Member of the Harley Street Group International- Dr Chow Yok Wai

The Harley Street Group (HSG) was formed by a group of established medical professionals who share a common philosophy in healthcare delivery. Medical care must be patient-centred, up-to-date and evidence-based and above all ethical and on par with the best in the Western World. The complex nature of many medical conditions often require an integrated multidisciplinary approach to care which we believe will be best served by a network of well qualified medical professionals. Harley Street Group doctors are within reach over all the major medical centres in the country. Wherever you are, there are always Harley Street Group doctors near you to serve your medical needs with our subscribed standard of care. Our members are recruited based on their sound all round clinical reputations which include their ethical standards and appropriate charges and not solely on their professional qualifications. Should you need a specific type of medical care that cannot be obtained locally, Harley Street Group can arrange and coordinate the medical care you need through our professional contacts overseas. "We heal, we cure, we care" is our motto as well as a guide towards our vision and mission. Our Vision To deliver a standard of healthcare equivalent with the best available anywhere in the world. Our Mission To coordinate quality control in healthcare delivery of our professional members based on our subscribed treatment philosophy and to bring this to the patient anywhere in Malaysia. To offer and market this brand of healthcare delivery to patients from anywhere in the world, whether resident or visiting in Malaysia. Visit me at http://harleystreetinternational.com/doctor.php?id=51

Hypertension- Translating guidelines into Clinical Practice- Dr Chow Yok Wai

Topic : Hypertension- Translating guidelines into Clinical Practice

Speaker: Dr Chow Yok Wai, Consultant Nephrologist and Physician,
Hospital Pantai Ayer Keroh, Melaka

Date: 16/7/2010 7.00pm

Venue: Ramada Renaissance Melaka

Who should attend?
General Practitioners/Primary care physicians
Physicians/Registrar/Medical Officers

Public Forum- Yong Peng by Dr Chow Yok Wai and Dr Pang Kim Keng

Date : 26/6/2010 (Saturday)

Venue : Yong Peng High School

(Jalan Sekolah Cina, 83700 Yong Peng, Johor)

Time : 6.30pm - 10.00pm

Target of Pax : 150 pax

Speakers: Dr Pang Kim Keng, Consultant Urologist, Hospital Pantai Ayer Keroh, Melaka

Dr Chow Yok Wai, Consultant Nephrologist, Hospital Pantai Ayer Keroh, Melaka



Programme : 6.30pm - Registration

7.00pm - Talk by Dr Pang and Q&A (Common Urological Diseases)

8.00pm - Talk by Dr Chow and Q&A (Protect you kidneys, Control diabetes)

9.00pm - Blood Pressure and Blood Glucose Screening

Mycophenolate mofetil and intravenous cyclophosphamide are similar as induction therapy for class V lupus nephriti

Original Article

Kidney International (2010) 77, 152–160; doi:10.1038/ki.2009.412; published online 4 November 2009
Mycophenolate mofetil and intravenous cyclophosphamide are similar as induction therapy for class V lupus nephritis

Jai Radhakrishnan1,6, Dimitrios-Anestis Moutzouris2,6, Ellen M Ginzler3, Neil Solomons4, Ilias I Siempos5 and Gerald B Appel1

Class V lupus nephritis (LN) occurs in one-fifth of biopsy-proven cases of systemic lupus erythematosus. To study the effectiveness of treatments in this group of patients, we pooled analysis of two large randomized controlled multicenter trials of patients with diverse ethnic and racial background who had pure class V disease. These patients received mycophenolate mofetil (MMF) or intravenous cyclophosphamide (IVC) as induction therapy for 24 weeks, with percentage change in proteinuria and serum creatinine as end points. Weighted mean differences, pooled odds ratios, and confidence intervals were calculated by using a random-effects model. A total of 84 patients with class V disease were divided into equal groups, each group had comparable entry variables but one received MMF and one received IVC. Within these groups, 33 patients on MMF and 32 patients on IVC completed 24 weeks of treatment. There were no differences between the groups in mean values for the measured end points. Similarly, no difference was found regarding the number of patients who did not complete the study or who died. In patients with nephrotic syndrome, no difference was noted between those treated with MMF and IVC regarding partial remission or change in urine protein. Hence we found that the response to MMF as induction treatment of patients with class V LN appears to be no different from that to IVC.

