diabetes insipidus case study

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ICEECE2012 Poster Presentations Clinical case reports - Pituitary/Adrenal (58 abstracts)

Central diabetes insipidus: about two clinical cases

C. nogueira 1, , m. matos 1, , c. esteves 1, , g. jorge 1 , j. couto 2 , c. neves 1, , j. queirós 1 , e. vinha 1 , i. bernardes 1 & d. carvalho 1,.

1 Centro Hospitalar São João, Porto, Portugal; 2 Instituto Português de Oncologia, Porto, Portugal; 3 University of Porto, Porto, Portugal.

Introduction: Central diabetes insipidus (CDI) is produced by the destruction of the magnocellular neurons of the hypothalamic supraoptic and paraventricular nuclei which results in decreased arginine vasopressin (AVP) synthesis and secretion.

Case report 1: Forty-five year old female, previously healthy, was observed in April 2011 complaining of polydipsia, polyuria, nocturia and weight loss since January. Diabetes mellitus (DM) was excluded and she was admitted for study of possible diabetes insipidus. Water deprivation test was suggestive of CDI. Magnetic resonance imaging (MRI) showed infundibular hypophysitis and no hyperintense signal in the neurohypophysis. Autoimmune diseases, infections and infiltrative diseases were excluded. Imaging (chest x-ray, abdominal ultrasound, mammography, breast ultrasound and thoracoabdominal CT) was normal. No other pituitary deficits were shown. She started therapy with oral desmopressin with clinical improvement.

Case report 2: Fourty-three year old man, previously healthy, was seen in August 2011 complaining of polydipsia, polyuria and nocturia during the previous 3 months. DM was excluded. Water deprivation test was positive for CDI. Pituitary MRI was normal, with normal signal of high intensity in the neutohypophysis. He had no other hormonal deficits. Autoimmune and infectous diseases were excluded. After initiation of oral desmopressin the symptoms disappeared.

Discussion: In both cases it was not determined the etiology of CDI, as it may occur in 20–50% of CDI cases. In our institution is not possible to determine antibodies towards vasopressin secretory cells, which does not allow the diagnosis of this autoimmune form of CDI. The infundibular hypophysitis, observed in the first case, can occur in about 50% of idiopathic cases and more frequently in women. The lymphocytic hypophysitis can be diagnosed by pituitary biopsy, but it’s a very aggressive procedure and almost never performed. These cases highlight the difficulty of the etiologic diagnosis of CDI. However, proper treatment allows the symptoms control.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.

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A Case of Diabetes Insipidus

By David F. Dean (rr)

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“Amanda Richards,” a 20-year-old junior in college, is majoring in biology and hopes to be a pediatrician one day. For about a month, she has been waking up frequently at night to go to the bathroom. Most recently, she has noticed that she needs to go to the bathroom during the day more often, almost hourly. Students read about these symptoms and then answer a set of directed questions designed to teach facts and principles of physiology using reference books, textbooks, the Internet, and each other as sources of information. The case has been used in a sophomore-level course in human anatomy and physiology as well as in senior-level course in general physiology.

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• Learn about the similarities and dissimilarities between diabetes insipidus and diabetes mellitus.
• Understand the basic differences between the four types of diabetes insipidus.
• Be able to define and describe excessive thirst and urination in adults.
• Understand the methods by which diabetes insipidus is diagnosed and treated.
• Learn about other conditions which produce symptoms similar to those produced by diabetes insipidus.
• Be able to describe the physiological effects of antidiuretic hormone other than the maintenance of body water balance.

Pituitary diabetes insipidus; diabetic; antidiuretic hormone; ADH; vasopressin; osmoreceptors; osmolarity; polyuria; polydipsia; supraoptic nuclei; kidney function

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Undergraduate lower division, Undergraduate upper division

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Diabetes Insipidus Case Study (60 min)

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You just started your shift, what nursing assessments will be your priority at this point?

• Assess ventilator and respiratory status, lung sounds, SpO2
• Assess EVD system for integrity and that it is draining appropriately
• Complete neuro exam including pupils, GCS, reflexes, and LOC.
• Full set of vitals plus assessing IV sites for signs of infiltration or infection
• Assessing foley site and urine output
• Turning and assessing skin top to tail

Mrs. Ford’s vital signs are as follows: BP 124/68 MAP 86

HR 84 Temp 98.9 RR 16 (ventilated) ICP 12

She is not on any sedation. You determine her GCS is 6, she withdraws to pain, but does not open her eyes. Her pupils are equal and reactive bilaterally, 4mm. For this hour she has put out 120 ml of urine that is clear and yellow. She is receiving normal saline at 75 mL/hour as well as tube feeds at 40 mL/hour. Her EVD is open at 15 cmH 2 O and draining a clear pink fluid, 6 ml this hour.

faq lesson=”true” blooms=”Application” question=”Calculate her cerebral perfusion pressure.”]

