PRACTICE For the full versions of these articles see bmj.

com

Diagnosis in General Practice

Self diagnosis
Clare Goyder,1 Ann McPherson,2 Paul Glasziou1

1
Department of Primary Health Some conditions can be diagnosed correctly Stage Strategy
Care, University of Oxford, Oxford
OX3 7LF by the patient, but self diagnosis should Initiation of
• Spot diagnoses
• Self labelling
always undergo challenge and refinement by
2
Health Experiences Research the diagnosis • Presenting complaint
Group (formerly DIPEx), • Patten recognition trigger
Department of Primary Care,
University of Oxford, Oxford
the general practitioner
• Restricted rule-outs
OX3 7LF • Stepwise refinement
Correspondence to: Clare Goyder A 26 year old postgraduate student presents with a 12 hour Refinement • Probabilistic reasoning
[email protected] history of a painful left eye. She feels her vision is reduced • Pattern recognition fit
• Clinical prediction rule
and her eye is watering more than usual. She has had a
Cite this as: BMJ 2009;339:b4418
doi: 10.1136/bmj.b4418 previous episode of iritis (anterior uveitis) and she suspects • Known diagnosis
• Further tests ordered
that this is the diagnosis today. Defining the
• Test of treatment
final diagnosis
• Test of time
• No label applied
What is self diagnosis?
The process of diagnosis is pivotal to the daily work of the Diagnostic stages and strategies
general practitioner. Despite the clinical importance of this
process, many of the diagnostic methods used by GPs have infection.2 Clinical cure was observed in 92% of those with
been elucidated only recently. Three key stages in diagnos‑ a confirmed urinary tract infection. Patients with symp‑
tic reasoning have been identified (figure).1 In the first stage toms and negative urine cultures were evaluated for other
diagnostic hypotheses are triggered, and sometimes this diagnoses, and one patient was diagnosed and treated for
is done by the patient: “Doctor, I think I have the flu/gout/ chlamydia. This study suggests that self diagnosis and self
tonsillitis/etc.” treatment of recurrent urinary tract infection can be both
convenient and safe. By replacing prophylaxis, self treat‑
When is it used? ment may reduce antibiotic use. Generally, this self manage‑
Several processes can initiate diagnostic hypotheses (fig‑ ment was met with high degrees of patient satisfaction.
ure). The most common is the patient presenting with a Self diagnosis occurs in resource poor settings. In Malawi,
particular key symptom. The “presenting complaint” is where qualified clinicians are scarce, national malaria pol‑
used in the initiation phase in almost 70% of consulta‑ icy supports self diagnosis and self medication,8 although
tions with general practitioners.1 Patients also present with evidence on the accuracy of self diagnosis of malaria is mea‑
preconceived diagnoses that may explain their symptoms. gre. Studies in Tanzania on schistosomiasis suggest that self
Heneghan et al found that this process of self diagnosis diagnosis is often accurate and could potentially replace
(also called self labelling) was responsible for initiating a more expensive and impractical laboratory methods.6 When
diagnosis in 18% of consultations.1 Conditions that were self diagnosis was confirmed by urine microscopy, schisto‑
commonly self diagnosed included tonsillitis, gout, and somiasis was correctly reported by 67% of infected children
chest infections. Using this process well relies on giving and by 87% who were heavily infected.
patients time to tell their story and then asking open ques‑
tions, such as “What are you worried about?” or “Did you How does self diagnosis go wrong?
have ideas about what this might be?” General practi‑ Some evidence suggests that certain conditions are often
tioners can then explore where these preconceived ideas misdiagnosed by patients. Examples from our litera‑
­originated. ture search include pregnancy, vaginal candidiasis, and
The few studies that have been performed on the accu‑ scabies.9‑13
racy of self diagnosis suggest that recurrent urinary tract In an observational study in the United States of 95
infection, recurrent anterior uveitis, schistosomiasis, and women who had purchased over the counter antifungal
head lice can all be self diagnosed correctly.2‑7 treatments, vaginal symptoms were evaluated through clin‑
A recent prospective study in the United States of 172 ical history, examination, and routine laboratory tests.11
women attending a primary health care clinic at a university The accuracy of self diagnosis of vulvovaginal candidiasis
found a concordance of 84% (95% confidence interval 77% was poor, with a sensitivity of only 34%, although 21%
to 90%) between the self diagnosis of recurrent, uncom‑ of women had candidiasis plus another cause, usually
plicated urinary tract infection and laboratory confirmed b­acterial. Despite the small size of the study and possible