Protect your kidneys control diabetes- Health Forum 6th March 2010

Dr Chow Yok Wai MRCP (UK) - Curriculum Vitae

1. Education
Basic Medical Qualification
University Attended: University of Science Malaysia
Degree Obtained: Doctor of Medicine (MD)
Date Awarded: 25th July 1999

MRCP (Member of the Royal College of Physicians)
Date Awarded: 22nd July 2003

2. Working Experience and Present Appointment
July 1999-October 2000
• Commenced internship training in Sultanah Aminah Hospital Johor Bahru
(HSAJB), Malaysia
• Underwent 18 months training in General Medicine, General Surgery
(Including Plastic Surgery, Urology, Neurosurgery and Paediatric Surgery),
Obstetrics and Gynaecology, Orthopaedics and General Paediatrics.
November 2000-March 2001
• Joined the Department of Medicine HSAJB as a medical officer
• Commenced subspeciality rotation in Nephrology
April 2001-October 2001
• Haematology rotation
November 2001-March 2002
• Neurology rotation
April 2002-November 2002
• Infectious Disease and Intensive Medicine rotation
December 2002-July 2003
• Cardiology, Respiratory Medicine, Gastroenterology and Endocrinology
rotation

July 2003-December 2004
• Granted membership to the Royal College of Physicians of United Kingdom
• Assigned to a 35 bedded general medical ward as general physician in Sultanah Aminah Hospital Johor Bahru, Malaysia upon completion of MRCP
January 2005-June 2006
• Commencement of Nephrology Subspeciality Training
(Nephrology Followship Programme) in HSAJB
July 2006-December 2007
• Completion of Nephrology Subspeciality Training in Kuala Lumpur
Hospital, Malaysia
January 2008- February 2010
• Attached to the Nephrology Unit, Department of Medicine, HSAJB as Consultant Nephrologist and Physician.

February 2010 – to date
• Consultant Nephrologist and Physician,
Hospital Pantai Ayer Keroh
75450, Melaka

3. Registration as a Medical Practitioner
5th July 2000
• Full registration with the Malaysian Medical Council

12th November 2008
• Full registration with the General Medical Council of United Kingdom

4. Official Gazettement by the Government of Malaysia (Ministry of Health)
22nd January 2005
• Gazetted as a Internal Medicine specialist

1st January 2008
• Gazetted as a Nephrologist


5. Professional Activities
2003
Clinical attachment in the New Royal Infirmary of Edinburgh, Scotland
Department of Nephrology

Position: Visiting Registrar
Supervisor: Dr Robin Winnie
Consultant Nephrologist
New Royal Infirmary of Edinburgh
Edinburgh


2008
Attended the Malaysian Nephrology Board Examination on 9th May 2008
Conducted by the Nephrology Board Malaysia
(Malaysian Society of Nephrology, Ministry of Health Malaysia, Academy of
Medicine, Malaysia)
Obtained the highest marks in the 2008 cohort


2008-2009
Awarded a full scholarship by the Public Services Department of Malaysia to
pursue a one year advance nephrology training in the field of vasculitis in Addenbrooke’s Hospital Cambridge University Hospitals NHS Foundation Trust


Position: Honorary Clinical Research Fellow

Supervisor: 1) Dr David Jayne
Director of Lupus and Vasculitis,
Addenbrooke’s Hospital
Cambridge University Hospitals NHS Foundation Trust

2) Professor Kenneth Smith
Cambridge Institute of Medical Research,
University of Cambridge,
United Kingdom.