• CPP = MAP – ICP
• 86 – 12 = 74 mmHg [/faq]

Given the assessment information that you have, what are you most concerned for with this patient?

• Immobility – skin and muscle breakdown
• Increased ICP → herniation → death
• Damage to Pituitary and/or Hypothalamus glands → can cause SIADH, DI, temperature regulation issues, as well as issues with CNS functions like breathing
• This patient clearly has a significant brain injury. I would be concerned for and monitoring for the following complications:

Hourly urine output for Mrs. Ford For the last 3 hours were 180 mL, 240 mL, and 440 mL. The urine is clear and barely pale yellow. Her blood pressure is 108/56, HR is 104. Her ICP is 15.

What could be going on physiologically with Mrs. Ford?

• This is likely Diabetes Insipidus due to the known neurological issue and the excessive output of clear, barely pale yellow urine.
• Neurological damage can cause damage to the pituitary gland – causing a LACK of secretion of ADH (Antidiuretic Hormone). This means the patient can no longer retain water and therefore begins to dump water excessively – this is why the urine looks almost like water.
• This will cause the blood to be super concentrated and could cause a lot of other issues because of it.

What further diagnostic testing do you expect the provider to order?

• Note: Polyuria WITHOUT hyperosmolality may indicate Primary Polydipsia – a condition in which patients literally drink water excessively and send themselves into a water intoxication/hypernatremic state.
• Check a CMP with serum osmolality to see if she is hyperosmolar or hypernatremic
• Check urine specific gravity and urine osmolarity – again this can tell us if she’s dumping lots of urine or if she’s just dumping a ton of water. Low specific gravity indiacates DI.

Lab Values: Na + 155 mg/dL Serum osmo 310 mOsm/kg Urine SG 1.005

Explain the significance of these lab values considering the patient's diagnosis.

• The patient is dumping excessive amounts of water in the urine, that is why her urine specific gravity is so low
• Because of the loss of water, the blood is now super concentrated, creating hypernatremia and a high serum osmolality.

What medications and or treatment changes do you expect the provider to order?

• The IV fluids need to be changed to D5W or D10W
• Free water via the OG tube will also help with the sodium levels
• DDAVP (Desmopressin) or Vasopressin should be ordered to replace the ADH that isn’t working

The provider orders the following:

Free water flush via OG Tube – 200 mL q4h

Change IVF to D5W at 125 mL/hr

Desmopressin (DDAVP) 2 mcg IV push q 12h

Daily weight

q4h Sodium and Serum Osmolality levels

You set the tube feeding pump to administer the free water and change the IV fluids while waiting for the DDAVP from the pharmacy

What regular monitoring will need to be done for Mrs. Ford during this treatment?

• Hourly urine output + urine specific gravity
• Continue frequent monitoring of vital signs and ICP/CPP
• Re-draw labs as ordered to ensure sodium is not being corrected too quickly

After 2 days of treatment, misses Fords urine output and urine specific gravity return to Baseline. However, she continues to have a GCS between 4 + 6, and now her left pupil is 8mm and fixed. The nurse notes her respiratory rate is erratic, her ICP is 18, and her heart rate is dropping.

What do you believe could be happening to Mrs. Ford at this time?

• Mrs. Ford may be experiencing brain herniation due to the bleeding and swelling in and around her brain
• Unfortunately, many times these patients cannot be returned to their normal baseline due to the extent of the damage.

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Preoperative peripheral inflammatory markers are predictors of postoperative central diabetes insipidus in craniopharyngioma patients: a retrospective study

• Jing Wang 1 , 2 ,
• Guanghui Wang 1 ,
• Lidong Cheng 1 ,
• Hongtao Zhu 1 ,
• Junwen Wang 1 ,
• Xinmin Ding 2 ,
• Hongquan Niu 1 ,
• Kai Zhao 1 &
• Kai Shu 1  

BMC Cancer volume  24 , Article number:  572 ( 2024 ) Cite this article

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Postoperative central diabetes insipidus (CDI) is commonly observed in craniopharyngioma (CP) patients, and the inflammatory response plays an important role in CPs. We aimed to evaluate the predictive value of preoperative peripheral inflammatory markers and their combinations regarding CDI occurrence in CPs.

The clinical data including preoperative peripheral inflammatory markers of 208 CP patients who underwent surgical treatment were retrospectively collected and analyzed. The preoperative peripheral white blood cells (WBC), neutrophils, lymphocytes, monocytes, platelet (PLT), neutrophil-to-lymphocyte ratio (NLR), derived-NLR (dNLR), monocyte-to-lymphocyte ratio (MLR) and PLT-to-lymphocyte ratio (PLR) were assessed in total 208 CP patients and different age and surgical approach CP patient subgroups. Their predictive values were evaluated by the receiver operator characteristic curve analysis.

