Misleading normal TSH and persistently elevated creatine kinase: clues to the diagnosis of chronic Sheehan’s syndrome

A 53-year-old woman was referred for medical evaluation of therapy-resistant dyslipidaemia accompanied by elevated creatine kinase levels. Because cessation or alteration of her medication did not improve laboratory abnormalities, hypothyroidism was considered, despite the fact that thyroid stimulating hormone levels were within the reference interval. On further evaluation, she was found to have panhypopituitarism and empty sella turcica as shown by MRI. These findings were unexpected since there was no clinical suspicion during detailed evaluation. When supplementary questions were asked, she brought up a history of severe postpartum haemorrhage 30 years ago, for which she underwent a hysterectomy. Based on these findings, the patient was diagnosed with Sheehan’s syndrome. This syndrome is a rare but potentially life-threatening complication of postpartum haemorrhage, characterised by varying degrees of hypopituitarism that are most commonly presented many years after delivery. The patient recovered after adequate hormone replacement therapy.

R116C mutation in PRSS1 gene causes hereditary pancreatitis and elevated creatine kinase in one child：a case report

Background Functionally acquired mutations in the PRSS1 gene can lead to autosomal dominant hereditary pancreatitis (Hereditary Pancreatitis, HP). The most frequently reported mutation sites are R122H, N29I, A16V, and R122C. R116C mutation was less frequently reported to be associated with HP. Moreover, there are few reports about association of hereditary pancreatitis with elevated creatine kinase in children. Case presentation: We reported a patient presented with repeated abdominal pain and recurrent acute pancreatitis accompanied by elevated creatine kinase. The genomic DNA of lymphocytes from peripheral blood was extracted for whole exon gene analysis. The patient had a heterozygous mutation in exon 3 c.346C > T, resulting in substitution of cysteine at position 116 with arginine (p.R116C). Her father had the same mutation in exon 3 c.346C > T. The diagnosis of hereditary pancreatitis due to R116C mutation in PRSS1 gene was confirmed. Conclusions The patient's hereditary pancreatitis is caused by the mutation of PRSS1 gene R116C, characterized by elevated creatine kinase in patient.

Rhabdomyolysis secondary to severe tic fits

Tourette syndrome (TS) is a condition wherein motor and vocal tics occur, provoked by an urge, but often not able to be completely voluntarily controlled. Tics are known to cause physical and emotional risks to quality of life, and in rare extreme cases, may have permanent consequences. We report the first cases, to our knowledge, of rhabdomyolysis due to extreme tic fits in two distinct patients with TS. Both patients presented with severe tics, leading to elevated creatine kinase and a diagnosis of rhabdomyolysis requiring hospitalisation and intravenous fluids. Neither had neuroleptic malignant syndrome. One patient was on concurrent neuroleptic therapy, but his laboratory parameters improved when tics subsided despite continued neuroleptic use. Our cases highlight the potential complication of rhabdomyolysis secondary to severe tic fits independent of neuroleptic use.

CK-MB Elevation in Mild Hypothermia: What We Did and We Should Have Done

An 88-year-old male patient with a past medical history of hypertension and gastroesophageal disease presented with nausea, vomiting, and hypothermia. He was admitted for further testing, which revealed elevated creatine kinase and its MB isoenzyme (CK-MB) and troponin with no significant electrocardiogram changes. He denied cardiac symptoms or any previous cardiac history. The patient was treated with fluids and antibiotics in which improvement in his symptoms was noted. In this article, we share this rare case of hypothermia associated with elevation of CK-MB.

Statin-associated necrotizing myopathy: a rare etiology

Introduction: Necrotizing autoimmune myopathy is a rare entity characterized by proximal muscle weakness, elevated creatine kinase levels, potential autoantibody presence, and myofiber necrosis with reduced or absent inflammation. Case description: We report the case of a 72-year-old female with a 3-week-history of asthenia, increasing proximal tetraparesis, without pain, fever, or other symptoms, and elevated creatine kinase levels. Previous history was remarkable for dyslipidemia controlled with statin therapy. A muscular biopsy was performed, leading to the diagnosis of necrotizing myopathy. A body computed tomography (CT) scan was normal. Corticotherapy was initiated with progressive clinical and analytical improvement. Discussion: This case depicts an uncommon and underdiagnosed pathology which may be associated with statin treatment or cancer, that requires an early diagnosis and close follow-up for better clinical outcomes.

Caffeine Overdose Complicated by Acute Kidney Injury despite Mild Creatine Kinase Elevation

Caffeine is a commonly used stimulant in our society. Prior case reports have described acute caffeine overdose resulting in rhabdomyolysis and acute kidney injury (AKI). We present the case of a 29-year-old man who presented to the emergency department after ingesting 20.1 g of caffeine in a suicide attempt and experienced AKI with only mildly elevated creatine kinase (CK). This case highlights the possibility that AKI can result from a caffeine overdose, even if the patient’s CK is only slightly elevated.