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 PRACTICE

selection bias, the results suggest that inappropriate treat‑ Key points
ment and delay in diagnosis are common and that self diag‑
Self diagnosis triggers the diagnostic hypothesis in 18% of
nosis of vaginal discharge is inaccurate, even in patients consultations with general practitioners
who had been previously been diagnosed by a clinician as Self diagnosis of recurrent uncomplicated urinary tract
having candidiasis. Many women may be unaware that it infection can be accurate and safe, but self diagnosis
is normal and indeed physiological to have a small amount can be inaccurate and unsafe—for example, in vaginal
• doc2doc.bmj.com of vaginal discharge and may purchase drugs to treat this. candidiasis and gout
“Google threw up a whole list When patients look for a diagnosis of a normal physiologi‑ Prevalence, previous episodes, general awareness of
of possibles, ranging from the
cal process, self diagnosis will definitely go awry.14 condition, and patient education affect the accuracy of self
sublime to the ridiculous, with diagnosis
some rather serious medical
Patients may often make incorrect self diagnoses
information in between. Top of without any consequences, particularly in regard to self Self diagnosis should always undergo subsequent
the list was leukaemia. Yikes— limiting infections, but this can be unsafe in some circum‑ refinement and challenge
this was certainly not what I stances. Although little has been published in this area,
had expected to find” anecdotal evidence abounds. Examples (from the authors’ rent episodes. Doctors could actively assist this process
Birte Twisselmann, assistant editor, and our colleagues’ experience) include an elderly man through patient education—giving patients feedback on
in a blog on doc2doc.bmj.com who attributed his chest pain to indigestion, thus ignor‑ what to watch out for. The patient may have acquired
ing an extensive myocardial infarction; a patient with a the knowledge underlying self diagnosis through media
colorectal malignancy who had ignored months of rectal reports, family experience of a condition, or observing oth‑
bleeding, assuming this was due to haemorrhoids; and the ers with the same symptoms. Public health campaigns can
patient with a history of arteriopathy who presumed that lead to specific conditions being incorrectly self diagnosed,
his acutely painful foot was due to gout. but this heightened public awareness may lead to detec‑
tion of rare but potentially life threatening conditions.
How can we improve?
No matter how diagnoses are triggered, the initial hypo­ Conclusions
theses should always undergo challenge and refinement. Knowing when patients are likely to be right about a self
Doctors should acknowledge the patient’s self diagnosis, diagnosis is useful, but the strength and relevance of
but what they say will depend on the probability of the research in this area is weak. The available studies pro‑
suggested diagnosis being correct. If the self diagnosis is vide some insight into the accuracy of self diagnosis and
likely to be right we could say “That sounds likely, but show that some conditions, such as recurrent urinary tract
there are a few other things we should check first.” For less infection, may be reliably self diagnosed and even safely
likely suggestions we could say “That sounds possible, but self treated.
there are other diagnoses that might be more likely.” This Learning when patients can appropriately and safely
approach—listening combined with verification—should diagnose and manage common conditions may eventually
enable the self diagnosis to be explored but should prevent lead to changes in health services. When managing recur‑
premature closure of the diagnostic process. rent conditions and chronic diseases, patients are often
Doctors are taught that a good consultation will address experts, and a collaborative approach within a traditional
the patient’s ideas, concerns, and expectations. Explor‑ diagnostic framework may yield the most satisfying results
ing the patients’ own views of their diagnosis is not only for all. As Herxheimer said, “Every encounter between a
about effective communication. Patients may have correct patient and a physician is a learning experience for both,”4
ideas that we had not thought of, or incorrect ideas that and this opportunity should be welcomed.
need to be discussed explicitly. Knowing when patients
are likely to be correct or incorrect will also help in inter‑ Case review
preting their ideas. Our search found such information An observational study analysed whether patients present‑
for only a few conditions (summarised in the table), but ing to Moorfields Eye Hospital, London, with a history of
some general principles apply. iritis could recognise recurrent attacks.5 Patients who had
Firstly, the more common the condition, the more likely a history of iritis were asked whether their current problem
it is to be identified by patients, whether malaria in Malawi represented a further episode of iritis or a different condi‑
or urinary tract infection in the United States. Secondly, tion. Their diagnosis was then compared to the ophthal‑
previous experience of some conditions (such as urinary mologist’s opinion; 86% of patients with recurrent iritis
tract infection) may allow accurate self diagnosis of recur‑ were able to correctly self diagnose this condition.

Accuracy of patients’ self diagnosis for some conditions

Reference Condition Accuracy
Gupta et al 20012 Recurrent urinary tract infection Sensitivity 84%
Ansell et al 19976 Schistosomiasis Sensitivity: 67% infected children,87% heavily infected childrenSpecificity: 96%
at the lowest prevalence (decreased with increasing prevalence)
Pearson et al 19915 Recurrent anterior uveitis Sensitivity 86%
Pilger et al 20087 Head lice Sensitivity 81%Specificity 92%
Strote and Chen 200610 Pregnancy (answer to question: “Do you Sensitivity 55%Specificity 95%
think you might be pregnant?”)
Wiley et al 200215 Genital warts Sensitivity 38%Specificity 91%
Laughey et al 199316 Different types of headache 56% with migraine were able to distinguish second headache type from migraine

BMJ | 23 january 2010 | Volume 340 205

 PRACTICE

We thank Kevin Barraclough, Peter Rose, and Nicholas Summerton for their 7 Pilger D, Khakban A, Heukelbach J, Feldmeier H. Self-diagnosis of
helpful comments, and Nia Roberts (outreach librarian, Oxford University active head lice infestation by individuals from an impoverished
Library Services) for her help. community: high sensitivity and specificity. Rev Inst Med Trop Sao
Contributors: CG and PG conducted the literature search and reviewed Paulo 2008;50:121-2.
8 Muula AS, Rudatsikira E, Siziya S, Mataya RH. Estimated financial
the studies. CG drafted the initial paper. AM reviewed drafts and made
and human resources requirements for the treatment of malaria in
suggestions for further revisions. PG reviewed drafts, revised and edited the Malawi. Malaria J 2007;6:168.
text, and approved the final version. CG is guarantor. 9 Ramoska E, Sacchetti A, Nepp M. Reliability of patient history in
Competing interests: None declared. determining the possibility of pregnancy. Ann Emerg Med 1989;18:
Provenance and peer review: Commissioned; externally peer reviewed. 48-50.
10 Strote J, Chen G. Patient self assessment of pregnancy status in the
Patient consent not required (patient anonymised, dead, or hypothetical). emergency department. Emerg Med J 2006;23:554-7.
1 Heneghan C, Glasziou P, Balla J, Rose P, Thompson M, Lasserson D, et 11 Ferris DG, Nyirjesy P, Sobel JD, Soper D, Pavletic A, Litaker MS.
al. Diagnostic strategies used in primary care. BMJ 2009;338:b946. Over-the-counter antifungal drug misuse associated with patient-
2 Gupta K, Hooton TM, Roberts PL, Stamm WE. Patient-initiated diagnosed vulvovaginal candidiasis. Obstet Gynecol 2002;99:419-
treatment of uncomplicated recurrent urinary tract infections in young 25.
women. Ann Intern Med 2001;135:9-16. 12 Sihvo S, Ahonen R, Mikander H, Hemminki E. Self-medication with
3 DeAlleaume L, Tweed EM. When are empiric antibiotics appropriate for vaginal antifungal drugs: physicians’ experiences and women’s
urinary tract infection symptoms? J Family Pract 2006;55:338,341-2. utilization patterns. Fam Pract 2000;17:145-9.
4 Herxheimer A. Helping patients take responsibility for their own 13 Kovacs FT, Brito MFDM. Disease perception and self medication in
health. Ann Intern Med 2001;135:51-2. patients with scabies. An Bras Dermatol 2006;81:335-40.
5 Pearson RV, Wilson-Holt NJ, Bates AK. Self diagnosis in recurrent acute 14 Summerton N. Patient-centred diagnosis. Abingdon: Radcliffe, 2007.
anterior uveitis. Eye 1991;5:145-6. 15 Wiley DJ, Grosser S, Qi K, Visscher BR, Beutner K, Strathdee A, et al.
6 Ansell J, Guyatt H, Hall A, Kihamia C, Kivugo J, Ntimbwa P, et al. The Validity of self-reporting of episodes of external genital warts. Clin
reliability of self-reported blood in urine and schistosomiasis as Infect Dis 2002;35:39-45.
indicators of Schistosoma haematobium infection in school children: a 16 Laughey WF, MacGregor EA, Wilkinson MI. How many different
study in Muheza District, Tanzania. Trop Med Int Health 1997;2:1180-9. headaches do you have? Cephalalgia 1993;13:136-7.