Preoperative peripheral WBC, neutrophils, NLR, dNLR, MLR, and PLR were positively correlated and lymphocyte was negatively associated with postoperative CDI occurrence in CP patients, especially when WBC ≥ 6.66 × 10 9 /L or lymphocyte ≤ 1.86 × 10 9 /L. Meanwhile, multiple logistic regression analysis showed that WBC > 6.39 × 10 9 /L in the > 18 yrs age patients, WBC > 6.88 × 10 9 /L or lymphocytes ≤ 1.85 × 10 9 /L in the transcranial approach patients were closely associated with the elevated incidence of postoperative CDI. Furthermore, the area under the curve obtained from the receiver operator characteristic curve analysis showed that the best predictors of inflammatory markers were the NLR in total CP patients, the MLR in the ≤ 18 yrs age group and the transsphenoidal group, the NLR in the > 18 yrs age group and the dNLR in the transcranial group. Notably, the combination index NLR + dNLR demonstrated the most valuable predictor in all groups.

Conclusions

Preoperative peripheral inflammatory markers, especially WBC, lymphocytes and NLR + dNLR, are promising predictors of postoperative CDI in CPs.

Peer Review reports

Introduction

Craniopharyngioma (CP) is a common benign tumor arising from squamous cell nests in the primitive Rathke’s pouch in the central nervous system. The point prevalence of CPs is approximately 0.5–2.5/1,000,000 in the population [ 1 ]. Accompanied by increased knowledge of CPs and improved endoscopic surgery and radiation therapy, the surgical outcomes for CPs have significantly improved [ 2 , 3 ]. However, the postoperative process in each patient is different due to various postoperative complications, including central diabetes insipidus (CDI) and multiple pituitary hormone deficiencies [ 2 ].

CDI is the most common complication in CPs after surgery mainly resulting from the impairment of hypothalamic posterior pituitary function [ 1 ]. Briefly, postoperative CDI is characterized as a triphasic response of urine volume. The prevalence of postoperative CDI in CPs has been reported elsewhere to be up to 90% [ 4 ]. Although CDI has been well studied for decades, the management of this entity remains controversial. Numerous factors for the prediction of postoperative CDI occurrence have been identified in previous publications, such as patient age, tumor histopathological type, tumor volume, and cerebrospinal fluid leakage [ 5 , 6 ].

A cerebral inflammatory response is often observed and displays a close relationship with tumor prognosis in multiple tumors, including CPs [ 7 , 8 ]. Increasing studies have demonstrated that inflammatory cytokines, including IL-6, IL-8, CXCL1, etc., are closely related to CPs development [ 9 , 10 ]. Although these inflammatory factors have shown predictive value, medical expenses have limited their clinical application. Thus, finding a simpler, readily available, inexpensive method is urgent. Numerous studies have demonstrated that peripheral inflammatory markers and their combinations can be used for monitoring nonspecific inflammatory responses in various pathological situations [ 11 , 12 , 13 ], as well as inflammation monitoring, differential diagnosis, and prognosis prediction of CPs [ 7 , 13 , 14 , 15 ]. However, there remains a lack of comprehensive investigations into whether there are correlations between preoperative peripheral inflammatory markers and postoperative CDI in CPs, which is the purpose of this study.

The clinical data of 267 patients diagnosed with CPs who underwent surgical treatment in the neurosurgery department of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, from January 2016 to October 2021 were retrospectively collected and analyzed. The exclusion criteria were as follows: (1) patients with preoperative CDI; (2) patients who underwent radiotherapy or surgical treatment before; (3) patients with an infectious disease or severe organ dysfunction, such as failure of the lung, heart, liver and kidney; (4) patients with incomplete clinical data; and (5) patients taking diuretics or anti-inflammatory reagents postoperatively.

Data collection and study design

Clinical variables, including sex, age, laboratory examinations and surgical approach, were recorded directly from the medical records. The location of tumors was analysed from magnetic resonance images (MRI) performed by two independent experienced senior neurosurgeons and classified into Q-type, S-type and T-type according to the criteria described in a previous report [ 16 ]. The volumes of tumors were measured with preoperative MRI and the extent of tumor resection was evaluated by postoperative MRI and described as gross total resection (GTR, more than 95% of tumor resected) or subtotal resection (STR, the residual tumor volume was less than 20%) [ 17 , 18 ]. The blood specimens for laboratory examination in our current study were collected from each patient at admission, daily during the first week after the operation and every 2–3 days during the subsequent weeks postoperatively. The preoperative pituitary functions were evaluated with blood tests and patients with hypopituitarism were given preoperative steroid replacement (PSR) treatment until the cortisone supplementation was adequate, and then the surgery was performed. The counts of white blood cells (WBC), neutrophils, lymphocytes, monocytes and platelet (PLT) were directly collected from the peripheral blood tests and the combined inflammatory markers, including NLR (neutrophil-to-lymphocyte ratio; NLR = neutrophils/lymphocytes), dNLR [derived-NLR; dNLR = (WBC-neutrophils)/lymphocytes], MLR (monocyte-to-lymphocyte ratio; MLR = monocytes/lymphocytes) and PLR (platelet -to-lymphocyte ratio; PLR = platelet /lymphocytes), were calculated. CDI was identified by two independently experienced neurosurgeons during treatments for CPs in the first week postoperatively, in terms of the diagnosis described previously [ 19 ]. In general, the laboratory tests used for monitoring CDI include: (1) increased urine output (more than 300 ml for 3 consecutive hours); (2) elevated serum sodium concentration (higher than 145 mmol/l); and (3) reduced urine specific gravity (less than 1.005).

