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Copper is an essential cofactor in many enzymatic reactions vital to the normal function of the hematologic, vascular, skeletal, antioxidant, and neurologic systems. Parenteral nutrition and chronic tube feeding are used in various mal-absorptive syndromes, including following gastrectomy and gastric bypass surgery. Features of copper deficiency include hematologic abnormalities (anemia, neutropenia, and leukopenia) and myeloneuropathy; the latter is a rarer and often unrecognized complication of copper deficiency. We describe a 36 -year-old Emirati woman who was referred to endocrinology service because of generalized body weakness and fatigue post bariatric surgery. The patient initially noted a lower extremity swelling in feet bilaterally that worsened in severity over time and progressed up to knees. Over a 3 month period, her ability to ambulate gradually deteriorated. She also noticed maculopapular skin rash over both shins. Patient had Sleeve Gastrectomy in 2011. Followed by conversion of sleeve to RYGB surgery in 2018 due weight loss failure. Patient is known to have well controlled hypothyroidism on thyroxine. She was prescribed vitamin D, neurobion, iron and multivitamins tablets post surgery but never been compliant. The patient was admitted with severe malnutrition due to poor oral intake over the last 5 months prior to admission. Her total weight loss was 34.5 kg (32% weight change, BMI 28 .52kg/m2) in less than 9 months post surgery. Initial labs revealed severe hypoalbuminemia, normochromic anemia and neutropenia. Iron, folate, thiamine, and vitamin B12 levels were normal. Vitamin B6 level was normal at 11 mcg/L (normal = 5-50 mcg/L). The serum copper level was low at 310 µg/l (normal = 794-2023µg/l). Zinc level was low at 447 µg/l (normal = 551-925µg/l). Nutritional needs were estimated using the following formulas; 22-25 kcal/kg ideal body weight (IBW)/d and 1.5-2.0 g protein/kg IBW/d, 30-35 ml IVF/kg /d. The patient’s input/output, body weight, and clinical status were monitored. Parenteral nutrition additive copper 0.3 mg/day and oral copper 8 mg daily, resulted in the rapid correction of hematologic indices over one week. Combined multivitamins supplementation and oral copper supplements alone normalized serum copper levels over 4 weeks and resulted in resolution of weakness and body edema. This report serves to alert physicians of the association between bariatric surgeries and subsequent severe copper deficiency in order to avoid diagnostic delays and to improve treatment outcomes.

Radioactive iodine ablation (RAI) has been used for the treatment of Graves’ hyperthyroidism since 1946 and it is the primary recommended modality for Graves’ disease treatment in many countries. Acute painful radiation thyroiditis after radioiodine treatment for hyperthyroidism of Graves’ disease is considered uncommon. The prevalence is 1-5% in patients treated with 131I therapy for hyperthyroidism. Dose of RAI and thyroid volume can be precipitating factors for post radiation thyroiditis. The higher RAI dose increases the chance of RAI thyroiditis while the larger goiter size decreases the absorbed radiation dose in the thyroid gland. We present a 25-year-old Emirati male previously healthy, who was referred to our service for hyperthyroidism management. He presented with thyrotoxicosis in absence of goiter. All investigations revealed that graves’ disease is the primary cause of his hyperthyroidism. He was treated with RAI ablation 18.3 mCi. Day four after RAI, he presented with severe pain in the anterior neck associated with fatigue, tremor, palpitation and weight loss. Symptoms lasted for 6 weeks post RAI. There was laboratory evidence of thyrotoxicosis presented with further suppression of TSH and higher fT4 than the baseline. Acute radiation thyroiditis was diagnosed and has been commenced on propranolol 10mg BID. Symptoms completely resolved after 6 weeks of treatment and thyroid function returned to normal level. The patient has remained asymptomatic on continued follow up care till eventually became hypothyroid clinically and biochemically. Our case reflects that radioiodine thyroiditis can last for longer period and occur after larger doses of 131I treatment in absence of goiter. Our patient has RAIA induced thyroiditis lasted for 6 weeks post 18.3mCi of 131I, and has no goiter, which were both contributing factors for RAIA induced thyroiditis

