Ectopic Locations Research Articles

ODP121 Recurrent atypical parathyroid adenoma: a case report

Abstract Background Atypical parathyroid adenoma is a rare cause of hyperparathyroidism, with an incidence ranging from 0.5 to 4.4%. Its recurrence rate is low, around 3%. We describe a young patient with an atypical parathyroid adenoma that recurred twice at the right neck. Case presentation A 39-year-old woman presented to the ER with low back pain, hyporexia, weight loss, and an oral lesion with purulent discharge. She was diagnosed with nephrolithiasis, severe hypercalcemia (serum calcium concentration: 21,2 mg/dl (Reference range 8,5-10,5) and hyperparathyroidism (serum PTH: 703 pg/mL; reference range 15-45pg/mL). Parathyroid scintigraphy identified an uptake at the site of the lower right parathyroid. A cervical US confirmed the presence of a 3 cm markedly hypoechoic nodule in that location. Fine needle aspiration (FNA) suggested parathyroid adenoma, and PTH washout levels were 1900 pg/ml. Screening for multiple endocrine neoplasia was negative. Biopsy of the mandibular alveolar bone, around the oral lesion, showed giant cell lesion. Lower right parathyroidectomy was performed, and the histopathology showed parathyroid neoplasm with features favoring atypical parathyroid adenoma (lesion measuring 3×2×1.8 cm). Fifteen months after the surgery, the patient presented symptoms of hypercalcemia, with a new elevation of serum PTH levels (738 pg/ml), confirmed with radiotracer uptake at the site of the upper right parathyroid gland. She underwent right parathyroidectomy and hemithyroidectomy. Histopathology revealed an atypical parathyroid adenoma. Immunohistochemistry was positive to galectin 3 in rare cells; Ki 67 positive (2%). After nine months, the patient noticed a subcutaneous nodule in the right anterior cervical region associated with symptomatic hypercalcemia, and a new increase in serum PTH levels (469.5 pg/mL). Parathyroid scintigraphy confirmed radiotracer activity at the nodule described, that was surgically resected. Histopathology was compatible with an atypical parathyroid neoplasm (uncertain malignant potential). The patient remains in regular follow-up, asymptomatic and normocalcemic. Conclusion While 96% of patients with atypical parathyroid adenomas are cured with parathyroidectomy, this case shows a very rare description of two recurrences in a short time of follow-up, with an ectopic location in the last one. It should be noted that atypical paratyroid adenomas are already an uncommon presentation of primary hyperparathyroidism. Genetic investigation is warranted in such cases. Presentation: No date and time listed

DNA sequence and chromatin modifiers cooperate to confer epigenetic bistability at imprinting control regions

Genomic imprinting is regulated by parental-specific DNA methylation of imprinting control regions (ICRs). Despite an identical DNA sequence, ICRs can exist in two distinct epigenetic states that are memorized throughout unlimited cell divisions and reset during germline formation. Here, we systematically study the genetic and epigenetic determinants of this epigenetic bistability. By iterative integration of ICRs and related DNA sequences to an ectopic location in the mouse genome, we first identify the DNA sequence features required for maintenance of epigenetic states in embryonic stem cells. The autonomous regulatory properties of ICRs further enabled us to create DNA-methylation-sensitive reporters and to screen for key components involved in regulating their epigenetic memory. Besides DNMT1, UHRF1 and ZFP57, we identify factors that prevent switching from methylated to unmethylated states and show that two of these candidates, ATF7IP and ZMYM2, are important for the stability of DNA and H3K9 methylation at ICRs in embryonic stem cells.

ПЕРВИЧНЫЙ ГИПЕРПАРАТИРЕОЗ, ОБУСЛОВЛЕННЫЙ АДЕНОМОЙ ПАРАЩИТОВИДНОЙ ЖЕЛЕЗЫ, ЭКТОПИРОВАННОЙ В ТИМУС: ОПИСАНИЕ КЛИНИЧЕСКОГО НАБЛЮДЕНИЯ