Guidelines
Diagnosis and pharmacological management of
Parkinson’s disease: summary of SIGN guidelines
D G Grosset,1 G J A Macphee,1 M Nairn,2 on behalf of the Guideline Development Group

1
Department of Neurology, Why read this summary? -A slow, progressive course
Southern General Hospital, Parkinson’s disease is a common neurodegenerative dis‑ -A good response to drug treatment for Parkinson’s
Glasgow G51 4TF
2 ease diagnosed in 1% of people aged over 65 years. It disease.
Scottish Intercollegiate Guidelines
Network, Edinburgh EH7 5EA has a considerable impact on patients and their families • Observe the patient for non-motor features (box),
Correspondence to: M Nairn as well as healthcare and social care systems. With an which may predate motor features, particularly
[email protected] ageing population, the number of cases in Scotland may impaired olfaction, REM (rapid eye movement) sleep
Cite this as: BMJ 2010;340:b5614
increase by 30% in the next 25 years.1 Accurate diagnosis behaviour disorder, constipation, and depression.4 A
doi: 10.1136/bmj.b5614 can be difficult, particularly at first presentation. As the combination of several such features raises diagnostic
disease progresses, treatment with complex combinations suspicion of Parkinson’s disease.
of drugs often becomes the norm. This article summarises • Be aware of the potential inaccuracy of clinical
the recommendations from the Scottish Intercollegiate diagnosis in the early stages of the disease. For
Guideline Network (SIGN) on the diagnosis and drug man‑ instance, not all patients with parkinsonism have
agement of Parkinson’s disease.2 Parkinson’s disease; the term parkinsonism does
not specify cause but describes a clinical syndrome
Recommendations of bradykinesia plus at least one of three features:
SIGN recommendations are based on systematic reviews tremor, rigidity, and postural instability. Consider this
of best available evidence. The strength of the evidence is diagnostic uncertainty when giving information to the
graded as A, B, C, or D (figure), but the grading does not patient and planning management.(C)
reflect the clinical importance of the recommendation. • Review the diagnosis regularly by assessing:
Recommended best practice (“good practice points”), -Response to treatment
This is one of a series of BMJ based on the clinical experience of the Guideline Devel‑ -Rate of disease progression
summaries of new guidelines, opment Group, is also indicated (as GPP). -Any new features, some of which may indicate
which are based on the best
available evidence; they highlight atypical parkinsonism caused by other conditions,
important recommendations for Diagnosis such as progressive supranuclear palsy (for
clinical practice, especially where • Diagnosis depends largely on: example, early swallowing difficulties; gaze
uncertainty or controversy exists.
An algorithm for drug treatment, -The presence of a specific set of clinical features paresis) or multiple system atrophy (for example,
further information about (using research derived diagnostic criteria, such as early severe autonomic problems such as postural
the guidance, and a list of the the UK Brain Bank criteria)3—bradykinesia, rigidity, hypotension, cerebellar ataxia). (GPP)
members of the guideline
development group are in the full rest tremor, and postural instability • While basing the diagnosis of Parkinson’s disease
version on bmj.com. -The absence of atypical features on diagnostic criteria, avoid over-rigid application of

206 BMJ | 23 january 2010 | Volume 340

 PRACTICE

the criteria. For example, in a patient who develops clinically helpful to identify the presence of structural
bradykinesia after taking a drug that may cause lesions that may cause or contribute to parkinsonism
parkinsonism, the diagnosis may be Parkinson’s or tremor. (D)
disease, drug induced parkinsonism, both of these, or • Do not use CT scanning or MRI scanning routinely in
another cause entirely. (D) diagnosing idiopathic Parkinson’s disease. (C)
• Instruct patients diagnosed with Parkinson’s disease • Use MRI in patients where it would be clinically
to inform the Driver and Vehicle Licensing Agency. helpful to identify:
-The degree of cerebrovascular disease (in
Who should diagnose Parkinson’s disease? differentiating idiopathic Parkinson’s disease from
• For all patients presenting to their general vascular parkinsonism), or
practitioner with symptoms suggesting Parkinson’s -The degree and distribution of brain atrophy (for
disease, refer to a hospital clinician with expertise in example, when clinical features suggest atypical
movement disorders. (C) parkinsonism such as multiple system atrophy). (D)
• Do not give a “trial of treatment” before referral • Do not use acute dopaminergic challenge testing,
as this may mask physical signs; treatment for transcranial sonography, or objective olfactory testing
Parkinson’s disease is rarely required urgently, and in routine clinical diagnosis of Parkinson’s disease.
no treatment delays disease progression. (C) (A, B, C)