Idiopathic transient osteoporosis of pregnancy (ITOP) is a rare and under-reported condition that has affected healthy pregnancies. ITOP usually presents in the final trimester of a normal pregnancy. Radiographic studies detect drastic loss of bone mass, elevated rates of turnover in the bone, and edema in the affected portion. We present a 26-year-old previously healthy woman, who was admitted at 39 weeks of gestation with severe left hip pain and inability to walk for one month.The pain was constant, progressive, involving left lower limb, and associated with numbness and weakness. Neurological exam revealed diminished power in the left hip (motor power was 2/5), and inability to stand and walk due to pain in the left hip. She was unable to stand by herself. Investigations revealed anemia, low vitamin B12, low vitamin D and magnesium. Bilateral hip MRI showed increased T2WI signal in the left femoral head consistent with idiopathic transient osteoporosis of the left hip (ITOP). DXA scan showed bone mass density (BMD) below expected for age.The patient had induced vaginal labor without complication. The left hip pain improved after delivery. She was treated conservatively with Calcium, Magnesium and vitamin D. The patient symptoms completely resolved in 3 months post-delivery. DXA scan and Hip MRI at 1 year interval showed normal BMD and complete resolution of previous bone marrow edema and changes seen in MRI hip. This case report serves to highlight the effect of pregnancy on bone mass during third trimester which may result in transient osteoporosis of pregnancy leading to weakness and gait disturbance. Clinical symptoms can be misdiagnosed as a peripheral neurological complications instead of bone metabolism changes of pregnancy.

Thyroid gland can affect kidney function in different ways. Thyroxine as a master hormone of metabolism and growth works in many cellular levels include the renal tubules. We present a 34-year-old Emirati gentleman who presented with multiple episodes of hypokalemic periodic paralysis. Blood test revealed thyrotoxic state, with highly positive serology for thyroid peroxidase, anti-thyroglobulin and thyrotropin receptor antibodies. Thyroid uptake scan confirmed homogenous diffuse uptake consistent with toxic diffuse goitre [Graves’ disease]. In view of recent fracture, bone profile and DXA scan were done. Investigations revealed vitamin D deficiency and below expected for age bone mass density. The patient was started on symptomatic treatment with propranolol, IV and oral potassium along with IVF hydration. Routine blood work during admission showed a persistent normal anion Gap metabolic acidosis, serum bicarb 15 mmol/l. 24 hours urine electrolytes revealed normal potassium, sodium, high magnesium, low calcium and PH levels. Biochemical lab results suggested type 1 renal tubular acidosis. As the patient had hypokalaemia, high urine magnesium and low urine calcium and limbs weakness, Gitleman Syndrome was considered in the differential diagnosis. Whole Exome Sequencing (CentoXome GOLD®) was sent which came back negative. The following gene panels were studied: Renal tubular acidosis panel: ATP6V0A4, ATP6V1B1, CA2, EHHADH, HNF4A, SLC34A1, SLC4A1, SLC4A4. Bartter Syndrome panel: ATP6V1B1, BSND, CA2, CASR, CLCNKA, CLCNKB, CLDN16, CLDN19, FXYD2, HSD11B2,KCNJ1, KCNJ10, KLHL3, NR3C2, SCNN1A, SCNN1B, SCNN1G, SLC12A1, SLC12A2, SLC12A3, SLC4A1, SLC4A4, WNK1. Gene related to Gitelman syndrome: SLC12A3 Renal tubular acidosis was treated with KCL 600mg PO TID, Na bicarb 1200mg PO BID and spironolactone 25 mg PO OD. The patient received radioactive iodine (RAI) as the ultimate treatment for Graves’ disease. He developed hypothyroidism post RAI ablation and commenced on levothyroxine. Improvement of the metabolic acidosis was noticed in line with improvement of thyroid function. Na bicarb and spironolactone tablets were stopped eventually as the patient was euthyroid clinically and biochemically. Overt hyperthyroidism is associated with accelerated bone remodelling, leading to hypercalciuria, which can predispose to nephrocalcinosis and renal tubular damage, and therefore causes type 1 renal tubular acidosis. Once the patient becomes euthyroid, bone remodelling and urine calcium return to normal levels and that would correct the renal acidosis. This case report serves to highlight the effect of Graves’ disease on renal tubules which may result in type 1 renal tubular acidosis. This effect could be reversible with normalization of thyroid function.