Primary hyperparathyroidism (or PHPT) is a rare pediatric disease occurring in 1 case per 200 to 300 thousand children. The most common cause of PHPT in the adult population is a solitary parathyroid (PT) adenoma with up to 16% of PT adenomas having an ectopic location. There are no epidemiological data on pancreatic adenomas in pediatric population including atypically located ones, and clinical data are extremely scarce. This article describes a clinical observation of an adolescent patient with PHPT whose disease has been manifested with increased fragility and deformation of the bones of the skeleton. Only one year after the onset of primary symptoms a complex set of diagnostic measures was initiated, as a result of which a diagnosis was established: PHPT against the background of adenoma of the pancreas, ectopic in the left lobe of the thymus. The surgical treatment was carried out in the amount of thoracoscopic hemithymectomy which led to the relief of hyperparathyroidism. Despite the surgical intervention the systemic osteoporosis and persistent pathological changes in the bone skeleton that have been formed by the time of diagnosis require long-term observation and treatment of the patient by a pediatric endocrinologist, pediatric orthopedist and rehabilitologist. Thus, based on the presented clinical observation, the conclusion is as follows: in order to minimize the risk of disability in children and adolescents with PHPT it is extremely important to establish the correct diagnosis as early as possible coupled with the timely etiotropic and pathogenetic treatment.

A “Two-bal” Pregnancy: A Case Report on Heterotopic Pregnancy

Heterotopic pregnancy is defined as the combination of an intrauterine pregnancy and a concurrent pregnancy with an ectopic location, often the fallopian tube. Implantation can also occur in the cervix, ovary, cornua, abdomen, and previous Cesarean scar . While heterotopic pregnancy is considered a rare finding, the incidence is increasing due to the increased use of Assisted Reproductive Technology (ART). Heterotopic pregnancy is suspected when an ultrasound reveals an intrauterine pregnancy in addition to a complex adnexal mass. Differential diagnoses include: threatened abortion, ruptured corpus luteum cyst, and isolated ectopic pregnancy. Correct diagnosis can be difficult to attain due to nonspecific symptoms and findings such as: free fluid in the abdomen, abdominal pain, and vaginal bleeding. Patients are often diagnosed later than in an isolated tubal pregnancy due to these nonspecific symptoms and confirmation of an intrauterine pregnancy . Delayed diagnosis often leads to greater risk of rupture, an acute abdomen, and hemodynamic instability. Since the extrauterine pregnancy is non viable, salpingectomy is the surgical standard and first line treatment . However, other treatment modalities such as local feticidal injection have been performed depending on the clinical status of the patient and physician expertise. Finally, an ultrasound is to be performed after the procedure to confirm viability of the intrauterine pregnancy. During this case study, the patient presentation, diagnosis, and treatment of heterotopic pregnancy will be discussed in detail. The objective of this case study is to review the events and management of this unique patient presentation and discuss the recommended diagnosis and treatment options, as well as the incidence and prognosis of patients with this rare diagnosis.

Lower pole obstructive megaureter of duplex kidney: an exception to the Weigert-Meyer rule

Introduction. Anatomical features of the urinary tract in patients with duplicate kidneys are described using the Weigert-Meyer rule, since the orifice of the upper ureter has an ectopic location (inferomedial) and the orifice of the lower ureter has an orthotopic location (superolateral). However, there are rare cases of violation of this rule, complicated by obstructive megaureter, ectopic ureteral orifice, the presence of ureterocele.Objective. To report the rare clinical case of a lower pole obstructive megaureter as a violation of the Meyer-Weigert rule in the patient with complete ureteral duplication and to describe the use of ureteroureterostomy as an effective and safe method of surgical correction of the presented anomaly.Clinical case. We present a case of the infant (5 months old) with a lower pole obstructive megaureter. This pathology was identified through intravenous urography and voiding cystourethrography. Laparoscopic proximal end-to-side ureteroureteroanastomosis was chosen as a surgical treatment. Postoperative control intravenous urography showed the effectiveness (a reduction in the lower pole collecting system of the duplex kidney was revealed) and the safety of this method of correction.Conclusion. There are only several clinical cases about exceptions to the Weigert-Meyer rule reported in literature, and most of them are about adult patients. The main surgical method of treatment in such cases is heminephrectomy. To our knowledge, this is the only reported case of using ureteroureterostomy in the patient with a lower pole obstructive megaureter. This technique has shown its effectiveness and safety for restoring the patency of the urinary tract, confirmed during the control postoperative examination.