2008- 2010
Coordinator for National Glomerulonephritis Registry, National Renal Registry
(Johor Bahru)


6. Professional Bodies
National
Member of the Malaysian Medical Association
Member of the Malaysian Society of Nephrology
Member of the Postgraduate Renal Society, Malaysia
International
Member of the Royal College of Physicians of Edinburgh
Member of the International Society of Nephrology
Member of the IgA International Network





7. Research Activities
Publications:-
Acute renal failure in the same hospital 10 years apart; A comparison of two prospective studies in Sultanah Aminah Hospital, Johor Bahru
Medical Journal of Malaysia Vol 62 No1 March 2007

Lactic acidosis in HIV patients receiving highly active antiretroviral therapy- the Johor Bahru experience
Medical Journal of Malaysia Vol 62 No 1 March 2007

Quality improvement in Department of Nephrology, Kuala Lumpur Hospital- an audit on clinical performance indicators
Journal of Quality Improvement Vol 10 No 2 2007

Rituximab in Behcet’s Disease
Submitted to Annals of Rheumatic Diseases for publication (May 2009)

Participation in clinical studies:-
National
HDP study- Hospitalisation rate among Dialysis Patients study (2007)

International
GIANT study- Greatest International Antibiotic Trial study (2006)

A randomized double blind placebo controlled multicenter study to evaluate the efficacy and safety of two doses of Ocrelizumab in patients with WHO or ISN Class III or IV nephritis due to systemic lupus erythematosus (2008)

A phase III multicentre, double blind, double dummy, randomized flexible dose comparative study of MCI-196 versus Simvastatin for the treatment of dyslipidaemia in subjects with chronic kidney disease on dialysis (2009)

Evaluation of chronic kidney disease patterns through the global information database (GRID) (2009)

Biologic therapies in neuro-behcet’s disease, an international collaborative case-series- neurobehcet study group, International Society of Behcet’s Disease (2009)

CHiC-TRIAD (Cambridge Hinxton Centre for Translational Research In Autoimmune Disease) (2008-2009)

MY-CYC (A randomised clinical trial of mycophenolate mofetil versus cyclophosphamide for remission induction in ANCA associated vasculitis) (2008-2009)



Abstracts:-
National
OUTCOME OF A COMMUNITY BASED HEALTH SCREENING PROGRAMME DURING THE PUBLIC AWARENESS CAMPAIGN ON KIDNEY CARE IN JOHOR BAHRU, MALAYSIA
Oral Presentation- 22nd MSN Annual Seminar in Nephrology
Prevention of Chronic Kidney Disease

MYCOPHENOLATE MOFETIL IN RELAPSING LUPUS NEPHRITIS
23rd Malaysian Society of Nephrology Annual Seminar
Johor Bahru, Malaysia
11-13th April 2007

MYCOPHENOLATE MOFETIL IN MEMBRANOUS NEPHROPATHY
23rd Malaysian Society of Nephrology Annual Seminar
Johor Bahru, Malaysia
11-13th April 2007

International
ACUTE RENAL FAILURE IN THE SAME HOSPITAL 10 YEARS APART;
A COMPARISON OF TWO PROSPECTIVE STUDIES IN SULTANAH AMINAH
HOSPITAL, JOHOR BAHRU, MALAYSIA
Poster Presentation- 3rd World Congress of Nephrology
Post Congress Satellite Symposium
Acute Renal Failure: From Bench to Bedside
1st -3rd July 2005

LACTIC ACIDOSIS IN HIV PATIENTS RECEIVING HIGHLY ACTIVE ANTIRETROVIRAL THERAPY- THE JOHOR BAHRU EXPERIENCE
Oral Presentation
14th IUSTI Asia Pacific International Conference- 27th to 30th July, 2006

ADULT POLYCYSTIC KIDNEY DISEASE IN PATIENTS ON DIALYSIS IN MALAYSIA
11th Asian Pacific Congress of Nephrology 2008

ELDERLY PATIENTS INITIATING DIALYSIS IN MALAYSIA
11th Asian Pacific Congress of Nephrology 2008

