Chronic neutropenia is a rare hematologic abnormality encountered in primary care. It can be caused by a wide range of acquired and congenital factors. Very rarely, it can occur as isolated chronic neutropenia where other hematologic cell lines are completely intact. The case discussed here dealt with a similar situation where a 29-year-old female patient presented with severe neutropenia and otherwise intact cell lines in an asymptomatic fashion. Laboratory testing conducted at multiple intervals showed a consistently and severely depressed absolute neutrophil count (ANC) for a prolonged time. In addition, the patient had some abnormalities in serum immunoglobulin levels that pointed towards an underlying autoimmune or malignant pathology but these were insufficient to arrive at a clear diagnosis. The unique presentation in this patient presents an opportunity to study the pathological causation for neutropenia and, more specifically, isolated neutropenia.
Creutzfeldt-Jakob disease (CJD) is known for a rapidly progressive decline in cognitive functions due to an underlying infection from a prion. This case involves a unique and atypical variant of CJD that was difficult to diagnose for the investigating medical teams. As such, it highlights the particular challenge of using traditional diagnostic algorithms for atypical variants of CJD, in terms of time-appropriate diagnostics. The patient presented with a sudden episode of vertigo which was treated as an isolated symptom. While succeeding investigations involving neurology and otolaryngology specialists were being carried out, the patient experienced progressively worsening and more frequent episodes of disequilibrium that required multiple visits to emergency care facilities. In such a facility, a repetitive battery of serum and cerebrospinal fluid testing confirmed the diagnosis of CJD. Subsequently, the patient was provided the necessary supportive care. While this case was successfully diagnosed, it showed that common presentations can have significant underlying neurological implications, and such atypical variants should be accounted for in traditional diagnostic algorithms. This can avoid unnecessary delays in therapeutic rehabilitation.
Social media platforms, such as YouTube and Instagram, have become the latest medium for communication with a vast potential for influencing society. With their rise, a virtual market now exists where attention in the form of "likes," "views," and "followers" is traded for a monetary and psychological benefit. Amid this trade, physically risky behaviors have arisen to become a new attraction for attention, leading to numerous "trends" that encourage the same risk-taking behavior. Such trends, even those with a positive goal, have simultaneously led to injuries and fatalities, which highlights the necessity of a proactive approach to curtail the same. While media outlets and some non-governmental organizations usually highlight the risks of participating in these trends, the healthcare community has yet to have a collective and organized response to extreme social media participation. As such, a collaborative effort involving multiple tiers of the healthcare community is required to successfully prevent vulnerable populations from falling prey to the virtual attention-based economy of extreme social media participation.
Case Presentation•A 39 years old lady withType1Diabetes was repeatedly hospitalised with seizures thought to be related to hypoglycaemia though capillary glucose was never documented in these episodes •She also had primary hypoparathyroidism for the last ten years and was on calcium and vitamin D supplements •She had cataract removal from right eye and also had early cataract in left eye •Her family also confirmed her declining memory over past 2 years. She would take long pauses trying to recall things •On examination she had slow speech, serpentine gaze and shuffling gait. Chvostek's sign and Trousseau's signs were negative. Rest of the systemic examination was normal •Her calcium was reasonable with adjusted calcium of 2.-2.5mmol/L on treatment Progress and ManagementShe was sent for neuropsychological assessment to ascertain the cognitive impairment and whether she would be capable of looking after her diabetes by herself. She was found to have marked cognitive impairment in everyday functioning, particularly planning & organisation, abstract reasoning, attending to verbal information and processing new information, recalling and decision making. Thus had CT brain which showed wide spread calcification in the brain. She was seen by a neurologist and started on anticonvulsant treatment. Her seizures improved with no improvement in her cognition and gait abnormalities CT Brain-showing calcification in basal ganglia involving caudate nucleus,lentiform nucleus and thalamus, in the centrum seim ovale bilaterally & also subcortical dense curvilinear calcification bilaterally Discussion•Hypoparathyroidism is the common cause of pathological calcification in the brain though 0.3-1.5 % cases are physiological •Seizures occur in up to 70% of patients with symptomatic hypoparathyroidism 1,2,3 •Parkinsonism, dystonia, hemiballismus, choreoathetosis, and oculogyric crises occur in 5-10% of patients with idiopathic hypoparathyroidism 4 but are less common in patients with surgical hypoparathyroidism or other causes of hypocalcemia 4 •Parkinsonism seems to be resistant to levodopa but in some cases improvement occur with calcium and vitamin D replacement 5,6,7 •The mechanism of intracranial calcification is not completely understood 8 .It may be related to the duration of hypocalcaemia and hyperphosphataemia than parathyroid hormone itself •The goal of therapy in hypoaparathyroidism is to control symptoms and minimise complications. Use of PTH is not recommended 9 •In our case, initially hypoglycaemia was thought to be the cause of patient's seizures and neuropsychiatric symptoms as serum calcium was stable (2.2-2.5mmol/L).However, her visit to the neurologist and subsequent CT brain findings and improvement in seizures (after anticonvulsant treatment) showed that her symptoms were due to hypothyroidism related brain calcification ConclusionThis case emphasizes the importance of thinking about the whole spectrum of the disease even though the biochemical markers are stable on treatment.
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