Clinical scenario :
A 60-year-old male presented with complaints of easy
fatigability of 3 months duration .it was followed by a fever of 3 weeks
duration
Fever was not associated with Rigors and Chills
more so in the evenings.
The patient also complained of reduced appetite
and weight loss-16kgs in 3 months. Before the current presentation, he
developed progressive deterioration in his sensorium and vomiting. The vomiting
was not bilious, not blood-tinged usually the food taken by him earlier.
There was no history of
cough with expectoration, no history of diarrhea, no dysphagia
No history of diabetes, hypertension in the past
or any other comorbidity
On examination:
The patient was irritable and disoriented to
time, place and person
Pallor was present
Generalised emaciation,BMI – 18.2kg/m2
No icterus, clubbing, cyanosis, pedal edema,
lymphadenopathy
Pulse rate- 100 bpm – Regular Rhythm
BP- 110/90 mmHg
RR- 23 cycles per minute
Found to have polyuria during input-output
monitoring
RS: No accessory muscles used, B/L Reduced breath
sounds at base of the lung
P/A : Umbilicus appears normal, distended
abdomen, No organomegaly,
and bowel sounds heard,
On Percussion – Shifting Dullness (+)
CNS: No focal neurological deficit
Differential diagnosis considered
were :
Chronic Infections-Tuberculosis/HIV
Malignancy-hematological/gastrointestinal/lung
Endocrine-diabetes, hyperthyroidism,
hyperparathyroidism
INVESTIGATIONS
CBC-Hb-9.4 g/dL ,TLC 5.5 X 103
/µL,Neutrophil-79.6% (25-50%)
Lymphocyte 12.8% (25-40%)Eosinophil 1.8%
(1-6%)Basophil0.4% (0-1%)
Monocyte5.4% (1-8%)
Blood sugars-normal, TSH-normal
Blood urea level -75mg/dL (15-36g/dL),Serum
Creatinine-3.1mg/dL (0.6-1.2mg/dL),
Serum Calcium-14.0mg/dL (8.4-10.2mg/dL),Serum
Albumin-3.2 g/dL (3.2-4.4g/dL),
Corrected Calcium level-14.64mg/dL
(8.5-10.2mg/dL),CRP-23.4mg/L (<10mg/L),
Serum phosphate-2.5mg/dL (2.5-4.5mg/dL),Serum ACE
Levels-Normal,
Parathyroid hormone (PTH)-1.60pg/mL
(15-68.3pg/mL)
Vitamin D-45ng/mL (20-50ng/mL)
Chest X-ray shows mild blunting of costophrenic
angle
(image enclosed)
(image enclosed)
USG Neck-Thyroid gland appears normal in size and
texture.
No evidence of enlarged Parathyroid glands. No
other significant abnormality detected
CECT Thorax and abdomen-Image shows pleural
thickening with enhancement
(costal, mediastinal and diaphragmatic pleura).
Mesothelioma to be considered and suggested
pleural biopsy(image enclosed)
Histopathology of pleura(CT guided
pleural biopsy)-
Section studied show thickened pleura with
numerous granuloma composed of epithelioid cells,
Langhan’s giant cells and few
lymphocytes-features are suggestive of tuberculosis of pleura
HOSPITAL COURSE
Differential diagnosis considered were: Chronic
Infections-Tuberculosis/HIV, Malignancy-
hematological/gastrointestinal/lung,
Endocrine-diabetes, hyperthyroidism, hyperparathyroidism.
On evaluation found to have severe hypercalcemia
with acute kidney injury.
His altered sensorium and polyuria were also explained by hypercalcemia.
His altered sensorium and polyuria were also explained by hypercalcemia.
Such severe hypercalcemia usually occurs with
malignancy. He was hyper hydrated with IV fluids.
Calcitonin, furosemide, and steroids were given
after correction of dehydration.
Acute kidney injury resolved and calcium levels
reduced.
His Thyroid,
PTH levels were normal.
CECT thorax and abdomen was done to screen any
internal malignancy /tuberculosis/sarcoidosis
which showed pleural thickening which was
biopsied.
Biopsy revealed granuloma with caseous necrosis.
ATT was started. Tapering dose of steroids were
given for 4 weeks to control hypercalcemia
as it was granuloma induced hypercalcemia.
The patient improved symptomatically, polyuria resolved,
sensorium normalized.
He gained weight of 4 kg at follow up and calcium
levels were 8.5mg/dl.
TEACHING MESSAGE
Though severe hypercalcemia more than 12mg/dl is
commonly seen in malignancy and
hyperparathyroidism reversible causes like
granuloma induced hypercalcemia should be
considered
in a case of Pyrexia of unknown origin. Severe hypercalcemia being
one of medical emergency aggressive hydration and
treatment of the primary cause
in our patient-led to complete reversal of his
AKI, hypercalcemia, and resolution of PUO
Dr.Balachandra S Bhat,
Assistant Professor,
Dept of General Medicine, Yenepoya Medical College