MALIGNANCY POST RENAL TRANSPLANTATION: A 25 YEAR EXPERIENCE
11th Asian Pacific Congress of Nephrology 2008

LATE ACUTE ANTIBODY MEDIATED REJECTION ASSOCIATED WITH CALCINEURIN INHIBITOR MINIMISATION
11th Asian Pacific Congress of Nephrology 2008

CASTLEMAN’S DISEASE OF THE KIDNEY IN PATIENT WITH SLE
11th Asian Pacific Congress of Nephrology 2008

CLINICAL BENEFITS OF ICODEXTRIN: A SINGLE CENTRE EXPERIENCE
11th Asian Pacific Congress of Nephrology 2008

‘SUDOKU’ INCREASES COGNITIVE FUNCTION IN HAEMODIALYSIS PATIENTS- A PROSPECTIVE PILOT STUDY (Awarded Best Abstract)
11th Asian Pacific Congress of Nephrology 2008

SHORT TERM INFECTIOUS COMPLICATIONS POST RENAL TRANSPLANT
11th Asian Pacific Congress of Nephrology 2008

Neuro Behcet's Disease

Types of NBD

NBD is sub-classified into two major forms: parenchymal and non-parenchymal. The two types rarely occur in the same individual and their pathogeneses are probably different (7).

A. Parenchymal NBD
The parenchymal form of NBD is characterized by focal or multifocal involvement of the brain parenchyma. It is the most common presentation reported in NBD (11), comprising 81% of cases in a study of 200 NBD patients (7). This form of NBD commonly presents with an attack of hemiparesis, cognitive changes, sphincteric troubles and possible fever in men in their third decade. The most common clinical findings are pyramidal tract and brain stem signs. An acute attack may be followed by a relapsing or progressive course (2, 7).

MRI findings in parenchymal NBD: MRI is the most sensitive imaging modality for assessing patients with NBD (18); it shows focal or multifocal CNS abnormalities in the clinically affected areas (17, 19, and 20). The distribution and the MRI signal behavior of parenchymal NBD lesions will be reviewed.

Distribution of parenchymal NBD: Lesions in parenchymal NBD are located in the brainstem, thalami and basal ganglia. However, it can also involve the cerebral hemispheres, cerebellum, spinal cord, and other sites.

Brainstem-thalamic-basal ganglia: Parenchymal NBD lesions have predilection to the brainstem-thalamic-basal ganglia region (Fig 1). They characteristically involve the junction of midbrain and thalamus (meso-diencephalic junction) (Fig 2). The reason for this predilection is unknown (10, 21, 22, and 23). Extensive large lesions are commonly seen in these regions during acute attacks (7).
In the brainstem, the midbrain is most commonly affected site (Fig 3), with the cerebral peduncles involved and the red nuclei characteristically spared (17). The next most common location is the ponto-bulbar region (7, 22), with lesions that usually involve the basis pontis (Fig 4) and occasionally extend to brachium pontis (17, 19, 20, and 21). Although the white matter is more often involved in NBD, lesions may also be seen within the grey matter structures, including brainstem nuclei, cortex and basal ganglia (21, 24). Figure 5 shows symmetrical involvement of midbrain colliculi in parenchymal NBD. The disease commonly involves the basal ganglia and internal capsule region unilaterally (Fig 6), or bilaterally in one third of the cases (7). The globus pallidus and adjacent internal capsule is the most common site affected in this region (Fig 7) (10, 22).
High linear signal intensity in T2 weighted images along the posterior limb of the internal capsule is highly suggestive of NBD (Fig 8). This sign can be seen unilaterally or bilaterally with variable symmetry and severity (7, 22, and 23).
Lesions located in the basal ganglia regions tend to extend caudally along the corticospinal tracts (Fig 9). High signal intensity changes may thus be seen in the fiber tracts of the brainstem and may further extend to the cervical cord (Fig 10). The reversibility of signal changes along this pathway in follow-up MR studies is suggestive that they may represent edema (22). However, in chronic NBD cases, non-reversible signal changes in this distribution can be attributed to wallerian degeneration of the tracts documented in pathological studies (16, 24).