In vivo characterization of Drosophila golgins reveals redundancy and plasticity of vesicle capture at the Golgi apparatus

The Golgi is the central sorting station in the secretory pathway and thus the destination of transport vesicles arriving from the endoplasmic reticulum and endosomes and from within the Golgi itself. Cell viability, therefore, requires that the Golgi accurately receives multiple classes of vesicle. One set of proteins proposed to direct vesicle arrival at the Golgi are the golgins, long coiled-coil proteins localized to specific parts of the Golgi stack. In mammalian cells, three of the golgins, TMF, golgin-84, and GMAP-210, can capture intra-Golgi transport vesicles when placed in an ectopic location. However, the individual golgins are not required for cell viability, and mouse knockout mutants only have defects in specific tissues. To further illuminate this system, we examine the Drosophila orthologs of these three intra-Golgi golgins. We show that ectopic forms can capture intra-Golgi transport vesicles, but strikingly, the cargo present in the vesicles captured by each golgin varies between tissues. Loss-of-function mutants show that the golgins are individually dispensable, although the loss of TMF recapitulates the male fertility defects observed in mice. However, the deletion of multiple golgins results in defects in glycosylation and loss of viability. Examining the vesicles captured by a particular golgin when another golgin is missing reveals that the vesicle content in one tissue changes to resemble that of a different tissue. This reveals a plasticity in Golgi organization between tissues, providing an explanation for why the Golgi is sufficiently robust to tolerate the loss of many of the individual components of its membrane traffic machinery.

The Arabidopsis SAC9 enzyme is enriched in a cortical population of early endosomes and restricts PI(4,5)P2 at the plasma membrane.

Membrane lipids, and especially phosphoinositides, are differentially enriched within the eukaryotic endomembrane system. This generates a landmark code by modulating the properties of each membrane. Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] specifically accumulates at the plasma membrane in yeast, animal, and plant cells, where it regulates a wide range of cellular processes including endocytic trafficking. However, the functional consequences of mispatterning PI(4,5)P2 in plants are unknown. Here, we functionally characterized the putative phosphoinositide phosphatase SUPPRESSOR OF ACTIN9 (SAC9) in Arabidopsis thaliana (Arabidopsis). We found that SAC9 depletion led to the ectopic localization of PI(4,5)P2 on cortical intracellular compartments, which depends on PI4P and PI(4,5)P2 production at the plasma membrane. SAC9 localizes to a subpopulation of trans-Golgi Network/early endosomes that are enriched in a region close to the cell cortex and that are coated with clathrin. Furthermore, it interacts and colocalizes with Src Homology 3 Domain Protein 2 (SH3P2), a protein involved in endocytic trafficking. In the absence of SAC9, SH3P2 localization is altered and the clathrin-mediated endocytosis rate is reduced. Together, our results highlight the importance of restricting PI(4,5)P2 at the plasma membrane and illustrate that one of the consequences of PI(4,5)P2 misspatterning in plants is to impact the endocytic trafficking.

Pituitary stalk interruption syndrome (PSIS): do not miss this diagnosis

BackgroundPituitary stalk interruption syndrome (PSIS) is one of the rare endocrinal aetiologies of the abnormal short stature. This is a syndrome characterized by a specific tirade, an absent or hypoplastic anterior pituitary gland, thin or absent infundibulum, and ectopic posterior pituitary location. This type of pituitary dwarfism is usually presented in the first decade of life and may be first isolated with normal other pituitary hormones.ResultsOnly 3 out of 117 dwarf patients (2.5%) were found to have pituitary stalk interruption syndrome.ConclusionAlthough of rare incidence, pituitary stalk interruption syndrome (PSIS) is an entity which leads to pituitary dwarfism and should be kept in mind while investigating a child with pituitary dwarfism and radiologists should be aware of its rarely encountered diagnostic MRI findings for early diagnosis and treatment.

Eps15/Pan1p is a master regulator of the late stages of the endocytic pathway.

Endocytosis is a multistep process involving the sequential recruitment and action of numerous proteins. This process can be divided into two phases: an early phase, in which sites of endocytosis are formed, and a late phase in which clathrin-coated vesicles are formed and internalized into the cytosol, but how these phases link to each other remains unclear. In this study, we demonstrate that anchoring the yeast Eps15-like protein Pan1p to the peroxisome triggers most of the events occurring during the late phase at the peroxisome. At this ectopic location, Pan1p recruits most proteins that function in the late phases-including actin nucleation promoting factors-and then initiates actin polymerization. Pan1p also recruited Prk1 kinase and actin depolymerizing factors, thereby triggering disassembly immediately after actin assembly and inducing dissociation of endocytic proteins from the peroxisome. These observations suggest that Pan1p is a key regulator for initiating, processing, and completing the late phase of endocytosis.

