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  1. Rajendra S, Kadir ZA, Karim N, Zain Z
    Singapore Med J, 2003 Aug;44(8):423-5.
    PMID: 14700423
    Neurological involvement associated with inflammatory bowel disease is well established though rarely reported in the literature. The coexistence of motor neurone disease with ulcerative colitis has never been previously documented. The case of a 53-year-old Indian male with distal ulcerative colitis who, two and a half years later, developed dysarthria, dysphagia, a wasted fasciculating tongue and palatal palsy characteristic of bulbar type motor neurone disease is described. Topical and oral steroids together with azathioprine and mesalazine suppositories controlled the bowel symptoms but did not improve the neurological deficit. Subsequently, the antiglutamate agent riluzole improved the mobility of his tongue. The close temporal relationship and relative infrequency of both these conditions in a Malaysian population along with the recognised association between ulcerative colitis and other neurological conditions deserve careful consideration as to whether a common denominator is involved. Documentation of coexistence of both disorders in a single patient is important in case similar associations are reported in future.
  2. Davis TM, Singh B, Choo KE, Ibrahim J, Sulaiman SA, Kadir ZA, et al.
    J Intern Med, 1998 May;243(5):349-54.
    PMID: 9651556
    OBJECTIVES: To investigate the dynamic parathyroid response to rapidly induced, sustained hypocalcaemia in patients with acute malaria and in healthy volunteers.

    DESIGN: Serum intact parathormone (PTH) concentrations were measured on samples taken before and during a variable-rate tri-sodium citrate infusion designed to 'clamp' the whole blood ionised calcium concentration 0.20 mmol L-1 below baseline for 120 min.

    SUBJECTS: Six Malaysian patients aged 17-42 years with acute malaria, four of whom were restudied in convalescence, and 12 healthy controls aged 19-36 years.

    MAIN OUTCOME MEASURES: Whole-blood ionised calcium and serum intact PTH concentrations.

    RESULTS: The mean (SD baseline ionised calcium was lower in the malaria patients than in controls (1.09 +/- 0.06 vs. 1.18 +/- 0.03 mmol L-1, respectively; P = 0.01) but PTH concentrations were similar (3.0 +/- 1.8 vs. 3.3 +/- 1.3 pmol L(-1); P = 0.33). Target whole-blood ionised calcium concentrations were achieved more rapidly in the controls than the patients (within 15 vs. 30 min) despite significantly more citrate being required in the patients (area under the citrate infusion-time curve 0.95 (0.25 vs. 0.57 +/- 0.09 mmol kg-1; P < 0.01). The ratio of the change in serum PTH to that in ionised calcium (delta PTH/ delta Ca2+), calculated to adjust for differences in initial rate of fall of ionised calcium, was similar during the first 5 min of the clamp (132 +/- 75 x 10(-6) vs. 131 +/- 43 x 10(-6) in patients and controls, respectively, P > 0.05), as were steady-state serum PTH levels during the second hour (7.0 +/- 2.2 pmol L-1 in each case). Convalescent patients had normal basal ionised calcium levels but the lowest serum intact PTH levels before and during the clamp, consistent with an increase in skeletal PTH sensitivity after treatment.

    CONCLUSIONS: There is a decreased ionised calcium 'set point' for basal PTH secretion but a normal PTH response to acute hypocalcaemia in malaria. Skeletal resistance may attenuate the effects of the PTH response but patients with malaria appear relatively resistant to the calcium chelating effects of citrated blood products.

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