Diagnostic tools Genetic testing

When the clinical picture is incomplete, or there are pointers Nearly all cases of Parkinson’s disease cases arise from no
to a possible alternative diagnosis, or dual pathology may apparent cause (so called sporadic Parkinson’s disease),
be present, the following diagnostic tests may be applied. although genetic susceptibility factors may be relevant.
• Perform an FP-CIT SPECT (fluoropropyl-carbomethoxy • Do not routinely incorporate gene testing of affected
iodophenyl tropane single photon emission computed individuals or asymptomatic family members for
tomography) brain scan when clinical diagnostic monogenic parkinsonism as no evidence of benefit
uncertainty exists about the presence of dopamine exists. Refer patients who request genetic testing
deficiency as the cause of parkinsonism or tremor. to a specialist movement disorders clinician for
FP-CIT SPECT is abnormal in Parkinson’s disease assessment. (GPP)
and other degenerative parkinsonism disorders and
is normal in cases of essential tremor, drug induced Management of non-motor neurobehavioural disorders
parkinsonism, and dystonic tremor. (B) Mood disorders including depression affect 30-50% of
• Use structural imaging (computed tomography (CT) or patients with Parkinson’s disease.5 However the diagnosis
magnetic resonance imaging (MRI)) where it would be of depression may be difficult in these patients as its fea‑
tures may overlap with those of cognitive impairment or of
Parkinson’s disease itself (such as flattened affect, lack of
The grade of recommendation relates to the strength of the supporting evidence on which
the evidence is based. It does not reflect the clinical importance of the recommendation motivation, and reduced motor activity).
• Use self rating scales (such as the Beck depression
A • At least one high quality meta-analysis, systematic review of randomised controlled trials, or inventory or the geriatric depression scale) or clinician
randomised controlled trial with a very low risk of bias and directly applicable to the target
population; or rated scales (such as the Hamilton depression rating
scale or the Montgomery-Asberg depression rating
• A body of evidence consisting principally of well conducted meta-analyses, systematic
reviews of randomised controlled trials, or randomised controlled trials with a low risk of bias
scale) to screen for depression in patients with
directly applicable to the target population, and demonstrating overall consistency of results Parkinson’s disease.6 Use the Hamilton depression
rating scale7 or the Montgomery-Asberg depression
B • A body of evidence including studies rated as high quality systematic reviews of case-control rating scale8 to help in determining the severity of
or cohort studies, and high quality case-control or cohort studies with a very low risk of
confounding or bias and a high probability that the relation is causal and which are directly depressive symptoms. (C)
applicable to the target population, and with overall consistency of results; or • Do not diagnose depression using rating scales alone.
• Extrapolated evidence from studies described in A
Clinical interview incorporating collateral information
from relatives and carers is required. (GPP)
C • A body of evidence including well conducted case-control or cohort studies with a low risk of No specific recommendation can be made for the choice of
confounding or bias and a moderate probability that the relation is causal and which are antidepressant agent as the evidence is limited. Amitriptyl‑
directly applicable to the target population and with overall consistency of results; or
ine and desipramine are associated with some benefit but
• Extrapolated evidence from studies described in B carry a risk of adverse effects.9 10 Many other antidepres‑
sants (such as selective serotonin reuptake inhibitors) are
D • Non-analytic studies, such as case reports, case series, expert opinion; or commonly used.11
• Extrapolated evidence from studies described in C
Drug management
Good Practice Points (GPP)
Initial treatment
Recommended best practice based on the clinical experience of the guideline development • Choose an initial therapeutic agent from the following
group drug classes:
-Dopamine agonists—a non-ergot dopamine agonist
Explanation of SIGN grades of recommendations (ropinirole, pramipexole, or rotigotine) is preferable

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PRACTICE

bmj.com: other recent SIGN • Do not use anticholinergic drugs because of the high
guidelines summaries Major non-motor symptoms of Parkinson’s disease
risk of adverse effects, particularly on cognition. (B)
• Diagnosis and management Non-motor features may occur at all stages of the disease.
of headache in adults Some non-motor features may fluctuate in response
to drug treatment, as do motor complications. Non-
Treating advancing disease with motor complications
(2008;337: a2329)
• Control of pain in adults motor features can be assessed using the non-motor Disease progression and treatment with levodopa based
with cancer: summary of SIGN questionnaire from the Parkinson’s Disease Society (www. drugs are associated with loss of smooth motor control
guidelines (2008;337:a2154) parkinsons.org.uk/pdf/nms_questionnaire.pdf). and with the emergence of motor fluctuations and dys‑
• Management of invasive Neuropsychiatric symptoms kinesia.12 Drug choice depends on clinical experience,
meningococcal disease in • Depression, anxiety, apathy comorbidity, and patient preference. There are no robust
children and young people: clinical triggers for adjunctive therapy. The initial choice
• Hallucinations, illusions, delusions*
summary of SIGN guidelines
• Dementia, cognitive impairment* will be from one of the drug classes below; over time, com‑
(2008;336:1367-70)
• Compulsive and impulsive behaviours* binations of drugs from each class may be necessary.
Sleep disorders • Use catechol-O-methyl transferase inhibitors,
• Insomnia* monoamine oxidase B inhibitors, or dopamine
• Sleep fragmentation*
agonists (oral or transdermal) to manage motor
complications. (A)
• Excess daytime somnolence*
• Use a non-ergot dopamine agonist (ropinirole,
• Restless legs syndrome
pramipexole, or rotigotine) to manage motor
• REM (rapid eye movement) sleep behaviour disorder
complications. (A)
• Vivid dreaming*
• Use apomorphine by subcutaneous infusion
• “Acting out” dreams, often including vocalisation when
asleep for severe motor complications where there are
sufficient expertise and resources. (D)
Autonomic disorders
• In patients with motor fluctuations use catechol-
• Bladder disturbance: nocturia, urgency, frequency
O-methyl transferase inhibitors or intermittent
• Heat or cold intolerance*
subcutaneous apomorphine to reduce “off” time
• Excess sweating*
(that is, symptoms that recur at the end of a dose
• Orthostatic hypotension*
cycle as the medication effect wears off). (A)
• Sexual dysfunction*
Neurosurgery can reduce motor fluctuations and dyski‑
• Drooling of saliva
nesia, but the selection of appropriate patients is outside
Gastrointestinal disorders (overlap with autonomic) the scope of this guideline.
• Dysphagia Intraduodenal levodopa is expensive but may be
• Ageusia (absence of taste) appropriate in selected patients with advanced motor
• Constipation or incomplete emptying of bowel* complications, after other options have been explored.
Sensory disorders It is not approved by the Scottish Medicines Consortium
• Pain, paraesthesia (which provides advice to Scottish NHS Boards and their
• Impaired olfaction area drug and therapeutics committees about all newly
Other symptoms licensed medicines).
• Fatigue*
• Pain* Daytime sleepiness
• Diplopia Up to a half of patients with Parkinson’s disease experi‑
• Seborrhoea ence excessive daytime sleepiness.13‑15
• Weight loss • Exclude reversible causes of excessive daytime
*May be intrinsic to disease and/or precipitated by, or related to, sleepiness—such as depression, poor sleep hygiene,
drug treatment for Parkinson’s disease and drugs associated with altered sleep pattern.
(GPP)
to ergot derived agonists (pergolide, cabergoline, • Do not use modafinil or melatonin to reduce
bromocriptine) (A) excessive daytime sleepiness in people with
-Levodopa with a dopa-decarboxylase inhibitor (A) Parkinson’s disease. (A)
-Monoamine oxidase B inhibitors (A)
• Choose an agent by taking into account its relative Dementia
efficacy and adverse effect profile; the patient’s Dementia is present in at least a third of patients with late
comorbidity, employment status, and own drug Parkinson’s disease.16
preference; and the clinician’s experience. Each • Withdraw non-parkinsonian drugs with potential
patient should have individual assessment and adverse effects on cognitive function (such as
discussion. tricyclic antidepressants). (GPP)
• Warn patients about the potential for dopamine • Withdraw sequentially and gradually
agonists to cause impulse control disorders anticholinergic agents, amantadine, selegiline, and
(pathological gambling, binge eating, compulsive dopamine agonists. (GPP)
shopping, and hypersexuality), and excessive • Exclude other causes of cognitive impairment or
daytime somnolence (and the implications for psychosis, particularly delirium, before adding a
driving and for operating machinery). (A) specific drug treatment for dementia. (GPP)

