysm, is a very rare complication of this syndrome. Malignant hypertension may play an important role in the aetiology of the aneurysm and early detection is essential in order to prevent organ damage. CONCLUSION:we report a new case of Seckel syndrome associated with malignant hypertension and cerebral haemorrhage.

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5/29. Hyponatremic hypertensive syndrome (HHS) in an 18-month old-child presenting as malignant hypertension: a case report.

BACKGROUND: The combination of hyponatremia and renovascular hypertension is called hyponatremic hypertensive syndrome (HHS). Malignant hypertension as a presentation has been reported in adults with HHS but is rare in children. CASE PRESENTATION: An eighteen month-old male presented with drowsiness, sudden onset status epilepticus and blood pressure of 210/160. The electrolytes on admission revealed sodium of 120 mEq/L and potassium of 2.1 mEq/L. The peripheral renin activity (PRA) was 172 ng/ml/min (normal 3-11 ng/ml/min) and serum aldosterone level was 91 ng/dl (normal 4 to 16 ng/dl). Patient underwent angioplasty with no success, followed by surgical correction. Two years since the diagnosis, the blood pressure is controlled with labetolol and amlodipine (at less than sixth of the pre-operative dosages). The PRA is 2.4 ng/ml/min and aldosterone 15.5 ng/dl. The child not only had three renal arteries on left but all of them were stenosed which to best of our knowledge has not been described. CONCLUSION: As uncommon as HHS with malignant hypertension may be in adults it is under-reported in children and purpose of the case report is to raise its awareness.

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6/29. Conn's syndrome can cause malignant hypertension.

We present a case in which a patient, having already sustained an episode of malignant hypertension, was subsequently found to have an underlying Conn's adenoma. Ablation of the adenoma improved control of her hypertension. When a second adenoma developed in her remaining adrenal gland, control of her hypertension deteriorated.

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7/29. Malignant hypertension secondary to cortisol-secreting adrenal tumour.

Adrenal cortical tumour-induced malignant hypertension is rare, except for some documented aldosterone-producing adenomas. hypertension is a common feature of Cushing's syndrome, whereas malignant hypertension is rarely seen. This case in taiwan is only the second reported case with malignant hypertension secondary to a cortisol-secreting adrenal tumour. The immunohistochemical study of the excised tumour showed strong positive staining of interleukin (IL)-6. IL-6 can trigger inflammatory vascular damage, which is typical in the malignant phase of hypertension. We hypothesise that IL-6 may have played an important role in this case.

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8/29. Infantile polyarteritis nodosa presenting as hyponatraemic hypertensive syndrome.

The association of arterial hypertension with hyponatraemic dehydration, known as hyponatraemic hypertensive syndrome (HHS), is a rare and serious hypertensive complication. Here, we describe a 17-mo-old girl who presented with severe hyponatraemic dehydration, hypokalaemia, polyuria, and nephrotic-range proteinuria associated with malignant arterial hypertension and systemic inflammatory disease. diagnosis of classic polyarteritis nodosa (c-PAN) was made on the basis of renal arteriography demonstrating small arterial aneurysms in association with non-aneurismal changes such as arterial cut-off, arterial tapering stenosis and nephrogram perfusion defect. A decrease of blood pressure by antihypertensive treatment resulted in the normalization of HHS abnormalities. However, c-PAN became well controlled only after 4 mo of immunosuppressive therapy. CONCLUSION: The main interest of this case was the uncommon presentation of systemic polyarteritis nodosa in a very young child. Renal ischaemia from intrarenal vessel disease may have been the trigger event for HHS in our case. Management of PAN-associated severe arterial hypertension is based on immunosuppressive and antihypertensive treatment.

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9/29. Posterior reversible encephalopathy syndrome: a variant of hypertensive encephalopathy.

Posterior reversible encephalopathy syndrome (PRES) is a recently described variant of hypertensive encephalopathy characterized by headache, visual disturbances and altered mental function. Its causes are diverse and in contrast to hypertensive encephalopathy, it can develop without significant elevation of blood pressure. This syndrome is mostly reversible when correctly managed; however, failure to recognize it can lead to cerebral infarction and death.

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10/29. Acute hypertensive encephalopathy in minimal change nephrotic syndrome.

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.

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