Hemispheric lesions: In sub-acute NBD (a few months after an acute attack,: during either remission or progressive worsening of an acute attack), hemispheric lesions may be seen concomitant with brainstem-thalamic-basal ganglia lesions (7). Hemispheric lesions of NBD are usually subcortical rather than periventricular (Fig 11) (25). However, extensive periventricular white matter changes have been reported (Fig 12) (19, 20, and 26).

Other brain lesions:Cerebellar lesions are less common in parenchymal NBD (7). However, lesions in the cerebellar white matters are occasionally encountered in parenchymal NBD (Fig 13) (7, 22). Involvement of the cranial nerves, rootlet of the spinal nerves and peripheral nerves is exceedingly rare. Contrary to the common belief, isolated aseptic meningitis is distinctly uncommon in BD. Instead, diffuse meningoencephalitis is common (22).

Brainstem atrophy:In chronic stage of NBD, gliosis and atrophy may occur (19, 23, and 27) with striking involvement of the brainstem (Fig 14). Isolated atrophy of the brainstem with relative sparing of the cerebral cortex, though not very frequent, is characteristic of chronic NBD (26).

Spinal cord:The spinal cord is less commonly involved in NBD compared to brainstem-thalamic-basal ganglia or hemispheric regions. The spinal cord lesions tend to extend over two or more vertebral segments posterolaterally and may involve the cervico-medullary junction (Fig 15) (22).

MRI signal behavior of parenchymal NBD:The parenchymal lesions of NBD are hyper intense on T2-weighted images. High-signal intensity lesions represent demyelination, gliosis or transient inflammation and secondary edema supported by the resolution of MR abnormalities in response to methyl-prednisolone and other immunosuppressive therapies (28). Most lesions are somewhat visible on T1 weighted images, but can be very subtle (Fig 8) (7, 19, 22, 23, and 27). Hypointense lesions on T1-weighted images may be seen in chronic lesions (Fig 7) (17). Fluid attenuation inversion recovery (FLAIR) sequences increase MRI sensitivity for NBD lesions, especially juxta-cortical and periventricular (Fig 16) (19). Some lesions may demonstrate contrast enhancement during the acute or the sub-acute phase that resolves in remissions (22, 30). The area of contrast uptake can be nodular, linear, crescentic or irregular and is usually smaller than 5 mm (Fig 17) (18, 25). These changes likely reflect a breakdown in the blood-brain barrier (18).

Temporal course of MRI lesions in parenchymal NBD: Acute phase: There are extensive large parenchymal lesions with predominant involvement of the brainstem-thalamic-basal ganglia region that tend to enhance in contrast studies (Fig 1).
Sub-acute phase: There is marked regression in the appearance of the lesions seen during the acute phase, while there may be smaller scattered lesions in the cerebral white matters and brainstem-thalamic-basal ganglia regions (Fig 11).
Chronic phase: There is marked reduction in the size of the parenchymal lesions that corresponds to clinical remissions and possible appearance of brainstem atrophy (Fig 18) (7, 27, and 31).

Pathological findings in parenchymal NBD:Autopsy studies and biopsy specimens of parenchymal NBD reveal widespread meningoencephalitis with multifocal necrotic foci that tend to accumulate mostly in the brainstem and basal ganglion region (23, 24). A non-specific inflammatory reaction with peri-vascular neurtorphilic or lymphocytic cuffing is commonly seen (23, 24). Gliosis and inflammatory axonal injury are reported in chronic lesions (Fig 19) (32, 33).
The precise pathologic mechanism of parenchymal NBD lesions has not been established. It has been hypothesized that parenchymal NBD lesions could be venous infarcts (22). This hypothesis needs more pathological support as vasculitis cannot usually be demonstrated within the parenchymal NBD lesions (17, 31-33). The presence of abnormal T-cell lymphocyte function points to a possible aberrant immune response to antigenic components of infectious agents such as Streptococcus species (6, 32 and 33).