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honorariums for talks from Boehringer-Ingelheim (BI), GE Healthcare,

Useful resources GlaxoSmithKline (GSK), Teva, and Union Chimique Belge (UCB); has
Parkinson’s Disease Society, Scottish Office (www. been reimbursed for conference attendance from Teva and UCB; and has
parkinsons.org.uk/scotland)—Offers support and received grant support for research staff from GSK and GE Healthcare.
information services for people with Parkinson’s disease, GM has participated in advisory boards for BI, GSK, Teva, and Solvay
Pharmaceuticals; has received speaker fees from BI, GSK, Orion, and
professionals, carers, and volunteers; also has a telephone
Solvay; and has received travel grants from BI and UCB Pharma. MN has
helpline (0808 800 0303) or email pds.scotland@ no relationships with any company that might have an interest in the
parkinsons.org.uk submitted work in the previous three years; (3) their spouses, partners,
Younger Parkinson’s Network (www.parkinsons.org.uk/ or children have no financial relationships that may be relevant to the
advice/younger-people.aspx)—Section of the Parkinson’s submitted work; and (4) DGG chaired the SIGN guideline development
Disease Society, Scottish Office , that offers support for group on diagnosis and pharmacological management of Parkinson’s
disease. GM and MN have no non-financial interests that may be relevant
younger patients (aged under 60)
to the submitted work.
National Tremor Foundation (www.tremor.org.uk)— Provenance and peer review: Commissioned; not externally peer reviewed.
Provides help, support, and advice to those of all ages with
1 General Register Office for Scotland. Projected population of
all forms of tremor; also has a telephone helpline (0800 Scotland (2008 based). 2009. www.gro-scotland.gov.uk/files2/
3288046) stats/projected-population-of-scotland-2008-based/projected-
population-of-scotland-2008-based-publication/projected-
population-of-scotland-2008-based.pdf
2 Scottish Intercollegiate Guidelines Network. Diagnosis and
Consider treating patients with mild to moderate pharmacological management of Parkinson’s disease. Edinburgh:
SIGN, 2010. (SIGN publication No 113) www.sign.ac.uk/
dementia (score 10-24 on the mini-mental state exami‑ guidelines/fulltext/113/index.html
nation) and Parkinson’s disease with the cholinesterase 3 Gibb WRG, Lees AJ. The relevance of the Lewy body to the
inhibitor rivastigmine, although the magnitude of benefit pathogenesis of idiopathic Parkinson’s disease. J Neurol
Neurosurg Psychiatry 1988;51:745-52.
is modest and tremor may be exacerbated and vomiting 4 Chaudhuri KR, Martinez-Martin P, Schapira AH, Stocchi F, Sethi
increased. 9 17‑ 19 In the absence of a submission from K, Odin P, et al. International multicenter pilot study of the first
comprehensive self-completed nonmotor symptoms questionnaire
the holder of the marketing authorisation, the Scottish for Parkinson’s disease: the NMSQuest study. Mov Disord
Medicines Consortium does not recommend rivastigmine 2006;21:916-23.
for use in the NHS in Scotland for the treatment of mild to 5 Starkstein SE, Merello M, Jorge R, Brockman S, Bruce D, Petracca
G, et al. A validation study of depressive syndromes in Parkinson’s
moderately severe dementia in patients with idiopathic disease. Mov Disord 2008;23:538-46.
Parkinson’s disease. 6 Schrag A, Barone P, Brown RG, Leentjens AF, McDonald WM,
Starkstein S, et al. Depression rating scales in Parkinson’s disease:
critique and recommendations. Mov Disord 2007;22:1077-92.
Psychosis 7 Hamilton M. A rating scale for depression. J Neurol Neurosurg
• Exclude other treatable causes of psychosis before Psychiatry 1960;23:56-62.
using antipsychotic drugs. (GPP) 8 Montgomery SA, Asberg M. A new depression scale, designed to be
sensitive to change. Br J Psychiatry 1979;134:382-9.
• Treat with low dose clozapine, monitoring blood 9 Miyasaki JM, Shannon K, Voon V, Ravina B, Kleiner-Fisman G,
tests for leucopenia or agranulocytosis weekly, and Anderson K, et al. Practice parameter: evaluation and treatment
of depression, psychosis, and dementia in Parkinson disease
with supervision by a registered specialist. (A) (an evidence-based review): report of the Quality Standards
• If weekly monitoring of blood is not possible, treat Subcommittee of the American Academy of Neurology. Neurology
with low dose quetiapine instead. (B) 2006;66:996-1002.
10 Devos D, Dujardin K, Poirot I, Moreau C, Cottencin O, Thomas P,
et al. Comparison of desipramine and citalopram treatments for
Overcoming barriers depression in Parkinson’s disease: a double-blind, randomized,
Ten to fifteen per cent of patients diagnosed with Par‑ placebo-controlled study. Mov Disord 2008;23:850-7.
11 Weintraub D, Morales KH, Moberg PJ, Bilker WB, Balderston C, Duda
kinson’s disease are managed in primary care, which is JE, et al. Antidepressant studies in Parkinson’s disease: a review
associated with a higher rate of diagnostic error than for and meta-analysis. Mov Disord 2005;20:1161-9.
patients seen in clinics specialising in movement disor‑ 12 Ahlskog JE, Muenter MD. Frequency of levodopa-related
dyskinesias and motor fluctuations as estimated from the
ders or Parkinson’s disease.20 If hospital referrals are to cumulative literature. Mov Disord 2001;16:448-58.
be increased, with long term follow-up in hospital clinics, 13 Tandberg E, Larsen JP, Karlsen K. Excessive daytime sleepiness and
sleep benefit in Parkinson’s disease: a community-based study.
reorganisation of services will be needed. Mov Disord 1999;14:922-7.
Psychosis is a key neuropsychiatric feature of Par‑ 14 Gjerstad M. Excessive daytime sleepiness in Parkinson disease: is
kinson’s disease and is associated with substantial dis‑ it the drugs or the disease? Neurology 2006;67:853-8.
15 Tan EK, Lum SY, Fook-Chong SM, Teoh ML, Yih Y, Tan L, et al.
ability. Clozapine is recommended as effective treatment Evaluation of somnolence in Parkinson’s disease: comparison with
but can be prescribed only by a specifically licensed age- and sex-matched controls. Neurology 2002;58:465-8.
physician (usually psychiatrist), and its use in patients 16 Aarsland D, Zaccai J, Brayne C. A systematic review of prevalence
studies of dementia in Parkinson’s disease. Mov Disord
with Parkinson’s disease in the United Kingdom is cur‑ 2005;20:1255-63.
rently minimal. Parkinson’s disease services need bet‑ 17 Leroi I, Collins D, Marsh L. Non-dopaminergic treatment of cognitive
impairment and dementia in Parkinson’s disease: A review. J
ter links with psychiatry services for this problem to
Neurol Sci 2006;248:104-14.
be tackled. 18 Maidment ID, Fox C, Boustani M. A review of studies describing
Contributors: All authors contributed to reviewing the evidence and writing the use of acetyl cholinesterase inhibitors in Parkinson’s disease
and correcting the article. dementia. Acta Psychiatr Scand 2005;111:403-9.
19 Aarsland D, Mosimann UP, McKeith IG. Role of cholinesterase
Funding: No funding was received for writing this summary.
inhibitors in Parkinson’s disease and dementia with Lewy bodies. J
Competing interests: All authors have completed the Unified Competing Geriatr Psychiatry Neurol 2004;17:164-71.
Interest form at www.icmje.org/coi_disclosure.pdf (available on request 20 Schrag A, Ben-Shlomo Y, Quinn N. How valid is the clinical
from the corresponding author) and declare that (1) No authors have diagnosis of Parkinson’s disease in the community? J Neurol
support from any company for the submitted work; (2) DGG has received Neurosurg Psychiatry 2002;73:529-34.

