Episcleritis is the inflammation of the thin, loose, highly vascular connective tissue layer that lies between the conjunctiva and sclera. Incidence is less than 1/1000. It is more common in women and those between 40 and 50 years of age. Most cases are idiopathic. It is classified into simple and nodular. Most attacks resolve within 1–3 months. The nodular type tends to be more recurrent and painful. It presents with acute onset of redness, lacrimation, and photophobia. The diagnosis of is essentially clinical, and eye pain or tenderness should raise the concern for scleritis. Ophthalmological referral is recommended to rule out scleritis. Bloodwork to diagnose associated systemic rheumatological disease may be helpful. Cold compresses and artificial tears provide symptomatic relief. Topical nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids are used for persistent symptoms. Rarely, systemic steroids may be necessary. Immunosuppressive treatment to control an underlying autoimmune disorder is the last resort for resistant cases.
Introduction/Background: Thyrotropin secreting pituitary adenomas (TSH-oma) are a rare cause of hyperthyroidism. They account for <1% of the cases of hyperthyroidism with a reported incidence of 2.8 per 1 million in Sweden. Diagnosis is suspected by the presence of elevated T4 and T3 in the setting of an unsuppressed TSH level. The presence of large pituitary adenoma is highly suggestive of the diagnosis and can be differentiated from thyroid hormone resistance by elevated alpha subunit and SHBG levels. Trans-sphenoidal surgery is the definitive treatment. Peri-operative medical treatment with somatostatin analogues is indicated to achieve euthyroidism and prevent surgical risks and thyroid storm. The use of somatostatin analogues as a primary treatment for TSH-oma is still under investigation. We hereby report a rare case of TSH-oma where somatostatin analogues successfully resulted in normalization of thyroid function and tumor size reduction. Clinical Case: A 61 years old gentleman with a history of hypothyroidism diagnosed three years before presentation to the Pituitary clinic. He was treated with Levothyroxine. On clinical examination, he had mild tremor and warm sweaty palms with no stigmata of Grave’s disease. The thyroid function test showed elevated free T4 of 3.6 ng/dl (0.9-1.7), elevated free T3 of 8.6 pg/ml (2.0-4.4), and a high TSH level of 9.10 μIU/ml (0.27-4.20). His prolactin level was mildly elevated at 24.8 ng/ml(4.0-15.2). Testosterone, IGF-1, and cortisol levels were normal. An MRI of his pituitary gland showed large pituitary macroadenoma with supra-sellar extension and mild compression of the optic nerve. He had an elevated alpha subunit of 5.6 ng/ml (<1.37) and a high SHBG level of 198 nmol/l(10-80). TSH adenoma was diagnosed and he was planned for trans-sphenoidal surgery. Pre-operative treatment with somatostatin analogue Lanerotide 90 mg monthly injection was initiated. Interestingly normal thyroid function was observed approximately 1 month after his first injection. Repeat MRI showed a considerable decrease in the size of the pituitary macroadenoma. The patient opted to hold on to surgery and to continue on medical treatment. His thyroid function remains normal 15 months after initiation of treatment and his MRI continues to show stable pituitary adenoma. Conclusion: Somatostatin analogues can be used as a primary treatment for thyrotropin secreting pituitary adenomas when the patient is unable or unwilling to undergo surgery. It is use is associated with normalization of thyroid function and in some cases with a reduction in the adenoma size.
