BackgroundGraves’ disease and Hashimoto’s thyroiditis are the two autoimmune spectrum of thyroid disease. Cases of conversion from hyperthyroidism to hypothyroidism have been reported but conversion from hypothyroidism to hyperthyroidism is very rare. Although such cases have been reported rarely in the past we are now seeing such conversions from hypothyroidism to hyperthyroidism more frequently in clinical practice.Case presentationWe are reporting three cases of middle aged Asian females who presented with classical symptoms of hypothyroidism and the investigations showed elevated thyroid stimulating hormone with positive thyroid antibodies. Diagnosis of autoimmune hypothyroidism was made and thyroxine replacement therapy was initiated. Patients became asymptomatic with normalization of thyroid stimulating hormone level. After few years they developed symptoms of hyperthyroidism with suppressed thyroid stimulating hormone level. Over replacement of thyroxine was considered and the dose of thyroxine was decreased, but they remain symptomatic. After gradual decrease in the dose of thyroxine it was stopped finally. Even after few months of stopping thyroxine, the symptoms of hyperthyroidism did not improve and the biochemical and imaging modalities confirmed that the patients have developed hyperthyroidism. Anti-thyroid treatment was then started and the patients became symptom free.ConclusionHigh index of suspicion should be there for possible conversion of hypothyroidism to hyperthyroidism if a patient with primary hypothyroidism develops persistent symptoms of hyperthyroidism. Otherwise it can be missed easily considering it as an over replacement with thyroid hormone.

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We are presenting a case of falsely elevated T3 levels in a patient due to interference from monoclonal immunoglobulins. A 56-year-old, clinically euthyroid man referred to the endocrinology clinic of the Aga Khan university, Karachi Pakistan, for possible T3 thyrotoxicosis after thyroid function tests revealed total T3 >12.32 nmol/L (reference range 0.6–2.79), normal TSH, and total T4 level. There was a mismatch in clinical and laboratory parameters and preliminary laboratory results were suggestive of thyroid binding globulin abnormalities. Further evaluation in this context unmasked multiple myeloma. The presence of monoclonal immunoglobulins can lead to assay interference and spurious results. To the best of our knowledge, this is the second case defining the cause of falsely elevated T3 levels, due to assay interferences with binding of T3 only to monoclonal immunoglobulins.

IntroductionScientific literature is scarce on the utility of estimated average glucose (eAG) from Pakistan. Hence, there is a dire need to evaluate the relationship between eAG and fasting plasma glucose (FPG), in order to enhance our understanding of eAG and its usefulness. This study aims to investigate the relationship between FPG and eAG in diabetic patients calculated using HbA1C.

Objective: Microcephalic osteodysplastic primordial dwarfism type II (MOPD II) is an extremely rare disorder. Studies have shown its association with polycystic ovary syndrome (PCOS) and severe insulin resistance. We are presenting a case of MOPD II with severe hyperandrogenism, which has never been reported before. Methods: We present the history, physical exam findings, and laboratory results of an 18-year-old girl with a known case of MOPD II, who presented with symptoms of hyperandrogenism. Results: An 18-year-old girl with a known case of MOPD II presented in the endocrine clinic with complaints of increased facial and body hair and amenorrhea for 5 years. On physical examination, she had short stature, scoliosis, and bowing of legs. Marked hirsutism was present in male pattern of distribution. Her lab investigations showed an extremely high testosterone level of 217 ng/dL and a free androgen index of 49%. 17-Hydroxyprogesterone was 1.48 ng/mL, dehydroepiandrosterone was 85.50 µg/dL, and serum insulin was 89.75 µIU/mL. Abdominal imaging was unremarkable, with normal ovaries and adrenal glands. Conclusion: PCOS has a known association with MOPD II, but this degree of clinical and biochemical hyperandrogenism is unusual in PCOS. In addition, imaging did not reveal any source of the high testosterone level. However, invasive testing to search for a cause is needed to find out if there is any association of MOPD II with testosterone-producing tumors. (AACE Clinical Case Rep. 2017;3:e166-e169) Abbreviations: MOPD II = microcephalic osteodysplastic primordial dwarfism type II; PCOS = polycystic ovary syndrome