Statistical analysis

All statistical analyses were performed using IBM SPSS statistics software, version 23.0. For the normally and abnormally distributed data, continuous variables were described as the mean ± standard deviation and median (interquartile range, IQR) [M (P25, P75)], respectively. Differences between the two independent groups were compared by Student’s independent t-test and the Mann-Whitney U test. Qualitative data were summarized as counts and percentages and were analyzed using the Chi-square tests or Fisher’s exact tests (expected count ≤ 5). We used multiple logistic regression to identify independent predictors of preoperative peripheral inflammatory markers for postoperative CDI of CPs patients. Meanwhile, to evaluate the predictive value of inflammatory markers on early postoperative CDI, we drew a receiver operator characteristic (ROC) curve. The area under the curve (AUC) was automatically calculated. p  < 0.05 was considered statistically significant.

Patients’ characteristics, peripheral inflammatory markers and CDI data

Of the 208 patients, postoperative CDI was identified in 93 patients (44.7%). Numerous clinical data regarding age, age groups, sex, surgical approach, tumor volume, preoperative pituitary functions, extent of tumor resection and tumor location displayed no significant differences between the CDI and non-CDI groups. The preoperative WBC and neutrophil counts in patients with postoperative CDI were significantly higher than those in patients without CDI ( p  < 0.001 and p  = 0.011, respectively), while the lymphocyte count in patients with CDI was lower ( p  = 0.008). The monocytes and PLT did not show a significant difference between the CDI and non-CDI groups. In addition, the combined inflammatory markers NLR, MLR, dNLR and PLR displayed higher levels in CPs with CDI than in CPs without CDI (all p  < 0.05) (Table  1 ).

Multiple logistic regression analysis showed that the incidence of CDI was increased when preoperative WBC was higher than 6.66 × 10 9 /L ( p  = 0.002) or lymphocyte was lower than 1.86 × 10 9 /L ( p  = 0.022) (Table  2 ).

In addition, although there was no significant difference, compared with patients with hypopituitarism and received PSR, patients with normal pituitary function had a tendency of higher levels of preoperative inflammatory markers including WBC, neutrophil, monocyte, PLT, NLR, MLR and PLR (Additional Table  1 ).

Clinical analysis in different subgroups

To evaluate the impact of preoperative inflammatory markers on postoperative CDI in young and adult patients, we divided participants into two age subgroups. As shown in Table  3 , the WBC, neutrophils and NLR displayed significant differences between the CDI and non-CDI in the > 18 yrs age group (WBC: p  = 0.001, neutrophils: p  = 0.024 and NLR: p  = 0.003), but not in ≤ 18 yrs age group (all p  > 0.05). The MLR was elevated in the ≤ 18 yrs age group with CDI compared with those without CDI ( p  = 0.007). However, the MLR was not evaluated differently in the > 18 yrs age group with and without postoperative CDI. Moreover, the dNLR was closely related to CDI occurrence in both ≤ 18 and > 18 yrs age groups ( p  = 0.014 and p  = 0.011, respectively).

Next, we further explored the preoperative inflammatory markers in patients who underwent surgery using different surgical approaches (Table  4 ). Of 189 patients undergoing the transcranial approach, the WBC, neutrophils, NLR and dNLR were predominantly higher in the CDI group than in the non-CDI group (WBC: p  = 0.001, neutrophils: p  = 0.030, NLR: p  = 0.004 and dNLR: p  = 0.003), while the lymphocytes was lower ( p  = 0.023). In addition, the monocyte, MLR and dNLR were associated with CDI prevalence in the transsphenoidal approach patients (monocytes: p  = 0.017, MLR: p  = 0.011 and dNLR: p  = 0.022).

Furthermore, multiple logistic regression analysis showed that the incidence of CDI was increased when preoperative WBC was higher than 6.39 × 10 9 /L ( p  = 0.035) in > 18 yrs age group, WBC was higher than 6.88 × 10 9 /L ( p  = 0.022) or lymphocyte was lower than 1.85 × 10 9 /L ( p  = 0.029) in transcranial group, respectively (Table  5 ).