BMJ | 23 january 2010 | Volume 340 209

PRACTICE

Lesson of the Week

Protein and creatine supplements and misdiagnosis
of kidney disease
Joanna Willis,1 Rachael Jones,2 Nneka Nwokolo,2 Jeremy Levy1

1
Imperial College Kidney and
Transplant Institute, Imperial
Check dietary supplement history before was taking the antiretroviral agents Kivexa (abacavir and
College Healthcare NHS Trust, investigating apparently declining renal function lamivudine), atazanavir, and ritonavir; no other drugs; and
London W12 0HS occasional non-steroidal anti-inflammatory agents. On
2
Chelsea and Westminster Hospital The past five years has seen increasing emphasis on the early examination he weighed 78 kg; blood pressure was normal
NHS Foundation Trust, London detection and treatment of chronic kidney disease, together (122/65 mm Hg); cardiovascular, respiratory, and abdomi‑
SW10 9NH
Correspondence to: J Levy
with reporting of estimated glomerular filtration rate (GFR) nal examination was unremarkable; and urine dipstick test‑
[email protected] alongside serum creatinine values.1 Most laboratories calcu‑ ing was negative for blood, protein, and glucose.
late estimated GFR automatically, using age, serum creati‑ His CD4 count had increased to 449 cells ×106/l and viral
Cite this as: BMJ 2010;340:b5027
doi: 10.1136/bmj.b5027
nine, gender, and ethnic group.2 Increasing reliance on this load was <50 copies/ml. He was hepatitis B and C virus
value as a marker of chronic kidney disease means that any negative. Urine protein:creatinine ratio was 11 mg/mmol
factor which affects creatinine independently of true changes (normal <25 mg/mmol), and a renal ultrasound scan was
in renal function may lead patients to be misdiagnosed with unremarkable. His serial biochemistry showed that over
kidney disease. Also, doctors have become more aware of the the course of the previous two months his estimated GFR
importance of reduction of estimated GFR. We report a series varied between 40 and 65 ml/min/1.73 m2 (figure). Urine
of patients referred for investigation of kidney disease (both dipstick testing was consistently negative. Intriguingly his
acute and chronic) in whom ingestion of protein and creatine renal function seemed to deteriorate during periods when
supplements led to a high serum creatinine and low reported he was well and improve during intercurrent illnesses or
estimated GFR in the absence of kidney disease. hospital admissions. His antiretroviral treatment was not
changed over this period.
Case reports The full history taken during the renal consultation estab‑
A 46 year old white man presented with a two month history lished that when he was well he regularly attended a gym
of flu-like symptoms and headache and was found to be HIV and he had been using whey protein and creatine supple‑
positive. Routine blood tests showed a serum creatinine of ments to enhance muscle profile, consuming 5-10 g creatine
113 μmol/l (normal <115 μmol/l), giving him an estimated monohydrate and 24-30 g whey protein daily. When first
GFR, as calculated by the hospital laboratory, of 64 ml/ diagnosed with HIV, during hospital admission to begin
min/1.73 m2 (normal >90 ml/min/1.73 m2). His CD4 count at treatment, and at times of intercurrent illness, he did not
the time of diagnosis was 320 cells ×106/l (normal >600 cells attend the gym or use the supplements, and since his diag‑
×106/l) with a viral load of 34 344 copies/ml. HIV antiretro‑ nosis he had been using them only when he felt well enough
viral therapy was started, and one month later at routine to train, resulting in sporadic intake. The periods of higher
review he was found to have a serum creatinine concentra‑ serum creatinine concentration (and lower reported esti‑
tion of 166 μmol/l and an estimated GFR of 41 ml/min/1.73 mated GFR) corresponded exactly to his periods of protein
m2. He was referred for a renal opinion, the concern being supplementation. He was advised to stop taking the sup‑
that he had underlying kidney disease associated with HIV plements, which he did, and when reviewed three months
or acute kidney injury induced by antiretroviral drugs. later his serum creatinine was 118 μmol/l and estimated
He had no family history of renal disease, no medical his‑ GFR 61 ml/min/1.73 m2. A chromium51-EDTA isotopic GFR
tory, and no urinary symptoms. At time of renal review he performed at the same time reported a rate of 88 ml/min.
Over the past six months we have seen three further
Periods of illness or hospital admissions
Return to gym and use of protein supplements patients who were referred for abnormal renal function
Supplements stopped after being told they had chronic kidney disease, in whom
70 close questioning identified intake of protein supplements
eGFR (ml/min/1.73 m2)

