HOSP #	42170712	WARD	Endocrinology OPD
CONSULTANT	Dr. Heleen Vreede	DOB/AGE	37y female

Abnormal Result

• The patient’s calcium measured 2.91 mmol/L on two occasions, with PTH measuring 40.6 pmol/L
• VitD 13.6 (<50 = deficient)
• TFT’s TSH 0.01 T4 26.7pmol/L

Presenting Complaint

Presented at the GIT clinic in Feb 2020 with persistent vomiting and abdominal cramps, which was ongoing since November 2019.

History

• Patient was diagnosed with hypertension in her early 20’s.
• Initiated on HCTZ – subsequently changed to Atenolol 25mg dly – not overweight at the time
• Gastroscopy was normal
• No psychiatric symptoms reported – mood swings are reported occasionally by the family
• Oligomenorrhoea – started in 2019 – nothing else wrong was noted.
• Normal menarche – normal regular menses until the diagnosis of hypertension was made.
• Amenorrhoeic last 4 years on no medication currently

Examination

• Increased BMI – quite significantly increased
• BP 170/90
• Skin: Significant amount of skin tags, acanthosis nigricans
• No striae or bruising
• No Sx of thyroid disease.
• Physical examination unremarkable.
• Normal pulses
• Essentially a normal examination other than the high BMI

Laboratory Investigations

Repeated bloods (5 days after initial presentation): 

• TSH 3.13 T4 12.5
• PTH 28 pmol/L (1.6 -6.9)
• Ca 2.79
• Inorganic phosphate 0.77 L mmol/L (0.78 – 1.42)
• LFT’s: Normal
• Creat Normal
• U-Ca 5.6 (no creatinine to compare ratio)
• FSH 3.2 IU/L
• LH 2.0 IU/L
• E2 244 pmol/L
• Dehydroepiandrosterone sulphate (DHEAS) 2.4 umol/L (1.7 – 9.2)
• Testosterone 0.5 nmol/L (0.3 – 1.7)
• SHBG 25.9 L nmol/L (32.4 – 128.0)
• Prolactin 11.5
• TSH-Receptor antibodies: Negative

Other Investigations

The patient still had occasional vomiting, abdominal cramps and unexplained muscle pain – other electrolytes apart from calcium, magnesium and phosphate is also advised, as is osmolarity as fluid and electrolyte imbalance may be an effect, rather than a cause of the nausea, vomiting and muscle pain – the sodium and potassium was normal however.

See below, for the hypertension, phaeochromocytoma can be excluded by a 24-hour fractionated urinary metanephrines analysis.

Final Diagnosis

• Primary hyperparathyroidism is on top of the differential diagnosis and is likely the cause of the raised total calcium.
• Another cause of the raised blood pressure could very likely be a phaeochromocytoma.
• It was also advised for replacement of Vitamin D, after a repeat measurement.
• Other features of MEN-1 syndrome needs to be excluded.

Take Home Message

For phaeochromocytoma, 3 separate days’ urine collection is recommended if the suspicion is high, which it isn’t in this case. This increases the sensitivity of the test.

Before testing for MEN-1: one needs to correct Calcium first – since the hypercalcemia could exacerbate gastrin levels.

Increased serum calcium and hypophosphatemia is the net-result of increased PTH. Urinary phosphate will also be high if measured.

HOSP #		WARD	Internal Medicine
CONSULTANT	Dr. Jody Rusch	DOB/AGE	21 y male

Abnormal Result

Potassium of 1.9 mmol/L was found on a blood gas analysis.

Presenting Complaint

Patient presented with a few isolated episodes of muscle weakness. This progressed from 2 weeks before, during the index episode, to become so severe that he couldn’t walk.

History

Patient was given IV potassium + MgSO4 upon which the potassium normalised to 5.5 mmol/L
History of muscle weakness was on and off over the last few months – unable to walk for brief periods of time.
No Family Hx of illnesses / hypokalmeia
No hypertension and no family Hx of hypertension
Patient had sweating more than usual. No other overt Sx of hyperthyroidism.
No medications

The mother had no similar symptoms ever.

The father was unfortunately not involved and not contactable.

Examination

Normal pulses
Small goiter, diffusely enlarger
No cardiovascular system abnormalities

Laboratory Investigations

Potassium upon the current consultation: 4.6 mmol/L
Normal Sodium, Creatinine, calcium, magnesium, phosphate and chloride

Normal pH 7.35
Normal HC03
Suspecting: Hypokalemic periodic paralysis
TSH < 0.01
Free T4: 59 pmol/L
Free T3: 21 pmol/L
TSH-Receptor Antibodies: Increased above the cut-off

Creatine Kinase 749

Other Investigations

The further investigations needed to confirm the diagnosis

Final Diagnosis

Considering the fact that the patient had no renal tubular acidosis, no medication which could cause the low potassium, it was, according to the endocrinologist, likely a diagnosis of Thyrotoxic Periodic Paralysis (TPP).

Patient was placed on Neomercazole and a Beta-adrenergic receptor blocker.

Take Home Message

I wasn’t aware of the condition until this case was brought up to the endocrinology meeting.

Thyrotoxic periodic paralysis is a rare cause of muscle paralysis.

TPP is a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis.

It has been increasingly reported in the USA due to the rise in the immigrant population. Hypokalemia in TPP results from an intracellular shift of potassium induced by the thyroid hormone sensitization of Na⁺/K⁺–ATPase rather than depletion of total body potassium. Treatment of TPP includes prevention of this shift of potassium by using nonselective beta-blockade, correcting the underlying hyperthyroid state, and replacing potassium.

It is important for physicians to distinguish TPP from familial hypokalemic periodic paralysis, a more common cause of periodic paralysis in Caucasians. The absence of a family history of paralysis, male sex, presentation in the second to fourth decades of life, and signs of thyrotoxicosis like sinus tachycardia help in the diagnosis of this disorder. Early recognition of TPP is vital to initiating appropriate treatment and to avoiding the risk of rebound hyperkalemia that may occur if high-dose potassium replacement is given.

It is most common in Asian populations – incidence approximately 2% in patients with thyrotoxicosis of any cause.

It has been recognized in Thais, Filipinos, Vietnamese, Koreans, Malaysians, Hispanics, African Americans, and Caucasians. It is characterized by acute onset of severe hypokalemia and profound proximal muscle weakness in patients with thyrotoxicosis.