ABSRTRACT 1

 

 

 

 

 

 

CONGENITAL HEPATIC FIBROSIS:

A STUDY OFA SAUDI FAMILY ANDREVIEW

 

 

Mohamed A. Laajam, MB(Lond), MRCP(UK); Ibrahim M. Al-Teimi, Facharzt; Abdullah A. Abba, MRCP(UK); SultanaM. Al-Mugairin, MBBS;

Mohammad Afzal, MD, FCAP

 

 

 

 

A Saudi family with three members afflicted with congenital hepatic fibrosis (CHF) is described.  CHF was associated withcystic dilatation of the intrahepatic bile ducts and autosomal dominant polycystic kidney disease (ADPKD) in all of the three siblings.  The proband’s case report is presented and the detection of the other two children by family screening is described.  This is the first report of CHF in a Saudi family.  Review of the disease is outlined.  Ann Saudi Med 1993;13(5):442-446.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Abstract 2

 

 

 

DELAYED MULTIPLE TOXIC REACTIONS POSSIBLY RELATED

TO VALPROATE THERAPY IN A SAUDI PATIENT

 

 

E. Ayobanji Ayoola, FACPO; Nabil S. Dahmash, MD; Dahish Ajarim, FRCPC; Sultan Mugrin Al-Mugairin. MBBS

 

 

 

To the Editor:  Valproate (2-propylpentanoic acid), and 8-carbon branch carboxylic acid has become a widely used antiepileptic agent since its introduction in 1967G.  Most of the side effects associated with its use are minor, transient, often dose-related, and are rare during long-term use.  However, potentially hazardous reactions such as hepatitis and pancreatitis have been reported in a few patients on valproic acid (VPA), especially when combined with other drugs.  Such serious reactions usually occur within one year of commencing VPA therapy.  We report the simultaneous occurrence of multiple adverse reactions in a 10-year old Saudi male who had received VPA therapy for a period of 12 years.  Annals of Saudi Medicine (Letter to Editors) 1994, 14(2):163-164.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Abstract 3

 

 

 

BRONCHIECTASIS IN MARFAN’S SYNDROME:

A STUDY OF A SAUDI FAMILY

 

 

Abdullah A. Abba, MRCP, DTCD, FCCP;

Sultan Al-Mogairin, MBBS, ABIM

 

 

 

Marfan’s Syndrome commonly presents with skeletal, cardiovascular and ocular features.  Bronchiectasis as a pulmonary manifestation has only rarely been reported.  A family study has never been reported.  We report a case of Marfan’s Syndrome presenting with bronchiectasis in which a full family study revealed two siblings of the proband case had Marfan’s Syndrome, one of whom had bronchiectasis.

 

We recommend a family study of patients with Marfan’s Syndrome and Bronchiectasis which may reveal bronchiectasis in a family members at an early stage. the aggressive management of which, may avert long term lung damage.

 

J.K. – Practitionerm Oct. – Dec. 2001, Vol. 8(4):245-247.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ABSTRACT 4

 

 

 

 

 

OUTCOME OF PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

 IN INTENSIVE CARE UNIT

 

 

 

AH Alzeer, A Al-Arfaj, SJ Basha, S. Alballa, J Al-Wakeel, S. Al-Sugair,            

 S. Al-Mugeiren, M. Al-Shamairi and EA Bamgboye

Department of Medicine, College of Medicine, King Saud University, Riyadh, Saudi Arabia

 

 

 

The objective of the study was to identify the causes, outcome and prognosis of severe illness in patients with systemic lupus erythematosus (SLE) requiring intensive care unit (ICU) care in a University Hospital over a five-year period.  The design was a cohort study.  Forty-eight SLE patients requiring ICU management over a five-year period (January 1997-December 2001) were studied prospectively.  Of 48 patients, 14 (29.2%) died, predominantly with multiorgan dysfunction syndrome (MODS).  Patients whose APACHE II score was equal to or greater than 20 had higher mortality than those with APACHEscore below 20 (60 versus 7.1% and P < 0.01).  All the 18 patients whose health status rated as “good” survived, while 46.7% of 30 patients whose health rated as “poor” died (P < 0.01).  Patients who had thrombocytopenia associated with sepsis and/or disseminated intravascular coagulopathy (DIC) had the highest mortality (75%) five-year survival).  IN conclusion, SLE patients admitted to the ICU had a lower mortality rate than some of the previous reports.  Patients with SLE with high APACHE score 20, poor health status, thrombocytopenia and multiorgan dysfunction syndrome had poor prognosis in the ICU.  Lupus 2004, 13:537-542.

 

 

 

 

 

 

Nickel-induced allergy and contact dermatitis: does it induce autoimmunity and cutaneous sclerosis? An experimental study in Brown Norway rats.