or creatine (table).
60

Discussion
50
Our patients had normal renal function. Their intake of
40 creatine (and concentrated protein) supplements led to a
high serum creatinine concentration and low reported esti‑
30
mated GFR, which was misconstrued as kidney disease.
20 Why the effects of the supplements were so marked is not
0 50 100 150 200 250
clear, but supplementation did not seem to be causing harm.
Days All four patients were HIV positive and exposed to various
Time course of variation in estimated glomerular filtration rate ­antiretroviral agents; the effect of protein and creatine

210 BMJ | 23 january 2010 | Volume 340

 PRACTICE

Patients with raised serum creatinine concentration who had function. A similar effect will occur with a high intake of
been taking high dose protein and creatine supplements protein supplements or a meat meal. Studies in normal vol‑
Serum creatinine (μmol/l) unteers and patients with diabetes have shown that serum
3 months after creatinine values can double 2-4 hours after a meal that
Urine stopping protein includes cooked meat, but not after vegetarian meals or
Patient Age Sex dipstick test Baseline supplements
meals containing raw beef.7
1 25 Male Normal 148 98
The impact of changes in muscle mass on serum creati‑
2 41 Male Normal 131 103
nine concentration is well known. As muscle mass represents
3 38 Male Normal 144 106
roughly 98% of total body creatine, people with substantial
s­ upplements on serum creatinine (and hence estimated GFR) muscle will have naturally higher serum creatinine levels
may be greater in such patients. than those without. This is important when interpreting
Creatine is a nitrogenous acid that is synthesised in the serum creatinine results, and is only partially corrected for
liver or ingested as dietary protein. It is transported to skel‑ by taking age and ethnic origin into account in calculating
etal muscle and stored in the form of creatine phosphate, estimated GFR; a creatinine concentration of 100 μmol/l
where it restores ATP after muscle contraction, before being may represent entirely normal renal function in a healthy
converted to creatinine by non-enzymatic dehydration. 90 kg young man, or impaired renal function in a frail 50
­Creatinine is mainly filtered in the glomerulus, with a small kg woman. Ingestion of large quantities of creatine will also
proportion excreted by active tubular secretion. Almost no result in misleadingly raised serum creatinine. Patients with
tubular reabsorption occurs, so the final creatinine levels HIV are particularly at risk of misinterpretation of estimated
in the blood and urine represent, in most situations, the GFR since they may be using protein supplements but may
amount filtered at the glomerulus, although the relation be malnourished and have low muscle mass as a result of
is not linear.3 HIV itself or changes in muscle and fat distribution induced
Competitive athletes have been taking creatine supple‑ by certain treatments.
ments for their potential ergogenic effects since the early Contributors: JL and RJ conceived this report. JL and JW wrote the paper
and all authors commented on drafts, had access to all data, and reviewed
1990s, and use has spread to amateur athletes and body
the paper. JL, RJ, and NN managed the patients and initiated the report. JL
builders. Creatine supplements and concentrated protein is guarantor.
supplements are advertised widely. Creatine can increase Competing interests: None declared.
muscle contractility and short term performance, par‑ Patient consent obtained.
ticularly in intense repetitive bouts of exercise, where it is Provenance and peer review: Not commissioned; externally peer
reviewed.
thought to shorten recovery time4; there is less evidence for 1 K/DOQI clinical practice guidelines for chronic kidney disease:
its benefit in endurance and incremental exercise. Creatine evaluation, classification, and stratification. Am J Kidney Dis
could be beneficial in physical rehabilitation by enhancing 2002;39:S1-266.
2 Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more
muscle building.5 Normal daily intake of creatine (mostly accurate method to estimate glomerular filtration rate from serum
in the form of dietary meat) is less than 1 g but with supple‑ creatinine: a new prediction equation. Modification of Diet in Renal
Disease Study Group. Ann Intern Med 1999;130:461-70.
mentation can reach 25-30 g. After increased intake, muscle 3 Cockcroft DW, Gault MH. Prediction of creatinine clearance from
concentrations of creatine and creatine phosphate remain serum creatinine. Nephron 1976;16:31-41.
4 Demant TW, Rhodes EC. Effects of creatinine supplementation on
raised for several weeks. The only important side effect exercise performance. Sports Med 1999;28:49-60.
seems to be a small increase in body weight, due to increased 5 Hespel P, Op’t Eijnde B, Van Leemputte M, Urso E, Greenhaff PL,
muscle mass and fluid retention within the muscle. Currently Labarque V, et al. Oral creatine supplementation facilitates the
rehabilitation of diuse atrophy and alters the expression of muscle
there is no evidence that creatine supplementation results myogenic factors in humans. J Physiol 2001;536:625-33.
in more serious harm, including renal impairment, but no 6 Bemben MG, Lamont HS. Creatine supplementation and exercise
performance: recent findings. Sports Med 2005;35:107-25.
long term studies exist.6 7 National Collaborating Centre for Chronic Conditions. Chronic
As creatine is converted to creatinine in proportion to its kidney disease: national clinical guideline for early identification
and management in adults in primary and secondary care. London:
concentration (and hence its intake), a high intake may lead Royal College of Physicians, September 2008. www.rcplondon.
to high serum creatinine and a reduced estimated GFR (as ac.uk/pubs/brochure.aspx?e=257
calculated from serum creatinine) despite normal kidney Accepted: 18 August 2009

What types of article does the BMJ consider?