CONGENITAL LABIAL NEVUS TREATED WITH PLASTIC SURGERY AND CRYOSURGERY

Congenital melanocytic nevi are lesions that present pigmentation at birth resulting from the accumulation of melanocytes in an ectopic location. In the labial region, they are rare. The diagnosis is clinical and must be confirmed with histopathology, because malignant lesions such as melanoma must be included in the differential diagnosis. A 32-year-old Black female patient presented with a lesion on the upper lip since birth. The patient did not have any health problems. On physical examination, a dark brown nodule located in the region of the tubercle of the upper lip, measuring 10 × 8 mm, sessile, painless, and with precise limits, was noted. Plastic surgery was performed by means of an excisional biopsy with a modified triangular incision, sutured by planes with catgut 5-0 and nylon 6-0 in the skin. The histopathologic exam confirmed the diagnosis of congenital nevus. The patient presented a discrete keloid that was treated with 3 cryosurgery sessions for aesthetic purposes, improving her lip appearance.

Dissecting the miR-451a-Mif Pathway in Endometriosis Pathophysiology Using a Syngeneic Mouse Model: Temporal Expression of Lesion Mif Receptors, Cd74 and Cxcr4.

Endometriosis is an enigmatic disease characterized by pain and infertility in which endometrial tissue grows in ectopic locations, predominantly the pelvic cavity. The pathogenesis and pathophysiology of endometriosis is complex and postulated to involve alterations in inflammatory, cell proliferation and post-transcriptional regulatory pathways among others. Our understanding on the pathogenesis and pathophysiology of endometriosis is further complicated by the fact that endometriosis can only be diagnosed by laparoscopy only after the disease has manifested. This makes it difficult to understand the true pathogenesis as a cause-and-effect relationship is difficult to ascertain. To aid in our understanding on endometriosis pathogenesis and pathophysiology, numerous rodent models have been developed. In this case, we discuss further assessment of a miR-451a—macrophage migration inhibitory factor (Mif) pathway which contributes to lesion survival. Specifically, we evaluate the temporal expression of lesion Mif receptors, Cd74 and Cxcr4 using host mice which express wild-type or miR-451a deficient lesions. Similar to that observed in humans and a non-human primate model of endometriosis, Cd74 expression is elevated in lesion tissue in a temporal fashion while that of Cxcr4 shows minimal increase during initial lesion establishment but is reduced later during the lifespan. Absence of miR-451a during initial lesion establishment is associated with an augmentation of Cd74, but no Cxcr4 expression. The data obtained in this study provide further support for a role of Mif receptors, Cd74 and Cxcr4 in the pathophysiology of endometriosis.

Synthetic regulatory reconstitution reveals principles of mammalian Hox cluster regulation.

Precise Hox gene expression is crucial for embryonic patterning. Intra-Hox transcription factor binding and distal enhancer elements have emerged as the major regulatory modules controlling Hox gene expression. However, quantifying their relative contributions has remained elusive. Here, we introduce "synthetic regulatory reconstitution," a conceptual framework for studying gene regulation, and apply it to the HoxA cluster. We synthesized and delivered variant rat HoxA clusters (130 to 170 kilobases) to an ectopic location in the mouse genome. We found that a minimal HoxA cluster recapitulated correct patterns of chromatin remodeling and transcription in response to patterning signals, whereas the addition of distal enhancers was needed for full transcriptional output. Synthetic regulatory reconstitution could provide a generalizable strategy for deciphering the regulatory logic of gene expression in complex genomes.

ЭФФЕКТИВНОСТЬ ОРГАНОСОХРАНЯЮЩЕЙ ТАКТИКИ ВЕДЕНИЯ ПРИ ШЕЕЧНОЙ БЕРЕМЕННОСТИ

Abstract. Diagnosis of cervical pregnancy is carried out based on the analysis of data obtained during the study of the gynecological status during bimanual abdominal - vaginal and ultrasound examinations. Treatment consists in performing organ-preserving manipulations and, in the absence of their effectiveness, extirpation of the uterus. Prevention of the development of cervical pregnancy consists in the rational treatment of gynecological diseases, refusal of abortions, carrying out full-fledged rehabilitation after intrauterine interventions. In this clinical case, prevention of unwanted pregnancy by prescribing rational contraception, timely diagnosis of the causes of infertility and miscarriage, as well as prevention and effective treatment of chronic endometritis would avoid the risk of cervical pregnancy. Careful management of pregnancy by an obstetrician-gynecologist made it possible to identify the ectopic location of the fetal egg in the early stages of pregnancy and prevent the occurrence of severe life-threatening complications, as well as perform organ-preserving surgical treatment, giving the patient the opportunity to realize the childbearing function in the future. Based on the study of this clinical case, it can be concluded about the effectiveness of the proposed management tactics of a patient with cervical pregnancy and the possibility of recommending this variant of medical tactics in the treatment of patients with this pathology.