Al-Mogairen SM, Meo SA, Al-Arfaj AS, Hamdani M, Husain S, Al-Mohimed B, Adam M, Al-Hammad A, Gad El Rab MO.

Department of Medicine, Rheumatology Division, College of Medicine, King Khalid University Hospital, King Saud University, P.O. Box 2925, Riyadh, 11461, Saudi Arabia, almogairin@hotmail.com.

Nickel sensitization is a growing problem and the most common cause of allergic contact dermatitis. The aim of this study was to investigate whether nickel chloride can induce autoimmunity and cutaneous sclerosis in immunosensitive rats. Nickel chloride, in a dose of 4.5 mg in 0.2 ml NS, was administered by the oral and subcutaneous routes to 20 Brown Norway rats. Autoantibodies (ANA, anti-RNP, anti-SCL70 and anti-centromere) were measured and compared in pre- and post-challenge serum samples. Histological studies were also performed in skin biopsies obtained from six positively responding rats and compared with an equal number of control rats at the 14th week post-challenge. Serum ANA was high in a significant number of rats in both the oral (P < 0.005) and subcutaneously nickel-treated groups (P = 0.02), while the anti-SCL70 was high in a significant number of rats in only the orally nickel-treated group (P = 0.04). Histologically, subcutaneous and oral nickel-treated groups showed sclerodermic features of the skin (P = 0.22, P = 0.5), respectively. It may be concluded that nickel chloride can induce scleroderma-related autoantibodies and cutaneous sclerosis. More prolonged duration of exposure is probably associated with greater risk. This is the first study showing the potential risk of nickel in triggering the development of cutaneous sclerosis in susceptible hosts.

Journal Rheumatology International, 2009 Sept.

 

 

 

 

 

 

 

Induction of autoimmunity in Brown Norway rats by oral and parenteral administration of sodium silicate.

Al-Mogairen SM, Al-Arfaj AS, Meo SA, Adam M, Al-Hammad A, Gad El Rab MO.

Department of Medicine, Rheumatology Division, College of Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia. almogairin@hotmail.com

Silica and silicate may disturb immune function such as autoimmunity and tumour immunity. The main objective of this study was to examine the relation between sodium silicate and induction of autoimmunity in genetically susceptible rats. In this study, thirty Brown Norway rats were randomised into four treatment groups, the first and second group receiving 3 mg of sodium silicate (NaSiO(4)) (equivalent to 2 mg silica) in 0.2 mL of normal saline either per oral or subcutaneously, and the third and fourth group (control) receiving 0.2 mL of normal saline (0.9%) through the same corresponding route. A significant number of rats (80%) (P < 0.05) which received sodium silicate by the subcutaneous route showed a high level of serum ANA compared with controls. In the oral, sodium silicate group showed high serum ANA in an insignificant number of rats. Other autoantibodies in both groups (anti-dsDNA, anti-Smith, anti-SSA, anti-SSB) showed gradual increased post exposure, but the numbers of rats with positive titres post exposure was statistically not significant. Silica exposure in rats appears to induce the development of autoimmunity. A longer duration post exposure to silicate seems to be associated with greater risks.

Lupus 2009 April 18 (05):413-7.

 

 

INDUCTION OF AUTOIMMUNITY IN BROWN NORWAY RATS

BY ORAL AND PARENTERAL ADMINISTRATION OF

 NICKEL CHLORIDE

 

S. M. AL-MOGAIREN

 

 

ABSTRACT

Objective:     Nickel intolerance due to its sensitization is a growing problem.  The main objective of this study was to examine the relation between nickel chloride and induction of autoimmunity in genetically susceptible rats.

Methods:      Thirty Brown Norway rats were randomized into four treatment groups; the first and second group received nickel chloride 4.5 mg in 0.2 ml normal saline either per oral or subcutaneously, and the third and fourth group (control) received normal saline (0.9%) 0.2 ml through the same corresponding route.

Result: A significant number of rats (P<0.05) which received nickel chloride by the subcutaneous and oral route showed a high level of serum ANA compared to controls. Significant number of rats (P<0.05) which received nickel chloride by the subcutaneous route showed high serum anti-SSA but the number of rats were insignificant in the group which received nickel by oral route.   Other autoantibodies in both groups (anti-dsDNA, anti-Smith, anti-SSB) showed a gradual increase but the number of rats with positive titer post exposure was statistically not significant.

Conclusion: Nickel chloride exposure in the rats appears to induce the development of autoimmunity.  A longer duration post exposure to nickel chloride seems to be associated with greater risks.

 

Accepted for publication in Lupus, Sept. 2009.