ROC curve analysis and predictive values

The corresponding ROC curves and AUC are shown in Table  6 ; Fig.  1 . Among the 208 CP patients, the AUCs were 0.641 (0.565–0.717) for NLR, which demonstrated the highest accuracy in predicting CDI occurrence. The evaluation of paired combinations of these inflammatory makers indicated that NLR + dNLR was the best predictor with an AUC of 0.681 (0.607–0.755) (Fig.  1 a). Further investigation revealed that the best accuracy for predicting CDI was obtained with MLR [AUC: 0.729 (0.580–0.878)] and NLR + dNLR [AUC: 0.731 (0.579–0.883)] in the ≤ 18 yrs age group (Fig.  1 b); NLR [AUC: 0.635 (0.547–0.722)] and NLR + dNLR [AUC: 0.667 (0.582–0.753)] in the > 18 yrs age group (Fig.  1 c); dNLR [AUC: 0.628 (0.545–0.711)] and NLR + dNLR [AUC: 0.661 (0.581–0.742)] in the transcranial approach group (Fig.  1 d); and MLR [AUC: 0.828 (0.643-1.000)] and NLR + dNLR [AUC: 0.889 (0.716-1.000)] in the transsphenoidal approach group (Fig.  1 e). Notably, among all inflammatory markers and their paired combinations, NLR + dNLR might be a discriminative parameter for predicting the prevalence of postoperative CDI.

The predictive value of the preoperative peripheral inflammatory markers. The predictive value of NLR, MLR, dNLR, PLR and their combinations in 208 CP patients ( a ), ≤ 18 yrs age group ( b ), > 18 yrs age group ( c ), transcranial approach group ( d ), and transsphenoidal approach group ( e )

Despite the fact that a long-term survival rate has been achieved in CP patients, the postoperative process is different in each individual, mainly resulting from multiple complications, particularly from CDI and the subsequent disturbance of water and electrolytes [ 19 ]. The incidence rate of CDI after surgery in CPs has been reported in an extensive range of 1.6–93% [ 5 , 6 ]. In our study, postoperative CDI was identified in 93 CP patients (44.7%), revealing a similar incidence to that in most previous reports. Inflammatory markers have been reported to play essential roles in tumor development, tumoral calcification, patient prognosis and the prevalence of postoperative complications including hypopituitarism [ 7 , 20 , 21 ]. However, little is known about the impact of the inflammatory markers on postoperative CDI in CPs.

Chronic inflammation plays pivotal roles in various brain diseases, such as hydrocephalus, cerebral hemorrhage, cerebral infarction, traumatic brain injury and gliomas [ 8 , 22 , 23 ]. Most recently, the inflammatory response in CPs has been well studied [ 9 , 24 , 25 ]. To quantitatively evaluate the inflammatory response, various inflammatory markers, either in cerebrospinal fluid (CSF) or in peripheral blood, have been evaluated in previous publications. The detection of inflammatory markers in CSF could directly reflect the inflammatory response in the brain. However, the clinical application has been limited for the following reasons: (1) CSF acquisition was invasive and inconvenient; (2) the value of inflammatory markers in CSF lacked certain reference intervals; and (3) these markers in CSF could not be detected continuously. Therefore, in our current retrospective study, we explored whether preoperative peripheral inflammatory markers and their combinations were associated with postoperative CDI occurrence in CPs.

The peripheral levels of WBC, neutrophils, lymphocytes and monocytes are identified as general markers of nonspecific inflammatory responses in the central nervous system (CNS). Increasing clinical data have indicated that peripheral WBC, neutrophils and monocytes play proinflammatory roles, while lymphocytes dominantly participate in the anti-inflammatory procedures [ 26 , 27 ]. For example, WBC and neutrophil counts were positively correlated with the malignancy of gliomas [ 28 ]. A higher peripheral blood WBC count and lower lymphocyte count indicated a poor prognosis in glioblastoma patients [ 29 , 30 ]. Moreover, higher levels of preoperative WBC and neutrophils might be potential markers to differentially diagnose papillary CPs [ 7 ]. In our study, we observed that higher WBC (≥ 6.66 × 10 9 /L) or lower lymphocyte (≤ 1.86 × 10 9 /L) in the total CP patients (Tables  1 and 2 ), higher WBC (> 6.39 × 10 9 /L) in the > 18 yrs age patients, higher WBC (> 6.88 × 10 9 /L) or lower lymphocytes (≤ 1.85 × 10 9 /L) in the transcranial approach patients (Tables  3 , 4 and 5 ) were closely associated with the elevated incidence of postoperative CDI. All of the above suggested that the inflammatory response might be closely associated with the prevalence of postoperative CDI in CPs and the WBC and lymphocytes may be the high-risk factors. Moreover, the WBC did not show differences between young patients with CDI and without CDI (Table  3 ). This result might have occurred because of: (1) the different clinical features of pediatric CPs; and (2) the statistical bias from the small young CP population in the current study. In addition, the dual function of monocytes has been demonstrated in various tumors [ 38 ]. However, monocyte function in CPs remains uncertain. Here, we report a relatively lower monocyte count in patients without CDI than in those with CDI after transsphenoidal surgery (Table  4 ). Unfortunately, multiple logistic regression analysis revealed that monocyte was insufficient for increasing the risk of postoperative CDI in patients with CPs (Table  5 ).

