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Biomedical subjects

M T Heafield

Publications and source records attributed to M T Heafield.

14 recordsLinked to original sources
PubMed1996

Idiopathic dysautonomia treated with intravenous gammaglobulin.

BACKGROUND: A previously healthy 23-year-old man presented with a short history of abdominal pain and diarrhoea followed by blurred vision, severe postural hypotension, reduced sweating and unremitting fever. METHODS: Examination revealed fixed dilated pupils, impaired sweating and postural hypotension. Clinical and neurophysiological examination showed no motor or sensory deficit. A diagnosis of idiopathic autonomic neuropathy was made. He became gravely ill with profound life-threatening hypotension and a prolonged ileus. FINDINGS: Within 36 h of receiving intravenous gammaglobulin (IVGG) his pupillary areflexia and severe hypotension resolved. 2 weeks later the autonomic failure recurred but again responded to treatment with IVGG. IVGG is a recognised treatment for Guillain-Barré syndrome. INTERPRETATION: This case report demonstrates that IVGG is also effective in the rare pure dysautonomic variant.

Adult↗
PubMed1992

Parkinson's disease: clinical and therapeutic aspects.

Recent developments on the clinical and therapeutic aspects of idiopathic Parkinson's disease (IPD) have focused on the role of monoamine oxidase B inhibition in IPD, strategies to manage the long-term levodopa (L-dopa) syndrome and attempts to replace nigral tissue by grafting. In addition, tools for community screening and possible identification of an 'at-risk' as well as presymptomatic population of sufferers have been suggested.

Antiparkinson Agents↗
PubMed1990

Plasma cysteine and sulphate levels in patients with motor neurone, Parkinson's and Alzheimer's disease.

Elevated plasma cysteine to sulphate ratios were found in patients with Motor neurone disease (MND), Parkinson's disease (PD) and Alzheimer's disease (AD). Cysteine and sulphate were measured by colourimetric methods. Following recent discovery of a defect in sulphoxidation and sulphation of xenobiotics in these diseases, this finding confirms that endogenous sulphur metabolism is disturbed. The mean cysteine:sulphate ratios (x 10(3] in fasting early morning plasma were 506, 521 and 477 for MND, PD and AD whereas it was 96 for normal controls (P less than 0.001). This excess of cysteine thiol groups may interfere with neural protein function. The deficiency of sulphate ions may lead to reduced xenobiotic detoxification.

Adult↗
PubMed1990

Xenobiotic metabolism in Alzheimer's disease.

Using 5 methods, we assessed the ability of patients with a clinical diagnosis of Alzheimer's disease (AD) to handle xenobiotics. Patients with AD, compared with controls, have reduced sulfoxidation of the probe drug S-carboxymethyl-L-cysteine; they also form less of the sulfate conjugate of acetaminophen. In addition, they have lower activity of the enzyme thiolmethyltransferase. In contrast, the capacity to oxidize debrisoquin and to acetylate sulfamethazine was normal. These findings suggest that a major risk factor for the development of AD is a skewed capacity for xenobiotic metabolism especially of compounds containing sulfur.

Acetaminophen↗
PubMed1990

Metabolism of low-dose paracetamol in patients with chronic neurological disease.

1. Low dose (500 mg) paracetamol (acetaminophen) was administered to patients with Parkinson's disease, motor neurone disease and to age-matched controls. 2. At this low dose level the controls excreted proportionately more sulphate and less glucuronide conjugate than has been reported for administration of 1000 mg of paracetamol. 3. Both groups of patients with chronic neurological disease excreted decreased amounts of paracetamol sulphate (control mean 11.2 +/- 5.4% dose; Parkinson's disease 3.9 +/- 3.7%; motor neurone disease, 5.0 +/ 4.1%). 4. The mean ratio of excretion of paracetamol sulphate/paracetamol glucuronide was 5.6 +/- 11.7 in controls, but 1.1 +/- 1.7 and 1.2 +/- 1.7 in Parkinson's disease and motor neurone disease respectively. These differences are statistically significant (p less than 0.001).

Acetaminophen↗
PubMed1989

S-methylation in motorneuron disease and Parkinson's disease.

Thiolmethyltransferase activity has been measured in newly diagnosed, untreated patients with idiopathic Parkinson's disease and motorneuron disease, and in normal volunteers. In Parkinsonian patients, mean thiolmethyltransferase activity was low (300 U/mg protein [SD 96]) compared with that in controls (947 [409]), whereas activity was high in patients with motorneuron disease (2077 [825]).

Adult↗
PubMed1989

Platelet monoamine oxidase-B activity in Parkinson's disease.

Platelet MAO-B levels have been investigated in seventeen consecutively diagnosed and previously untreated patients with idiopathic Parkinson's disease using the non-hydroxylated catecholamine, beta-phenylethylamine, as substrate. Patients with Parkinson's disease had MAO-B activity levels that were considerably higher than sex and age matched normal controls or patients with Motor neurone disease or Myasthenia gravis.

Adult↗
PubMed1989

Xenobiotic metabolism in Parkinson's disease.

We studied 68 patients with Parkinson's disease (PD) with probe drugs to determine whether a defect in metabolism might be an etiologic factor and found no difference between patients and controls in their ability to form the 4-hydroxy metabolite of debrisoquin. However, using S-carboxymethyl-L-cysteine, 63.2% (43/68) of PD patients had reduced S-oxidation capacity, while 35.3% (24/68) produced no sulfoxides (controls, 35.2% and 2.5%). When we studied acetaminophen (paracetamol) metabolism, only 29.6% of PD patients excreted greater than 5% of the dose as the sulfate conjugate; the corresponding figure for controls was 83.9%. These results suggest a deficiency in detoxication pathways involving sulfur metabolism. PD patients may be unusually susceptible to exogenous or even endogenous toxins.

Acetaminophen↗
PubMedDate not supplied

Neoplastic angioendotheliomatosis: a treatable "vascular dementia" occurring in an immunosuppressed transplant patient.

A 53-year-old right-handed woman presented with headaches and dizziness. She had been well for ten years following successful cadaveric renal transplantation and was taking prednisolone and azathioprine. Two months later she had more headaches with transient dominant hemisphere disturbances and then suffered a completed right hemisphere deficit. As this was recovering, she developed an ischemic optic neuropathy, Computerized tomography (CT) was then normal although CSF analysis showed lymphocytosis and high protein. Steroid trial led to dramatic symptomatic and clinical recovery. On tailing off steroids, progressive bilateral hemisphere disturbance occurred. She was bedbound, with fever, headache, incontinence and disturbed consciousness. New evidence of infarction in watershed territories on CT led to temporal lobe biopsy. Cortical arterioles and venules showed proliferation of lymphoid cells staining for leucocyte common antigen and B-cell markers characteristic of Neoplastic Angioendotheliomatosis (NAE). After chemotherapy she regained independence and mobility and CSF protein fell. This is the first case of NAE to our knowledge in association with immunosuppression for renal transplant and is further evidence that NAE is malignant lymphoma. Cerebrovascular disease is common in such patients, the simultaneous events in differing territories is typical of NAE. Response to chemotherapeutic agents occurred although the typical natural history was unchanged.

Brain Neoplasms↗