Hypophosphatemic rickets can cause a variety of bone and joint symptoms, one of its rare presentations is sacroiliac joint involvement, which may be mistaken for inflammatory spondylitis. Here, we report the case of a 31-year-old African American woman who presented with a two-year history of lower back pain and morning stiffness, initially suspected to be due to inflammatory spondyloarthritis. Laboratory tests revealed negative inflammatory markers, normal serum calcium, vitamin D3, and parathyroid hormone levels; however, the alkaline phosphatase levels were elevated and serum phosphorus level was low. Magnetic resonance imaging (MRI) of the lumbosacral spine revealed mild widening of the sacroiliac joint with periarticular sclerosis with no signs of osteitis or bone marrow edema. Her condition was attributed to a known diagnosis of X-linked hypophosphatemic rickets affecting her sacroiliac joints. Her symptoms gradually improved after conservative treatment with physical therapy, nonsteroidal anti-inflammatory drugs, phosphate, and vitamin D supplementations. Based on our literature review, we have come across only five rickets cases with similar presentations. Two patients had previously undiagnosed hypophosphatemic rickets at 15 and 35 years of age. One case was related to vitamin D-deficient rickets, and the final two cases were adult-onset vitamin D-resistant rickets misdiagnosed as ankylosing spondylitis. Radiological signs of sacroiliac joint involvement in these cases include narrowing of the sacroiliac joints, fusion of the sacroiliac joints, subchondral hypointense signal changes, and chondral surface irregularities. Vitamin D supplementation has significantly reduced the incidence of rickets; however, there are still cases of familial rickets that can present with a variety of symptoms, including signs and symptoms consistent with inflammatory spondylitis, which can be easily misdiagnosed or mistreated if this presentation is not recognized.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome involving excessive immune activation. It can be primary (familial) or secondary (triggered by infection, malignancy, or rheumatological disease). This is a case of a previously healthy 43-year-old African American woman who presented with fever and confusion. The patient was eventually diagnosed with pulmonary aspergillosis and responded well to antifungal therapy. She met the diagnostic criteria of HLH-2004 trial for hemophagocytic lymphohistiocytosis. She also fulfilled the 2019 classification criteria for systemic lupus erythematosus (SLE) without the classical signs and symptoms of SLE.HLH management includes supportive management, treatment of underlying condition, and immunosuppressive treatment. Etoposide and dexamethasone are commonly used treatments for HLH; however, underlying active infection can limit the treatment options. In our case, the patient was treated with steroids and hydroxychloroquine. Her condition gradually improved and she recovered without complications.Based on our literature review, we encountered six cases of HLH secondary to Aspergillosis with a mean age of approximately 47 years. The diagnosis of HLH is often delayed because of nonspecific presentation. Early identification and treatment are crucial to improve the survival rate.

Corticosteroid therapy is a known risk factor for osteonecrosis, more commonly with chronic use and high cumulative dose. Osteonecrosis (avascular necrosis) has been described in pregnancy involving primarily the femoral head. To our knowledge, only rare cases of femoral meta diaphysis or knee osteonecrosis in pregnancy have been documented in the literature.We report a 28-year-old woman with sickle cell trait and beta-thalassemia trait who developed severe bilateral knee pain shortly after corticosteroid therapy. She was 34-weeks pregnant when she presented with the signs of preterm labor and was found to have oligohydramnios and preeclampsia. She was given two intramuscular injections of betamethasone 12 mg one day apart to enhance the fetal lung maturity. Within hours of the second injection, she developed acute and severe bilateral knee pain affecting her mobility and ambulation. Bilateral knee x-rays were unremarkable. Given the severity and persistence of her pain, magnetic resonance imaging (MRI) of bilateral lower extremities was done few days later and showed signs of early osteonecrosis involving bilateral distal femoral meta diaphysis and right lateral femoral condyle.Other than the steroid therapy she had received, no additional extrinsic risk factors for osteonecrosis were identified. Potential intrinsic risk factors were thought to include her combined sickle-beta-thalassemia traits and pregnancy. She was diagnosed with steroid-induced osteonecrosis, given the temporal relationship. Her presentation was unique, because osteonecrosis affected unreported sites during pregnancy, and it started shortly after a brief course of antenatal steroid. She was treated conservatively with analgesics, and outpatient orthopedic follow-up was recommended. She was advised to avoid prolonged weight-bearing and strenuous activities. On a follow-up appointment two months later, she was still complaining of bilateral knee pain with ambulation though it was less severe. She did not return for follow-up thereafter.We suggest the possibility of osteonecrosis in pregnancy involving uncommon sites, such as distal femur and femoral condyle in this case, following one or two doses of systemic steroid. Obstetricians need to consider osteonecrosis when evaluating an unexplained musculoskeletal pain after betamethasone that is used for preterm labors. More studies, including reporting more cases with unusual presentation and prospective studies following pregnant patients receiving steroid therapy, are needed to better understand the causes, associations, management, and clinical course of osteonecrosis in pregnancy.