Considering the coexistence of pro-inflammation and anti-inflammation in the pathological circumstances of patients, the combined inflammatory markers NLR, dNLR, PLR and MLR have been used to evaluate the balance between pro- and anti-inflammation [ 20 , 31 ]. Moreover, these combined markers were more reproducible and accurate than routine blood cell counts. Higher NLR and MLR were associated with elevated mortality, neurological deterioration and poor outcome in cerebral hemorrhage patients [ 22 , 32 ]. In glioma patients, elevated NLR, PLR and MLR are reliable predictors of a poor outcome [ 8 , 33 ]. A higher NLR was correlated with a poor outcome in CPs [ 15 ]. In addition, PLR played roles in predicting neurological outcomes in comparison to PLT count alone [ 34 ]. Our study found that CP patients with postoperative CDI had higher levels of combined inflammatory markers, including NLR, MLR, dNLR and PLR (Table  1 ), indicating that the balance shifting towards a proinflammatory effect in CPs might result in a higher incidence of CDI. For single inflammatory markers, ROC curve analysis showed that NLR in the total CPs and the > 18 yrs age group, MLR in the ≤ 18 yrs age group and the transsphenoidal group, and dNLR in the transcranial group were the most valuable predictive markers for postoperative CDI occurrence (Table  6 ; Fig.  1 ), indicating that preoperative peripheral neutrophils and monocyte can also mediate the effect of the proinflammatory response on postoperative CDI. Meanwhile, for the paired combination of these four markers, the best predictive performance for CDI was proven in the application of preoperative NLR + dNLR in CPs regardless of age and surgical approach (Table  6 ; Fig.  1 ), suggesting that the combination of preoperative peripheral NLR + dNLR might be used as a promising potential biomarker for postoperative CDI prediction in CP patients.

In addition, a growing number of researchers have reported that the location, removal rate and tumor volume of CPs can affect the occurrence of postoperative CDI [ 35 , 36 ]. However, we did not draw these conclusions in this study. One possible reason of this inconsistency may depend on definition of the extent of tumor resection. Although we defined GTR as more than 95% of tumor resected and defined STR as 80–95% of tumor resected in this study [ 17 , 18 ], majority of the reported investigations were stood on another standard as GTR as 100% and STR as more than 90% [ 37 , 38 , 39 , 40 ]. This may reflect the inconsistency between our study and previously reported statistical results. In addition, for tumor locations, QST classification was used. Previous studies have shown that patients with T-type CPs are more likely to have postoperative sodium metabolism disorder and hypothalamic-pituitary dysfunction [ 16 ]. In this study, only 23 of the 208 patients with CPs had T-type CPs, 17 of the 208 patients with CPs accept STR of the tumor. The small sample size may be the reason why this study did not reach the above conclusions, and further studies with larger sample sizes are needed in the future. Meanwhile, previous studies have suggested that the incidence of postoperative CDI in CP patients is not determined by a single factor, but by a combination of various factors such as GTR/STR removal rate, tumor location, tumor volume, surgical approach, etc., among which whether the pituitary stalk is preserved is particularly important [ 41 , 42 , 43 ]. The lack of further distinction between whether the tumor invaded the pituitary stalk and whether the pituitary stalk was preserved by surgery may be another reason why we were unable to reach the above conclusions. Of note, although there was no statistical significance, the location, removal rate and tumor volume of CPs had a tendency to affect postoperative CDI in this study (Table  1 ). Furthermore, although there was no significant difference, this study found that preoperative PSR might have an effect on preoperative inflammatory markers in patients with CPs, but this effect did not interfere with postoperative CDI (Table  1 and Supplementary Table 1 ). Due to the fact that the dose of corticosteroids could not be extracted from the patient’s medical records, the effect of cortisone dose on preoperative inflammatory markers and postoperative CDI could not be determined. Follow-up studies are needed to further prove whether the use of PSR will affect the stability of the prediction model constructed in this study.

There are still some limitations of this retrospective study. (1) Our study only collected data from a relatively small proportion of CP patients in a single clinical center. Therefore, multicenter studies and larger numbers of patients are needed to verify our preliminary results; (2) the time interval between CPs onset and blood collection are different in each patient, which might have caused bias in data collection due to the differences in the inflammatory response at different stages of disease.

In this study, we observed that preoperative peripheral inflammatory markers, especially WBC, lymphocytes and NLR + dNLR, were promising predictors of postoperative CDI occurrence in CPs. This method of calculating preoperative circulation inflammatory markers can more accurately predict postoperative CDI and provide guidance for perioperative fluid management in CP patients.

