Karma and Diabetes Mellitus

1. Suter PM, Locher R, Häsler E, Vetter W. Is there a role for the ob gene product leptin in essential hypertension? Am J Hypertens 1998;11:1305-11. 2. Kennedy A, Gettys TW, Watson P, Wallace P, Ganaway E, Pan Q, et al. The metabolic significance of leptin in humans: Gender-based differences in relationship to adiposity, insulin sensitivity, and energy expenditure. J Clin Endocrinol Metab 1997;82:1293-300. 3. Makris TK, Stavroulakis GA, Krespi PG, Hatzizacharias AN, Kyriaki DK, Chronakis EV, et al. Elevated plasma immunoreactive leptin levels preexist in healthy offspring of patients with essential hypertension. Am Heart J 1999;138:922-5. 4. Karlsson C, Lindell K, Ottosson M, Sjöström L, Carlsson B, Carlsson LM, et al. Human adipose tissue expresses angiotensinogen and enzymes required for its conversion to angiotensin II. J Clin Endocrinol Metab 1998;83:3925-9. 5. Dunbar JC, Hu Y, Lu H. Intracerebroventricular leptin increases lumbar and renal sympathetic nerve activity and blood pressure in normal rats. Diabetes 1997;46:2040-3.

Sir, I read the editorial by Dr. Kalra et al. [1] on the concept of metabolic karma published in the May-June issue of the Indian Journal of Endocrinology and Metabolism with keen interest. With the understanding that I was raised the European cultural sphere and that Eastern spiritual concepts were imparted on me only through one of my professors at the Charles University, Zbavitel, a Scholar of Bengali Literature, translator from Sanskrit and Pali and more, [2] and through my professional experience in Nepal, [3] I would like to make a few notes. As described in the editorial, the concept of metabolic karma is logical but can potentially lead to dangerous results. Presenting this concept as stated to patients with type 2 diabetes mellitus could lead them to the conclusion that it is not necessary to make an effort to change their lifestyle habits, which we know to be key for improving metabolic control, and that the impetus for melioration can come from the outside, mainly through medication. And, we all know that for a significant portion of patients even in very developed parts of the world, modern antidiabetic medication is still not available due to financial limitations.

Preservation of Thyrotroph Function in Sheehan's Syndrome
Sir, Although Sheehan's syndrome (SS) is now rarely described from developed nations, physicians from developing nations need to keep the entity in mind wherein with modern hormone assays, and imaging diagnosis is not difficult. Atypical or partial presentation of SS is described from India; with the preservation of gonadotroph and corticotroph function, [1,2] preservation of thyrotroph has not been described.
A 38-year-old female was suspected to have primary hypothyroidism a year back on the basis of clinical features, and thyroid function tests revealed total T3 of 0.51 ng/ml (range: 0.8-1.8), T4 of 1.2 μg/dl (range: 4-13), and thyroid-stimulating hormone (TSH) of 100 mIU/L (range: 0.5-6.5). She was put on thyroxine 50 μg/day which she was taking intermittently. Recently, she presented to our hospital and detailed history revealed that she was married at the age of 31 years. She conceived 5-year postmarriage and terminal event was intrauterine death followed by postpartum hemorrhage. She required blood transfusion during the postpartum period. She also had history of easy fatigability, regression in breast size, and loss of axillary and pubic hair following the delivery of the dead fetus. Examination revealed blood pressure of 90/60 mmHg with no postural drop, respiratory rate of 18/min, and oral temperature of 97.6°F (36.4°C). There was no goiter or lymphadenopathy. She had atrophy of breasts and sparse axillary and pubic hair. Chest, cardiovascular, and abdominal examinations were noncontributory. Central nervous system examination revealed slow mentation in the form of delayed response to verbal commands. Examination of motor system did not reveal any focal neurodeficit, but deep tendon jerks were markedly delayed. Evaluation revealed hypoglycemia (blood glucose of 38 mg/dl), normal hemogram, kidney, and liver function, with normal serum sodium and potassium; electrocardiogram revealed bradycardia and low-voltage complexes. Abdominal ultrasound was normal. Hormonal investigations revealed TSH of 23 mIU/L with T3 of 1.64 ng/mL, T4 of 8.5 μg/dl and anti-thyroid peroxidase (TPO) antibody titer of 46 IU/L (normal value <35). Basal (8 am) serum cortisol 0.07 mcg/dl, adrenocorticotropic hormone <5 pg/ml (range: 9-52), prolactin 19.4 ng/ml (range: 4-23), follicle-stimulating hormone 16 IU/ml, luteinizing hormone 3.74 IU/ml, and serum insulin-like growth factor-1 was 39 ng/ml (range: 109-284). Magnetic resonance imaging of pituitary revealed empty sella. On the 2 nd day of admission, the patient developed acute adrenal crisis and was managed with intravenous (IV) fluids and IV hydrocortisone. Levothyroxine was restarted. The patient improved clinically. Appetite improved and there was an improvement in general well-being. The patient was given oral prednisolone, and levothyroxine was continued at the same dose. She was discharged on the 5 th day of admission.
Preservation of various anterior pituitary functions in SS has been reported previously. Of all the cell lines in the anterior pituitary, gonadotroph and corticotroph cell lines are the most often preserved. Because of the location of somatotroph and lactotrophs in the lateral and posterior portion of the pituitary, the location is supposed to be the most susceptible to ischemic necrosis. [3,4] However, some previous studies have reported thyrotroph involvement in 90%-100% of women with SS; [1] at the same time, preservation of thyrotroph has not been described. Some elevation in TSH has been reported in these women; it usually does not cross >20 mIU/L. [5] In the present, patient's initial TSH was more than 100 mU/L suggesting preservation of thyrotroph function which responds to failing thyroid by marked elevation of TSH as is seen in primary hypothyroidism. The possibility of autoimmune polyglandular disease is less likely in view of the absence of the elevation of TPO antibodies.

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Bashir Ahmad Laway, Sajad Sumji
Department of Endocrinology, Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India