B. Non-parenchymal NBD:
In the non-parenchymal group, CNS dysfunction is due to involvement of major vessels (vascular NBD) or rarely aseptic meningitis (7). The vascular form of NBD is more often reported from the Middle East (14, 34) and France (35), and less often from other parts of the world (7, 17) with geographical and ethnic variations in disease expression and severity (36).
Vascular NBD usually affects major intracranial vessels with frequent involvement of the venous sinuses, cerebral veins and less commonly the intracranial arteries (7, 35, 37-39). The rare arterial involvements in NBD include thrombosis and aneurysms of the large cerebral arteries (37, 38). Venous sinus thrombosis is the most frequent vascular manifestation in NBD (35, 40) followed by thrombosed deep and cortical cerebral veins (41). The association of venous parenchymal infarcts with venous thrombosis depends on the efficacy of the collateral circulation within the cerebral venous system. The extensive collateral circulation usually allows for a significant degree of compensation in the early stages of sinus venous thrombosis (42).
Vascular NBD usually manifests with acute neurological attacks. The arterial involvement usually presents with stroke that evolves over several hours (7). Raised intracranial pressure is the main clinical manifestation of venous sinus thrombosis with a spectrum of clinical presentations such as headaches, papilloedema, focal neurological deficits, seizures and coma. However, the clinical diagnosis of acute dural sinus occlusion can be difficult to make and is frequently delayed (42).

MRI findings in vascular NBD: The most common MRI findings in vascular NBD are occlusion of the cerebral venous sinuses without or with venous infarcts (7). MRI in conjunction with MR venography (MRV) is highly sensitive in detecting such lesions (42-44).
Venous sinus thrombosis: MRI findings include:
Direct visualization of a thrombus within the vessel. The increased intensity thrombus, detected on T1- and T2- weighted images, may partially or totally replace the flow void of the normal venous channel (Fig 20) (42).
MR venography (MRV) shows lack or impaired flow in the occluded sinus and identifies venous collaterals (Fig 21) (45, 46).

Venous infarcts: Venous infarcts are characterized by their non-arterial distribution. They involve the white matter and/or the cortical-white matter junction, and are often associated with hemorrhage. Bilateral cerebral involvement can occur, including the superior cerebral white matter of the convexities from superior sagittal sinus thrombosis (Fig 22) or the basal ganglia and thalami from internal cerebral vein thrombosis (41, 42).

Parenchymal versus non-parenchymal NBD:
Differentiating between parenchymal and non-parenchymal NBD has significant diagnostic, pathologic, therapeutic, and prognostic implications. Vascular NBD due to isolated intracranial hypertension and dural venous sinus thrombosis have better prognosis if detected and treated early. Acute lesions of parenchymal NBD can be reversible with appropriate treatment such as corticosteroids (11).
The most common forms of NBD, parenchymal and vascular, are distinguished by their unique clinical presentations, characteristic changes in the cerebrospinal fluid (CSF), and MRI findings. Clinically, the parenchymal form manifests with signs and symptoms referable to the brainstem with pyramidal findings, cognitive impairment, ataxia and sphincter disturbance; while the vascular form usually causes raised intracranial pressure due to occlusion of the dural sinuses or very rarely an arterial stroke. CSF findings are different in both groups. In parenchymal NBD, CSF shows pleocytosis with predominance of polymorphonuclear cells, with or without elevated protein level and rarely positive oligoclonal bands. In vascular NBD, the CSF is usually normal except for elevated pressure (22). Conventional MRI can usually differentiate between parenchymal and vascular NBD. However, in some cases, the differentiation between vascular and parenchymal NBD may be difficult because of the presence of parenchymal lesions in the former or in rare instances the coexistence of the two forms. In such cases, special sequences of MRI, such as diffusion-weighted imaging (DWI) or magnetic resonance spectroscopy (MRS), can provide additional information.