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June 2009KUWAIT MEDICAL JOURNAL 151lesions. It is known however, that patients withscrub typhus may not show the typical eschar orskin rashes. In our patient, even if there were skinlesions, they could have been attributed to the skinmanifestations of SLE, but the presence of an escharwould have pointed to an earlier diagnosis. Theraised liver enzymes associated with scrub typhuswere also present in this patient [7] . Though thedrug of choice in the treatment of scrub typhus isdoxycycline 100 mg orally or intravenously twicedaily, tetracycline 500 mg four times daily has alsobeen used with success, and chloramphenicol is stillcommonly used in some endemic areas. Tetracyclinewas initially prescribed for the patient. Changingtetracycline to doxycycline was considered buteventually not done as she had improved markedlywithin 48 hours. The drug was prescribed for twoweeks to reduce the risk of relapse. No vaccine ispresently available and chemoprophylaxis witha weekly dose of 200 mg of doxycycline is highlyeffective when used by non-immune individualsvisiting or working in endemic areas.This case report highlights the fact that scrubtyphus may rarely occur in non-endemic areasand that prolonged fever in SLE should be fullyinvestigated for associated viral, bacterial, protozoal,fungal and rickettsial diseases.CONCLUSIONSLE sometimes presents as unexplainedprolonged fever. But, if fever persists inspite of adequate dose of steroids and otherimmunosuppressants in a patient with SLE, thepossibility of an associated infection should beseriously considered and detailed investigationsperformed. Scrub typhus may rarely complicatethe course of SLE. In our patient, the diagnosisof the associated scrub typhus infection wasslightly delayed but the infection was quicklycontrolled with tetracycline and there were nocomplications.REFERENCES1. Lee PP, Lee TL, Ho MH, Wong WH, Lau YL. Recurrentmajor infections in juvenile-onset systemic lupuserythematosus - a close link with long-term diseasedamage. Rheumatology (Oxford) 2007; 46:1290-1296.2. Ogawa M, Hagiwara T, Kishimoto T, et al. Scrubtyphus in Japan: epidemiology and clinical featuresof cases reported in 1998. Am J Trop Med Hyg 2002;67:162-165.3. Swaak AJ, van de Brink H, Smeenk RJ, et al. Incompletelupus erythematosus: results of a multicentre studyunder the supervision of the EULAR StandingCommittee on International Clinical Studies IncludingTherapeutic Trials (ESCISIT). Rheumatology (Oxford)2001; 40:89-94.4. Isenberg DA, Manson JJ, Ehrenstein MR, RahmanA. Fifty years of anti-ds DNA antibodies: are weapproaching journey’s end? Rheumatology (Oxford)2007; 46:1052-1056.5. Sirisanthana V, Puthanakit T, Sirisanthana T.Epidemiologic, clinical and laboratory features ofscrub typhus in thirty Thai children. Pediatr InfectDis J 2003; 22:341-345.6. Liu YX, Cao WC, Gao Y, et al. Orientia tsutsugamushiin eschars from scrub typhus patients. Emerg InfectDis 2006; 12:1109-1112.7. Hu ML, Liu JW, Wu KL, et al. Short report: Abnormalliver function in scrub typhus. Am J Trop Med Hyg2005; 73:667-668.
152KUWAIT MEDICAL JOURNAL June 2009Case ReportA Case of Severe Primary Hyperthyroidism, SecondaryHyperparathyroidism, Adrenal Insufficiency andOsteoporosis with Multiple FracturesRamen C Basak, Manas Chatterjee, Mahmoud W RassemDepartment of Internal Medicine, King Khaled General Hospital, Hafr Al Batin, Kingdom of Saudi ArabiaABSTRACTOsteoporosis is generally known to be one of the most seriousadverse effects of long-term corticosteroid administration.Recently it was discovered that corticosteroid-inducedosteoporosis occurs not only in trabecular bone but alsoin cortical bone, leading to the reduction in the strength ofbones and subsequent fracture. We report a case of severeKuwait Medical Journal 2009; 41 (2): 152-155hyperthyroidism, secondary hyperparathyroidism, adrenalinsufficiency and osteoporosis with multiple fractures (mostlikely collectively due to chronic steroid intake because ofsteroid dependant bronchial asthma, hyperparathyroidismand hyperthyroidism) which was treated appropriately andmade an uneventful recovery.KEY WORDS: corticosteroid therapy, hyperparathyroidism, hyperthyroidism, osteoporosisINTRODUCTIONBone loss and relevant pathological fracturesare major serious adverse effects of long-termcorticosteroid therapy [1] . It has been well documentedthat trabecular bone injury predominates,especially in this entity [1] and few studies havefocused on the cortical bone too [2] . Alendronate,one of the bisphosphonates, has been reported tobe effective in prevention and treatment of steroidinducedosteoporosis [3] . The active vitamin Dmetabolites (alfacalcidol, 1-hydroxyvitamin D3,calcitriol, 1, 25 dihydroxy vitamin D3) have alsobeen reported to be beneficial but these are inferiorto bisphosphonates [4] . Furthermore, the combineduse of both drugs was shown to be more effectivethan either alone [5] . Parathormone (PTH) analogue(teriparatide) is superior to bisphosphonatesnot only in terms of increasing bone density andreducing fracture risk in vertebrae but also effectiveat non-vertebral sites [6] . Recently it is approved byFDA though long term safety is yet to be established.Osteoporosis induced fractures frequently involvethe spine, hip and wrist. The best screening test isdual energy X-ray absorptiometry (DEXA) which isquick, simple and yields accurate result. It measuresthe density of bones in these areas and accuratelyfollows the changes over time.CASE HISTORYThis 26-year-old female, married, havingregular menstruation, was a known asthmatic onprednisolone 10 mg daily for about 10 years. Shewas admitted in the medical department of KingKhaled General Hospital, KSA with suspecteddeep vein thrombosis (DVT). In the course of herinvestigation DVT was ruled out but she was foundto have severe hyperthyroidism though clinicallymildly symptomatic. She had severe osteopenia withmultiple pathological fractures with sign of healingover the shaft of both fibulae and femur bilaterally,detected on plain X-ray (Fig. 1 and Fig. 2).Examination revealed a conscious and orientedpatient. Pulse and BP were 120/min and 90/60 mmHgrespectively. She had mild diffuse goiter withoutbruit, fine tremor and no ophthalmopathy or pre-tibialmyxedema. The proximal muscles were weak withtenderness in thigh muscles on both sides. She couldbarely stand with support and hence postural drop ofblood pressure could not be assessed. Other systemicexamination revealed no significant abnormalities.Laboratory evaluation depicted that she had primaryhyperthyroidism as her FT 3was 30.19 pmol/l (N= 2.8 – 7.1 pmol/l), FT 457.70 pmol/L (N = 12 – 22pmol/l), and TSH 0.006 µU/ml (N = 0.27 - 4.2 µU/ml). Secondary hyperparathyroidism was diagnosedAddress correspondence to:Dr Ramen Chandra Basak, MD, Endocrinologist, King Khaled General Hospital, PO Box. 591, Hafr-Al-Batin, KSA. Tel: 037228179, Mobile:0551106087, E-mail: basakrc@yahoo.com
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