Data availability

The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.

Abbreviations

Area under the curve

Magnetic resonance images

Central diabetes insipidus

• Neutrophil-to-lymphocyte ratio

Central nervous system

Platelet-to-lymphocyte ratio

• Craniopharyngioma

Cerebrospinal fluid

Preoperative steroid replacement

Derived-NLR

Receiver operator characteristic

Gross total resection

Subtotal resection

Interquartile range

White blood cells

Monocyte-to-lymphocyte ratio

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This study was funded by the National Natural Science Youth Foundation of China (No.81602204); the funding from the Hubei Province Association of Pathophysiology, China (No.2021HBAP007); and the Scientific Research Initiation Fund for Talent Introduction of Shanxi Bethune Hospital, Shanxi Province, China (2021RC006).

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All authors contributed to the study conception and design. Data collection was performed by J.W., G.W., L.C. and H.Z. Data analysis was performed by K.Z., K.S., X.D. and JW.W. Material preparation was performed by H.N., K.Z. and K.S. The first draft of the manuscript was written by J.W. and all authors commented on previous versions of the manuscript. All authors reviwed the manuscript.

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Wang, J., Wang, G., Cheng, L. et al. Preoperative peripheral inflammatory markers are predictors of postoperative central diabetes insipidus in craniopharyngioma patients: a retrospective study. BMC Cancer 24 , 572 (2024). https://doi.org/10.1186/s12885-024-12324-4

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A Rare Case of Coexisting Psychogenic Polydipsia and Nephrogenic Diabetes Insipidus With Lithium Therapy

Drashti antala.

1 Internal Medicine, AMITA Health Saint Francis Hospital, Evanston, USA

Alisha Sharma

Arjab adhikari, pankaj luitel, sheldon hirsch.

2 Nephrology, AMITA Health Saint Francis Hospital, Evanston, USA

Lithium is a commonly used medication for mood stabilization and a well-known cause of nephrogenic diabetes insipidus (DI). Coexistent psychogenic polydipsia with nephrogenic DI is uncommon, and its management is challenging due to the wide variation in serum sodium based on fluctuations in water intake. Here, we describe the case of a 56-year-old male with psychogenic polydipsia and nephrogenic DI which manifested in wide swings of serum sodium over a short interval. He initially presented with hyponatremia with low urine osmolality consistent with psychogenic polydipsia. His serum sodium began to improve after free water restriction. However, later in the course, he developed an increase in serum sodium levels and polyuria with persistent low urine osmolality consistent with DI.

Introduction

Psychogenic polydipsia is a well-known phenomenon characterized by excessive fluid intake and polyuria. It is found in 11-20% of patients with schizophrenia spectrum disorder [ 1 ]. Lithium is a medication used for mood stabilization in many psychiatric disorders. Nephrogenic diabetes is a known adverse effect associated with lithium therapy. Underlying nephrogenic diabetes insipidus (DI) predisposes patients to urinary water loss and hypernatremia unless patients replace the water loss with an increase in fluid intake. However, in the event of coexisting psychogenic polydipsia, patients can consume enough water to overcome the kidney’s ability to excrete it which can result in hyponatremia. Therefore, a patient with both psychogenic polydipsia and nephrogenic DI can develop either hypernatremia or hyponatremia or swing rapidly from one to the other depending on access to and intake of water.

Case presentation

A 56-year-old male with a history of schizoaffective disorder (diagnosed 20 years ago) presented to the Emergency Department with generalized weakness, fatigue, and fever for a day. His home medications included lithium, amitriptyline, and valproic acid. His vital signs were stable except for a temperature of 103.2°F. A physical examination was remarkable for crackles on the right lower region of the chest. A chest X-ray revealed an infiltrate in the right lower lobe for which he was started on broad-spectrum antibiotics amoxicillin/clavulanate and doxycycline (Figure ​ (Figure1). 1 ). Urine antigens for Legionella and Streptococcus pneumoniae were negative, and mycoplasma immunoglobulin M was not elevated. Labs were remarkable for serum sodium of 127 mmol/L and serum creatinine of 1.48 mg/dL. Serum osmolality was 271 mOsm/kg (reference range: 275-295 mOsm/kg), and urine osmolality was 83 mOsm/kg (reference range: 50-1,200 mOsm/kg) which in the presence of hyponatremia suggested a diagnosis of psychogenic polydipsia. The patient was placed on fluid restriction of 1 L. Repeat labs in eight hours showed sodium of 133 mmol/L and creatinine of 1.08 mg/dL. The patient had a urine output of 2,700 cc over 24 hours, and the next day sodium corrected to 142 mmol/L with fluid restriction. Urine output subsequently increased to 4,400 cc in 24 hours and sodium increased to 145 mmol/L. Once his sodium level increased, his fluid restriction was stopped. He continued to have polyuria with urine output on average 5.5 L/24 hours for the next few days. At this time, despite the rise in serum sodium, his urine osmolality remained low at 103 mOsm/kg which was consistent with DI due to long-standing lithium use. He then maintained serum sodium in the high normal range because of spontaneous water intake. During hospitalization, he underwent informal water deprivation by being started on fluid restriction after which he developed a rise in sodium level and polyuria with low urine osmolality, essentially consistent with DI.