An Ectopic location of papillary carcinoma of the thyroid

An Ectopic location of papillary carcinoma of the thyroid

Heterotopic Pregnancy Secondary to in vitro Fertilization-Embryo Transfer: Risk Factors and Pregnancy Outcomes.

BackgroundWith the widespread application of assisted reproduction technology (ART) and increased pelvic inflammatory disease, the incidence of heterotopic pregnancy (HP) has risen. However, the risk factors and treatment of HP remain indefinite.ObjectivesTo explore risk factors affecting the incidence of HP secondary to in vitro fertilization-embryo transfer (IVF-ET) and pregnancy outcomes after surgical treatment of HP.Methods29 patients with HP and 116 with an intrauterine-only pregnancy (IUP) after IVF-ET during the same period were included retrospectively from January 2015 to September 2020.ResultsPatients with HP had a higher proportion of previous ectopic pregnancies, multiple abortion history (≧2 times) and tubal indication for IVF than IUP. Besides, they had a greater possibility to end in spontaneous abortion (31.03 vs.13.79%, P = 0.028) and preterm delivery (25.00 vs. 7.00%, P = 0.035), less possibility to result in a live birth (58.62 vs. 78.45%, P = 0.028). History of multiple abortions (≥2 times) [odds ratio (OR) 3.031, 95% confidence intervals (CI) 1.087–8.453; P = 0.034], tubal infertility (OR 3.844, 95% CI 1.268–11.656; P = 0.017), previous ectopic pregnancies (OR 2.303, 95% CI 0.625–8.490; P = 0.021) and number of embryo transfer (OR 0.300, 95% CI 0.092–0.983; P = 0.037) resulted in an elevated proportion of HP in IVF treatment. Shorter operative duration, smaller size of the ectopic mass and location in the ampulla of the fallopian tube were associated with higher chance of survival in the coexistent intrauterine pregnancy after surgical treatment.ConclusionsPrevious history of ectopic pregnancy, multiple abortions, tubal infertility and multiple-embryo transfer may be considered as meaningful risk factors of subsequent HP following IVF-ET. In patients with HP treated by surgery, shorter operative duration, smaller size of the ectopic mass and location in the ampulla of the fallopian tube means better reproductive prognosis.

The PLEKHA7–PDZD11 complex regulates the localization of the calcium pump PMCA and calcium handling in cultured cells

The plasma membrane calcium ATPase (PMCA) extrudes calcium from the cytosol to the extracellular space to terminate calcium-dependent signaling. Although the distribution of PMCA is crucial for its function, the molecular mechanisms that regulate the localization of PMCA isoforms are not well understood. PLEKHA7 is implicated by genetic studies in hypertension and the regulation of calcium handling. PLEKHA7 recruits the small adapter protein PDZD11 to adherens junctions, and together they control the trafficking and localization of plasma membrane associated proteins, including the Menkes copper ATPase. Since PDZD11 binds to the C-terminal domain of b-isoforms of PMCA, PDZD11 and its interactor PLEKHA7 could control the localization and activity of PMCA. Here, we test this hypothesis using cultured cell model systems. We show using immunofluorescence microscopy and a surface biotinylation assay that KO of either PLEKHA7 or PDZD11 in mouse kidney collecting duct epithelial cells results in increased accumulation of endogenous PMCA at lateral cell–cell contacts and PDZ-dependent ectopic apical localization of exogenous PMCA4x/b isoform. In HeLa cells, coexpression of PDZD11 reduces membrane accumulation of overexpressed PMCA4x/b, and analysis of cytosolic calcium transients shows that PDZD11 counteracts calcium extrusion activity of overexpressed PMCA4x/b, but not PMCA4x/a, which lacks the PDZ-binding motif. Moreover, KO of PDZD11 in either endothelial (bEnd.3) or epithelial (mouse kidney collecting duct) cells increases the rate of calcium extrusion. Collectively, these results suggest that the PLEKHA7–PDZD11 complex modulates calcium homeostasis by regulating the localization of PMCA.

The Double Engines and Single Checkpoint Theory of Endometriosis.