Back ground: Autoimmune progesterone dermatitis (APD) or progesterone hypersensitivity (PH) is a rare hypersensitivity reaction to progestogen that exclusively occur in women of childbearing age of which is the underlying mechanism remains not well understood. Clinical case: A 44 years old lady was referred to our endocrine outpatient clinic by her dermatologist for treatment of a recently diagnosed autoimmune progesterone dermatitis. She was initially evaluated for a skin rash that started during the second trimester of her second pregnancy in 2009. Her initial diagnosis was pregnancy induced eczema which was treated with topical steroid with no significant improvement. Her rash worsens after delivery and had persisted since then. She failed chronic systemic steroid treatment and multiple immunosuppressive medications over the years. She had regular menstrual period since her menarche at age of 11 years old. She was on oral contraceptive medication prior to her second pregnancy which she resumed after delivery. She then switched to IUD. Her rash typically gets worse 7-10 days before the onset of her menstrual period with some improvement after her period. Her initial clinical exam showed erythematous papules over her extensor elbows, thighs and genital area with scattered eczematous excoriated plaques over her extremities and trunk. She underwent skin patch test which showed that she is allergic to class A, B, and D1 steroids PH was suspected based on her history and confirmed by a positive progesterone skin test. She was referred to reproductive endocrinology for consideration of ovulation suppression using GnRH agonist. Conclusion: APD is a rare hypersensitivity reaction that can be triggered by endogenous progesterone (menses, pregnancy) or exogenous progestin (OCP, IUD, IVF) exposure. Women between menarche and menopause can be affected with the average age of onset to be in the third decade of life. The underlying mechanism is not well known with several hypotheses being postulated (e.g hypersensitivity reaction type I and IV, hormone cross reactivity and autoimmunity) Clinical presentation is variable and can range from mild dermatitis to life threatening anaphylaxis with some extra dermal manifestations have been described. Detailed history taking is the key to diagnosis as the most consistent features is the presentation of symptoms during the luteal phase of the menstrual cycle. The goal of treating APD is to suppress ovulation which can be achieved by the use of GnRH agonist, selective estrogen receptor modulator or oophorectomy. Progesterone desensitization has been tried in women desiring pregnancy.
Humans and mice with Melanocortin 4 receptor (MC4R) deficiency remain protected from hyperglycemia despite chronic obesity and insulin resistance. We have observed that elevated glycosuria in MC4R deficient mice protects them from hyperglycemia. Moreover, our results indicate that circulating epinephrine may couple MC4R signaling with kidney glucose reabsorption. However, the direct role of epinephrine in regulating kidney glucose reabsorption remains unclear. We hypothesize that epinephrine is essential for maintaining glucose homeostasis via kidney glucose reabsorption. To test this hypothesis, we performed oral glucose tolerance tests (OGTTs) and intraperitoneal insulin tolerance tests (ITTs) in phenylethanolamine-N-methyltransferase (Pnmt) knockout (KO) mice that specifically lack epinephrine but have normal norepinephrine levels. Pnmt KO mice exhibited reduced insulin sensitivity compared to their Wild-Type (WT) littermates (Area under the curve for ITT: 9,700±256 vs. 8,482±417 mg/dL.min, p<0.05). Paradoxically, we observed improved rather than impaired glucose tolerance in Pnmt KO mice compared to their WT controls (Area under the curve for OGTT: 32,546±1,592 vs. 40,058±1,918 mg/dL.min, p<0.05). To ascertain if Pnmt KO mice, like MC4R deficient mice, show elevated glycosuria, we quantified their 24 urine glucose levels after oral glucose (250 mg) challenge. Indeed, Pnmt KO mice demonstrated elevated glycosuria compared to their WT littermates (Urine glucose: Baseline, 24.63±2.2 vs. 11.14±0.82 mg/dl; post glucose challenge: 67.83±5 vs. 16.09±1.13 mg/dl, p<0.001), again validating the phenotype similar to that of MC4R deficient mice. To determine the glucose transporters involved in mediating elevated glycosuria in the Pnmt KO mice, we measured the levels of different renal glucose transporters using western blot. We found that GLUT2 was decreased by ~26% in Pnmt KO mice compared to their WT littermates. Levels of other glucose transporters were not changed, indicating that suppression of renal GLUT2 mediates elevated glycosuria in the epinephrine deficient mice. We validated the direct effect of epinephrine on GLUT2 levels in vitro using mouse primary renal proximal tubule epithelial cells. Indeed, epinephrine selectively increased GLUT2, but did not affect other glucose transporters in the mouse kidney primary cells. Our findings establish the essential role of epinephrine in glucose reabsorption via the renal glucose transporter GLUT2. Therefore, modulating the renal adrenergic system, or, kidney-specific GLUT2 may afford alternative strategies to regulate glycosuria and ultimately mitigate diabetes.
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