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Malar rash, also named a butterfly rash, is a common facial presentation of multiple disorders.[1] characterized by an erythematous flat or raised rash across the bridge of the nose and cheeks, which usually spares nasolabial folds. It may be transient or progress to involve other areas of facial skin.[2] This is mainly seen in patients with systemic lupus erythematosus. As per the American College of Rheumatology, Malar rash is one of the criteria for systemic lupus erythematosus (SLE); it may also be present with other types of lupus including discoid lupus and subacute cutaneous lupus.[2] Differential diagnoses for malar rash are as follows: systemic lupus erythematosus, cellulitis, rosacea, erysipelas, dermatomyositis, and pellagra. Treatment starts with sun protection, including appropriate clothing, sunscreens, and behavior change and management of the underlying disease., (Copyright © 2022, StatPearls Publishing LLC.)

Osteitis fibrosa cystica (OFC) is a disorder involving the bone which is resulted from excessive production of parathyroid hormone (PTH) due to parathyroid gland hyperactivity. It was first described by Recklinghausen in 1891. Bone changes are a late presentation of hyperparathyroidism. Bone involvement in hyperparathyroidism has shown a significant decrease in incidence over the past decades (from 80% to as low as 15%). This fact might be due to the early detection of asymptomatic cases via serum calcium monitoring.[1] PTH induces osteoclast activity which results in a bone break down. Hyperparathyroidism (PHP) might be due to parathyroid adenoma (up to 85% of cases), parathyroid hyperplasia, parathyroid carcinoma, renal osteodystrophy, and hereditary factors.[2] Up to 5% of PHP cases develop OFC which can indicate a prolonged or more severe disease. Osteitis fibrosa cystica presents as bone pain and characteristic radiologic findings including subperiosteal bone resorption in middle phalanges and distal radius, thinning of distal clavicle, bone cyst formation, “salt and pepper” pattern of the skull, brown tumor involving long bones and generalized osteopenia (up to 5% of cases). Brown tumors are caused by bone demineralization due to osteoclast activation, microfractures, and microhemorrhages. Its name comes from characteristic color resulting from hemosiderin deposition. OFC and its radiologic findings are more common in cases with parathyroid carcinoma compared to benign causes of PHP.[3][4], (Copyright © 2021, StatPearls Publishing LLC.)

Postpartum thyroiditis (PPT) is a destructive autoimmune disease occurring in the first year after delivery in women without a history of thyroid disease prior to pregnancy. Postpartum thyroiditis could cause transient or permanent thyroid disease. Three clinical presentations have been suggested for postpartum thyroiditis are as follows: (1) transient hyperthyroidism (32% of patients), (2) transient hypothyroidism (43% of patients), and (3) transient hyperthyroidism followed by hypothyroidism and then recovery, which is the classic form of PPT (25% of patients). Postpartum thyroiditis is an autoimmune disease and associated with the presence of antibodies to thyroid peroxidase (TPO). Chances of developing postpartum thyroiditis in pregnant women who have positive TPO antibodies early in pregnancy are 30% to 52%.[1] Postpartum thyroiditis could occur after the loss of a pregnancy at 5 to 20 weeks gestation.[2] During pregnancy level of TPO antibodies naturally decreases due to the immunosuppressed state of pregnancy. Women who remain positive for TPO antibodies in the third trimesters of pregnancy will have an 80% chance of developing postpartum thyroiditis.[3] Screening of high-risk women for developing postpartum thyroiditis, such as a positive test for antithyroid peroxidase antibody, history of postpartum thyroiditis, type 1 diabetes mellitus, is recommended by Endocrine Society clinical guidelines. High-risk women should be evaluated for serum TSH levels at three and six months postpartum.[1], (Copyright © 2021, StatPearls Publishing LLC.)