We are delighted to receive articles for publication— or if the authors make an inquiry about the suitability
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All original research articles are submitted, although article) before submitting your article. Some types of
we may invite submission (without ­promising article—news, features, observations, head to head,
­acceptance) if we come across research being views and reviews—are commissioned by the editors.
­presented at conferences, if we see it in abstract form, Cite this as: BMJ 2009;339:b3112

BMJ | 23 january 2010 | Volume 340 211

 PRACTICE

10-Minute Consultation
Tennis elbow
Christian David Mallen, Linda S Chesterton, Elaine M Hay

Arthritis Research Campaign

National Primary Care Centre,
A 47 year old decorator presents with a two Useful reading
Keele University, Keele, month history of right elbow pain. The pain Arthritis Research Campaign (www.arc.org.uk/arthinfo/
Staffordshire ST5 5BG
Correspondence to: C D Mallen is worse when he grips a paintbrush or uses patpubs/6044/6044.asp)—Information for patients
Bisset L, Beller E, Jull G, Brooks P, Darnell R, Vicenzino
[email protected] a paint roller on the ce­iling. B. Mobilisation with movement and exercise,
Cite this as: BMJ 2009;339:b3180 corticosteroid injection, or wait and see for tennis elbow:
doi: 10.1136/bmj.b3180 randomised trial. BMJ 2006;333:939 (doi:10.1136/
What issues you should cover bmj.38961.584653.AE)
bmj.com archive Tennis elbow (lateral humeral epicondylitis) is com‑ Calfee R, Patel A, DaSilva M, Akelman E. Management of
• Editorial. Tennis elbow in mon, peaking at age 35-55 and typically affecting the lateral epicondylitis: current concepts. J Am Acad Orthop
primary care (2006;333:927-8) dominant arm. Men and women are equally affected. It Surg 2008;16:19-29
• Research. Mobilisation is probably an overload injury related to minor or unrec‑ Lewis M, Hay E, Paterson S, Croft P. Local steroid
with movement and exercise, ognised injury (microtrauma). A careful taken history injections for tennis elbow: does the pain get worse
corticosteroid injection,
can exclude differential diagnoses, including referred before it gets better? Results from a randomized
or wait and see for tennis
elbow: randomised trial
pain and local elbow causes such as olecranon bursitis controlled trial. Clin J Pain 2005;21:330-4
and osteoarthritis. (doi:10.1097/01.ajp.0000125268.40304.b3)
(2006;333:939)
• Clinical review. Tennis elbow Tennis elbow pain is often mild. Episodes typically Smidt N, van der Windt D, Assendelft W, Deville
(2008;336:1367-70) last six months to two years and usually resolve within W, Korthals-de Bos I, Bouter L. Corticosteroid
12 months. Acute pain typically lasts 6-12 weeks. Anal‑ injections, physiotherapy, or a wait-and-see policy
for lateral epicondylitis: a randomised controlled
gesics, such as over the counter paracetamol, co-coda‑
trial. Lancet 2002;359:657-62 (doi:10.1016/S0140-
mol, or topical non-steroidal anti-inflammatory drugs, 6736(02)07811-X)
provide adequate pain relief for most patients. Injection
of corticosteroids (including triamcinolone, methylpred‑
nisolone, and hydrocortisone) with local anaesthetic can common extensor tendon or lateral epicondyle.
produce short term pain relief (with mean pain scores • Look for localised pain in the elbow when pressure
(0-100) falling from 60 to 20 over two weeks), but long is applied to the extended wrist (in the “stop traffic”
term effectiveness is less clear. At one year, seven of 10 position) or when the patient lifts, grips, or squeezes
people who received an injection will be pain free, com‑ an object.
pared with eight of 10 who did not. • Check whether the patient has paraesthesia or
Progressive exercise is beneficial. Splints and orthoses pain above the elbow (rare).
are best used in conjunction with physiotherapy • Diagnose tennis elbow following history
p­rogrammes. and examination. Do not request further
investigations.
What you should do • Give the patient an information and exercise
History leaflet.
• Ask the patient about the severity of pain and how he • Provide practical advice on avoiding aggravating
has tried to resolve it. factors, including muscle overload and strong
• Ask about the duration of symptoms. repetitive motion with the elbow extended.
• Take a detailed social and occupational history to • Inject about 1 ml of corticosteroid-anaesthetic
determine the cause of the epicondylitis and its mixture into the site of maximal tenderness until
effect on his everyday life. Repeated movements you can feel the periosteum. Spread the injection
of the wrist, especially those associated with using a “pepper pot technique” (multiple sites
resistance (such as backhand tennis stroke) usually around the epicondyle).
make tennis elbow worse. Occupations that involve • Demonstrate basic exercises and stretches or
repetitive turning or lifting at the wrist, such as prescribe a programme of physiotherapy.
gardening, keyboard use, plumbing, decorating, and • Prescribe pain relieving drugs.
bricklaying, are particularly likely to cause tennis
elbow. Funding: CDM is funded by an Arthritis Research Campaign career
development fellowship

This is part of a series of Examination and treatment Competing interests: None declared.
occasional articles on common • Reassure your patient. Provenance and peer review: Not commissioned; externally peer
problems in primary care. The
BMJ welcomes contributions • Palpate around the effected elbow joint to identify reviewed.
from GPs the area of maximum pain—usually over the Accepted: 26 June 2009

212 BMJ | 23 january 2010 | Volume 340