Hematologic & Urinary Excretion Anomalies in ME/cfs

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*Hematologic and Urinary Excretion Anomalies in

Patients with Chronic Fatigue Syndrome*

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See also: *Amino Acid Disturbances in ME/cfs*; Help

ME circle 24 June 2012, Co-Cure: http://bit.ly/OkRKaN

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Experimental Biology and Medicine

Hematologic and Urinary Excretion

Anomalies in Patients with Chronic

Fatigue Syndrome

Suzanne H. Niblett*, Katrina E. King*, R. Hugh

*,1, Clifton-Bligh†, Leigh A.

Hoskin‡, K. *, Greg R.

Fulcher†, Neil R. McGregor§, C.

Dunsmore†, Henry L. Butt§, Iven Klineberg||

and T. B. Rothkirch*

Author Affiliations

*Environmental and Pathogenic Microbiology

Laboratory, Discipline of Biological Sciences, University

of Newcastle, Callaghan 2308, Australia; †Department

of Endocrinology, Royal North Shore Hospital,

University of Sydney, St. Leonards 2065, Australia;

‡Service Improvement Unit, Westmead Childrens’

Hospital, Westmead 2145, Australia; §Bio21 Molecular

Science and Biotechnology Institute, University of

Melbourne, Parkville 3012, Australia; and ||Neurobiology

Research Unit, Centre for Oral Health Research,

University of Sydney, Westmead Hospital, Westmead

2084, Australia

1Environmental and Pathogenic Microbiology

Laboratory, School of Environmental and Life Sciences,

The University of Newcastle, Callaghan, NSW 2308,

Australia. E-mail: hugh.dunstan@...

Abstract

Patients with chronic fatigue syndrome (CFS) have a

broad and variable spectrum of signs and symptoms

with variable onsets.

This report outlines the results of a single-blind,

cross-sectional research project that extensively

investigated a large cohort of 100 CFS patients and 82

nonfatigued control subjects with the aim of performing

a case-control evaluation of alterations in standard

blood parameters and urinary amino and organic acid

excretion profiles.

Blood biochemistry and full blood counts were

unremarkable and fell within normal laboratory ranges.

However, the case-control comparison of the blood cell

data revealed that CFS patients had a significant

decrease in red cell distribution width and increases in

mean platelet volume, neutrophil counts, and the

neutrophil-lymphocyte ratio.

Evaluation of the urine excretion parameters also

revealed a number of anomalies.

The overnight urine output and rate of amino acid

excretion were both reduced in the CFS group (P <

0.01).

Significant decreases in the urinary excretion of

asparagine (P < 0.0001), phenylalanine (P < 0.003), the

branch chain amino acids (P < 0.005), and succinic

acid (P < 0.0001), as well as increases in

3-methylhistidine (P < 0.05) and tyrosine (P < 0.05)

were observed.

It was concluded that the urinary excretion and blood

parameters data supported the hypothesis that

alterations in physiologic homeostasis exist in CFS

patients.

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Introduction

Chronic fatigue syndrome (CFS) is a clinically defined

illness that is characterized by unexplained, persistent,

excessive and debilitating fatigue that presents in

conjunction with a complex and variable constellation of

other multisystemic symptoms (1, 2).

Debilitating neuropsychologic, endocrinologic,

immunologic and gastrointestinal symptoms are

frequently associated with the disorder.

Known also as myalgic encephalomyelitis (ME) and

chronic fatigue and immune dysfunction syndrome

(CFIDS), prevalence estimates suggest that the

condition affects between 0.002% and 2.6% of the

general population (3–8), including individuals of both

sexes, all ages, and from many regions of the world (9).

Research hypotheses seeking to explain CFS have

been diverse.

However, despite substantial research efforts, details of

the etiologic and pathophysiologic processes that

contribute to CFS have not been forthcoming.

Although physiologic anomalies have been noted in

many studies to date, no single etiological agent or

consistent cellular or biochemical alteration has been

associated with the disorder.

A major feature of CFS is the extremely diverse

symptom presentation and the presence of variable

types of onsets (10–12).

This inherent heterogeneity has frustrated efforts to

identify an etiological agent or agents and has

contributed to the plethora of conflicting reports.

The use of small patient groups has therefore been a

primary limitation to the interpretation and extrapolation

of CFS study findings in the past.

The future investigation of patients with CFS should

clearly involve larger patient numbers to address the

problem of symptom diversity and minimize the

potential confounding or bias introduced into data

derived from various heterogenous cohorts.

Several studies have suggested that disturbances in

amino acid homeostasis occur in CFS (13–18) and

other clinically overlapping syndromes (19–22).

In a recent study, CFS subjects were shown to have

significant reductions in the urinary excretion of

beta-alanine, hydroxyproline, histidine, methionine,

cystine, and phenylalanine compared with nonfatigued

controls (18).

Importantly, this report also showed that the excretion

profiles of CFS patients were different from patients with

depression and rheumatoid arthritis, suggesting that

the urinary excretion in CFS patients reflects different

metabolic perturbations compared with other patient

groups.

Significant reductions in plasma taurine, histidine,

alpha-aminobutyric acid, and tyrosine were also noted

for the CFS group.

It was concluded that the results were consistent with

inflammatory disease and warranted further

investigation.

However, the patient size used in this research project

was small (30 subjects), and therefore caution should

be applied in attempting to generalize these findings to

all CFS patients.

The aim of this investigation was to assess urine

metabolite excretion and blood cell parameters from

100 CFS patients who have been compared with 82

control subjects to test the hypothesis that CFS

patients have a molecular and cellular basis to the

disorder.

This study forms part of a larger multidisciplinary

investigation of subject parameters.

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Conclusions.

The results of this study revealed that patients with

CFS/ME had anomalies in blood parameters, urine

excretion volume, and urinary excretion of amino acids

compared with age- and sex-matched nonfatigued

controls.

Reductions in overnight urinary output and a generalized

depletion in the rate of amino acid excretion, in

particular, depletions in the excretion of branched chain

amino acids, were the most prominent alterations

observed.

These findings indicated significant disturbance to

amino acid and nitrogen metabolism and homeostasis.

Further investigation into the mechanisms underlying

these changes and their etiologic and clinical

significance is warranted.