<Case
Presentation>
A 75-year-old female patient was sent to emergency room
(ER) due to consciousness disturbance for one day. She had
diabetes mellitus, complicated with diabetic retinopathy and
nephropathy, with oral antidiabetic agent treatment for 6-7
years. Besides, she had osteoporotic compression fracture of
L1 and received calcium carbonate treatment since one month
ago. She was noticed to have disorientation and agitated
behavior abruptly one day prior to admission. There was no
fever or head injury, but body weight loss (10 kgs/ 6 months)
was noted.
At ER, her consciousness was drowsy (Glasgow coma scale:
E4V4M5). The blood pressure was 202/104 mmHg. The body
temperature was 36.8 C, pulse rate was 89 beats per minute,
and respiration rate was 18 per minute. Her skin was dry
without petechiae. Her conjunctiva was pale and the neck was
supple. The other physical findings were nonremarkable. The
brain CT revealed no definite acute intracranial lesion.
Laboratory data showed hypercalcemia (13.57 mg/dl),
hypophosphatemia (1.8 mg/dl) and hyperglycemia (337.9 mg/dl).
Other data are listed in Table 1 and 2.
After admission, normal saline
hydration, furosemide (Lasix) and clodronate sodium (Bonefos)
infusion were given. Consciousness recovered after
hypercalcemia improved. The plasma intact parathyroid hormone
(i-PTH) level was found to be elevated (330 pg/ml). Thyroid
echo showed left thyroid hypoechoic nodule and one hypoechoic
nodule (0.9 x 0.4 cm) behind the right thyroid lobe (Figure
1). Parathyroid sestamibi scan revealed persistent
abnormal accumulation of radioactivity at the inferior right
thyroid bed in the early (15 min) and delayed (3 hr) imaging
(Figure
2
).
Parathyroidectomy was done later and pathology report was
adenoma of right lower parathyroid.
She was discharged on the
4th day after operation when relative hypocalcemia
(7.4 mg/dl) was noted. She was admitted again because
progressive consciousness disturbance was found on the
7th
day after operation when the serum calcium level
was 5.29 mg/dl. She received oral calcium carbonate supplement
and calcitriol treatment later.
Table 1.
Hematologic laboratory values on admission
WBC K/μL |
RBC M/μL |
Hb g/dl |
Hct % |
MCV fL |
PLT K/μL |
Seg % |
Lym % |
Mono % |
Eosin % |
Baso % |
7.1 |
4.21 |
11.7 |
35.2 |
83.6 |
393 |
67.4 |
26.3 |
5.9 |
0.4 |
0.0 | Table 2. Blood chemical values on
admission
BUN mg/dl
|
Cre mg/dl
|
Glu mg/dl
|
Na mEq/L |
K mEq/L |
Ca mg/dl |
P mg/dl |
GPT IU/L |
NH3 μg/dl
|
Alb g/dl |
Ketone body |
12.7 |
0.71 |
337.9 |
138.2 |
3.10 |
13.57 |
1.8 |
26.6 |
32 |
4.59 |
Neg. | Table
3. Endocrinology laboratory tests
Cortisol (random) μg/dl (N: 3-25) |
T4 μg/dl (N: 5-12) |
Free T4 ng/dl (N: 0.9-1.8) |
T3 ng/dl (N: 70-190) |
TSH μIU/ml (N: 0.4-5.0) |
PTH-intact pg/ml (N: 10-60) |
15.63 |
4.91 |
1.09 |
48.39 |
0.41 |
330 | EKG:
non-specific ST-T change CXR: cardiomegaly, no active lung
lesion 24-hrs urine calcium excretion: 811 mg/ day (normal
range 100-300) CCr: 72.7 ml/ min Post-OP: serum i-PTH 3.5 pg/ml
<病案分析>
這是一個原發性副甲狀腺功能亢進造成高血鈣症的案例,其臨床表現包括意識變化、骨折、體重減輕等。意識變化除了考慮腦血管病變、高低血糖的問題外,電解質不平衡亦應考慮。此案例曾因骨質疏鬆、腰椎骨折住院,沒有檢驗血中鈣離子濃度,而接受碳酸鈣補充治療。體內的總血鈣值受血中白蛋白的影響,所以要先校正或直接測量游離鈣。要鑑別診斷高血鈣症,要先檢查血中的完整型副甲狀腺素(i-PTH)
。除了副甲狀腺功能亢進,其他高血鈣症的原因還有惡性腫瘤、腎衰竭末期、內分泌疾病如甲狀腺功能亢進、腎上腺功能不足,肉芽腫病如結核病,藥物因素如Thiazide、Lithium及家族性低尿鈣高血鈣症等(familial
hypocalciuric
hypercalcemia)。原發性副甲狀腺功能亢進要尋找有無家族史,約有1-3%的病人是第一型多發性內分泌腫瘤(multiple
endocrine
neoplasia)。原發性副甲狀腺功能亢進有百分之八十以上是單一腺瘤所引起,15-20%為副甲狀腺增生,目前的標準療法是手術切除腺瘤或增生的腺體。高血鈣危症的治療除了大量的等張輸液灌注、視情形投與利尿劑,臨床上常用的降血鈣藥物為雙磷酸類(包括pamidronate、clodronate)及抑鈣素(calcitonin)。術前對副甲狀腺的定位檢查包括超音波、核醫攝影、電腦斷層、核磁共振等。有1-5%的病人術後因為骨骼的remineralization,會產生慢性低血鈣症,稱為hungry
bone
syndrome,須服用鈣片及維生素D治療。
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