Endometriosis is a chronic disease characterized by the ectopic localization of the endometrial tissue in the peritoneal cavity. Consequently, it causes local pathological changes and systemic symptoms, affecting at least one in every ten women. This disease is difficult to diagnose early, it is prone to dissemination, is difficult to eradicate, tends to recur, and is regarded as “a cancer of no kill”. Indeed, the development of endometriosis closely resembles that of cancer in the way of mutagenesis, pelvic spreading, and immunological adaptation. While retrograde menstruation has been regarded as the primary cause of endometriosis, the role of ovulation and menstrual stimuli in the development of endometriosis has long been overlooked. The development of ovarian and peritoneal endometrioses, similar to the development of high-grade serous carcinoma in the fallopian tube fimbriae with intraperitoneal metastasis, depends highly on the carcinogens released during ovulation. Moreover, endometriosis carries an extremely hypermutated genome, which is non-inferior to the ultra-mutated endometrial cancer. The hypermutation would lead to an overproduction of new proteins or neoantigens. Because of this, the developing endometriosis may have to turn on the PD-1/PDL-1 “self-tolerance” checkpoint to evade immune surveillance, leaving an Achilles tendon for an immune checkpoint blockade. In this review, we present the double engines and single checkpoint theory of the genesis of endometriosis, provide the current pieces of evidence supporting the hypothesis, and discuss the new directions of prevention and treatment.

The transcription factor Atf1 lowers the transition barrier for nucleosome-mediated establishment of heterochromatin.

Transcription factors can exert opposite effects depending on the chromosomal context. The fission yeast transcription factor Atf1 both activates numerous genes in response to stresses and mediates heterochromatic gene silencing in the mating-type region. Investigating this context dependency, we report here that the establishment of silent heterochromatin in the mating-type region occurs at a reduced rate in the absence of Atf1 binding. Quantitative modeling accounts for the observed establishment profiles by a combinatorial recruitment of histone-modifying enzymes: locally by Atf1 at two binding sites and over the whole region by dynamically appearing heterochromatic nucleosomes, a source of which is the RNAi-dependent cenH element. In the absence of Atf1 binding, the synergy is lost, resulting in a slow rate of heterochromatin formation. The system shows how DNA-binding proteins can influence local nucleosome states and thereby potentiate long-range positive feedback on histone-modification reactions to enable heterochromatin formation over large regions in a context-dependent manner.

Early Life Events and Maturation of the Dentate Gyrus: Implications for Neurons and Glial Cells.

The dentate gyrus (DG), an important part of the hippocampus, plays a significant role in learning, memory, and emotional behavior. Factors potentially influencing normal development of neurons and glial cells in the DG during its maturation can exert long-lasting effects on brain functions. Early life stress may modify maturation of the DG and induce lifelong alterations in its structure and functioning, underlying brain pathologies in adults. In this paper, maturation of neurons and glial cells (microglia and astrocytes) and the effects of early life events on maturation processes in the DG have been comprehensively reviewed. Early postnatal interventions affecting the DG eventually result in an altered number of granule neurons in the DG, ectopic location of neurons and changes in adult neurogenesis. Adverse events in early life provoke proinflammatory changes in hippocampal glia at cellular and molecular levels immediately after stress exposure. Later, the cellular changes may disappear, though alterations in gene expression pattern persist. Additional stressful events later in life contribute to manifestation of glial changes and behavioral deficits. Alterations in the maturation of neuronal and glial cells induced by early life stress are interdependent and influence the development of neural nets, thus predisposing the brain to the development of cognitive and psychiatric disorders.

Intrahepatic Gallbladder: A Case Report

Ectopic gallbladder is a very rare congenital anomaly with total recorded incidence of 0.1 – 0.7 % 1. Multiple ectopic locations of the gallbladder have been described in the medical literature and the second commonest site is intrahepatic location2. It is associated with increased risk of several gallbladder pathologies and possible misinterpretations in their diagnosis due to unusual location may delay initiation of the treatment or may pose risk during the surgery. Therefore, prompt diagnosis is of utmost importance particularly in surgical setting.3 In this case report we present a 13-year-old girl who was lingering with on and off vague abdominal pain for many months before was diagnosed with this rare anomaly.
 How to cite this: Ibrahim MI, Saim M, Khan RA, Mehmood R, Hasan R. Intrahepatic Gallbladder: A Case Report. Life and Science. 2022; 3(2): 88-90. doi: http://doi.org/10.37185/LnS.1.1.231
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