Diabetic ketoacidosis (DKA) is an acute, life threatening complication of diabetes characterized by hyperglycemia, ketonemia and acidosis. It is known to commonly present with hyponatremia and rarely with hypernatremia. DKA can present with hypernatremia in pediatric population which carries poor prognosis when present. We present a 27 year- old Ethiopian lady, previously healthy who was brought to emergency department (ED) with decreased level of consciousness. She had polyuria and polydipsia associated with weight loss for 1 month and flu like symptoms for 3 days prior to admission. On day of presentation, she was found to be confused, sleepy and not able to recognize people around her. In ED, patient was confused, GCS 8 severely dehydrated with poor skin turgor and marked delay in capillary refill >3s. Patient was afebrile, with HR 115 bpm, BP 95/60mmHg, and BMI 20kg/m2. Initial labs revealed; severe acidosis pH 6.8, blood glucose (BG) >38 mmol/l and corrected Na 155 mmol/l. Calculated serum osmolality 357mOsm/kg, lactic acid 5 mmol/l and HCO3 3 mmol/l. Further labs revealed K 4.4 mmol/l, Urea 10 mmol/l, Cr 150 micromole/l, WBC 26 and Ketones 3+ in urine. DKA was diagnosed and treated in ED with 4L IVF (2L bolus NaCl and other 2L of 0.23% NaCl given at 15 ml/hr) and NaHCO3 150 mmol. Continuous insulin regular infusion at rate of 0.1U/Kg/hr as per protocol was initiated. Patient was admitted to ICU for close monitoring of BG, GCS and electrolytes. After 9 hours of management, patient GCS improved to 13-14. Repeated labs revealed; improvement in PH 7.17, BG 22mmol/l, HCO3 5 mmol/l and lactic acid 1 mmol/l. There was worsening of Na 159 mmol/l and K dropped to 2.6 mmol/l. IV KCL bolus 20mmol followed by 40mmol IV continuous in IVF was initiated. IVF was changed from NaCl to D5W at 125ml/hr. Electrolytes were repeated after 7 hours and showed improvement in and Na and k levels. During her stay in ICU, patient recovered to baseline GCS 15 with no residual symptoms. IV insulin infusion was stopped on 3rd day and commenced on Insulin glargine and insulin Aspart boluses. Further investigations confirmed DM type 1; HbA1c 15%, C-peptide 0.08 nmol/l, IA2Ab of >400 and GAD Ab >250. Patient had an uneventful hospital course, she stayed in ICU for 3 days and then shifted to medical floor. She was discharged on basal bolus insulin regimen. In patients with uncontrolled DM/DKA, serum Na level is variable, reflecting the balance between the hyperglycaemia induced water movement out of the cells that lowers serum Na level, and the glycosuria induced osmotic diuresis, which tends to raise serum Na. When there is marked osmotic diuresis, DKA may present with a normal or even elevated serum Na concentration, despite a markedly elevated serum BG. To best of our knowledge, this is the second case to report an unusual DKA presenting with hypernatremia in adult patient.

Anabolic steroid injections widely used by athletes during strength training period, all studies were done in this field showed transient effect of androgenic anabolic steroids on thyroid which were mainly causing hypothyroidism, However hyperthyroidism cases were never reported up to our knowledge. We present a 25-year-old Emarati male previously healthy, who is referred to endocrine service for hyperthyroidism management. He presented with thyrotoxicosis manifestations. Medical history revealed that he was using anabolic steroids, testosterone, and gonadotropin injection which were prescribed in private gym by trainer. Anabolic steroids were taken twice for few months over 2years prior to his current presentation with hyperthyroidism. Autoimmune profile was negative for thyroid disorder. Radioiodine uptake scan was normal initially then after a year showed diffuse uptake. No evidence of clear cause of his hyperthyroidism. He remained in thyrotoxic state for more than a year post stopping the anabolic steroids. He was treated with radioactive iodine ablation (RAI) according to his preference. Develop post-RAI thyroiditis treated with beta blockers and analgesia. Symptoms completely resolved after 6 weeks and thyroid function returned to normal. The patient has remained asymptomatic on continued follow up care. This case points to the effect of anabolic steroids on thyroid function. Hence all published studies showed that it could cause hypothyroidism not hyperthyroidism. few Literatures are showing that anabolic steroid’s prominent effect on human thyroid function is reduction of TBG with consequent reduction of Total T3 and T4. In rats, anabolic steroids also act in the peripheral metabolism of thyroid hormones and seem to exert an important proliferative effect on thyroid cells. By this effect we believe that, anabolic steroid might cause hyperthyroidism in our patient. To our knowledge, this is the first case report addressing anabolic steroids causing permanent hyperthyroidism. Our patient proved that the effect of anabolic steroid was not transient as he remained in thyrotoxic state for more than a year after stopping steroids and uptake scan showed diffuse high uptake which goes with thyroid cells proliferation hypothesis.