Lithium is one of the oldest mood stabilizers and was approved in 1970 by the Food and Drug Administration [ 2 ]. It remained the first line of management for many years. However, its use has been declining due to its toxicity and narrow therapeutic window [ 2 ]. Lithium is not protein-bound and is freely distributed throughout the body. It is not metabolized, and almost 95% of it is excreted unchanged through the kidney [ 3 ]. The plasma elimination half-life of a single dose ranges from 18 to 20 hours in young adults to approximately 36 hours in elderly patients. The half-life is also affected by the duration of therapy, increasing with the duration the patient has been on the treatment [ 4 ].

Because lithium has the same charge as sodium, its mechanism of filtration and reabsorption is very similar to sodium. It is freely filtered in the kidney, and 70% of it is reabsorbed in the proximal tubule. However, compared to sodium, lithium is less absorbed and delivered more to the distal part of the nephrons [ 5 ]. Overall, 3-10% of lithium is absorbed in the loop of Henle while the remaining is reabsorbed by transcellular uptake via epithelial sodium channel in the distal tubule and collecting duct [ 6 , 5 ]. The serum lithium concentration may not correlate with toxicity. Around 40% of patients who receive lithium therapy develop nephrogenic DI [ 7 ], which can sometimes persist for years after discontinuing lithium [ 8 ], even becoming irreversible after chronic use [ 9 ].

Nephrogenic DI is characterized by an inability of the kidneys to concentrate urine in the presence of antidiuretic hormone causing polyuria [ 10 ]. The aquaporin-2 water channel (AQP2) is expressed in the principal cells and plays an essential role in the reabsorption of water in the collecting ducts via the type 2 vasopressin receptor (V2R)-mediated mechanism. The dysfunction of the AVP-V2R-AQP2 system can result in DI [ 11 ]. Lithium prevents the insertion of cytoplasmic urinary aquaporin (AQP2) to the apical membrane because of which more hypo-osmotic fluid is delivered to the medullary collecting duct resulting in large-volume dilute urine excretion [ 12 ]. An open clinical trial with amiloride showed that impaired concentrating ability in lithium-induced nephrogenic DI was associated with decreased urinary aquaporin excretion, and this association correlated with the duration of lithium exposure [ 12 ].

Our patient had been on lithium for a long time and may have developed chronic nephrogenic DI. The diagnosis was obscured on admission due to hyponatremia. Nephrogenic DI manifested only after water restriction was enforced. He underwent an informal water deprivation test by being started on fluid restriction, after which the serum sodium increased to 145 mEq/L while the urine osmolality remained low (103 mOsm/kg), which is essentially diagnostic of DI. Polyuria tends to decrease in patients with primary polydipsia after eight hours of water deprivation and urine osmolality increases, whereas in DI, polyuria does not improve after water deprivation and serum osmolality remains low, as seen in this patient. The desmopressin test was not done due to concerns regarding cost and clinical correlation. As he was on lithium for a long duration, it was likely nephrogenic DI. Another case has been described of a patient with both psychogenic polydipsia and lithium-induced nephrogenic DI [ 13 ]. Further studies are needed to study whether lithium has any effect on the thirst mechanism and a role in developing primary polydipsia.

Polyuria-polydipsia syndrome describes a clinical syndrome of excessive intake and urinary output, with the usual differential diagnosis including psychogenic polydipsia and central or nephrogenic DI [ 14 ]. In rare cases, when polydipsia and nephrogenic DI coexist, multiple tests are needed at different times in the clinical course to provide a complete analysis. The water deprivation test is the best diagnostic test to differentiate among the different etiologies [ 1 ]. Studies have also found that copeptin, the c-terminal part of the AVP precursor peptide, can serve as a sensitive surrogate marker for AVP. Copeptin has been shown to improve the diagnostic accuracy of water deprivation test and help discriminate between primary polydipsia and DI [ 1 ]. Further studies are needed to accurately determine the objective way of differentiating between the two entities.

Conclusions

Having psychogenic polydipsia and diabetes insipidus at the same time can be challenging to manage due to wide fluctuations in sodium with changes in water intake, and can even prove catastrophic if sodium drops or rises to extreme levels. Because psychogenic polydipsia is widely prevalent in psychiatric patients and many patients are on lithium therapy, this condition may be more common, though very few cases have been reported. Further studies are needed to study this and explore the pathophysiology behind the possible role of lithium in the development of psychogenic polydipsia.

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The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study